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Ali Khoshbaten

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I am so keen in knowing about the role of scientific researches on human life style. I am also trying to improve human life style somehow to make life much more suitable and comfortable for everyone. Therefore I do continue researches on this subject “better life style, better living “

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Papers by Ali Khoshbaten

The Inhibition of Carrageenan Induced Inflammation by Atropine and Substance P Antagonist in Rabbit

Trauma monthly, 2017

The pathophysiology of acute joint inflammation remains unclear. Evidence is available to suggest... more The pathophysiology of acute joint inflammation remains unclear. Evidence is available to suggest a neurally mediated component to the inflammatory process. Acute joint inflammation in the rat knee, induced by intra-articular injection of 2% carrageenan, was reduced by 44% in animals whose knee had previously been injected with 1% capsaicin, while chronic joint denervation produced a 37% reduction. These results indicate a significant neurogenic component in this model of acute joint inflammation. Substance P may be the mediator of this response as intra-articular injection of this agent provoked an acute inflammatory response. Pretreatment of the test knee with the substance P antagonist d-Pro4,d-Trp7 9 10-SP(4-11), however, resulted in a 93% reduction of the inflammatory response to carrageenan. This unexpectedly large effect suggests that this substance P antagonist blocks both neurogenic and non-neurogenic mediators of inflammation. Sympathetic efferent fibres innervating the knee joint were not found to contribute to the neurogenic component of the inflammatory process.

Effects of Fundermol Ointment on Second Degree Burns in Rats

Trauma monthly, 2000

Investigation of circulatory and tissue ACE activity during development of lead-induced hypertension

Toxicology Letters, Nov 1, 2004

Prolonged exposure to low levels of lead causes systemic hypertension. Several mechanisms have be... more Prolonged exposure to low levels of lead causes systemic hypertension. Several mechanisms have been proposed to explain lead-induced hypertension. Recently, the etiological role of the renin-angiotensin system (RAS) has been investigated in this context. This study assessed the alterations of circulatory and tissue angiotensin converting enzyme (ACE) activity during development of lead induced hypertension. Male rats were divided to two main groups: lead-treated animals which received lead acetate, 100 ppm, in drinking water for 2, 4, 6, and 8 weeks and a control group given distilled water. The ACE activity in serum and tissues was analyzed by HPLC. The blood pressure gradually increased in correlation with lead exposure with time. The study also revealed significant elevation of local and serum ACE activity in the early phase of lead treatment; however, chronic lead exposure suppressed ACE activity in serum and tissues. These results emphasize the etiological role of ACE activity in the early phase of lead-induced hypertension.

CARDIOVASCULAR RESPONSES TO HYPERCAPNIA AND VARYING LEVELS OF ARTERIAL pH IN THE ANESTHETIZED CAT

The Medical Journal of The Islamic Republic of Iran, Feb 10, 1996

Effects of acute hypercapnia on the cardiovascular system (CYS) were studied in the anesthetized ... more Effects of acute hypercapnia on the cardiovascular system (CYS) were studied in the anesthetized cat. After surgery the animal was exposed to a gas mixture of 12% CO2 and 25% O2 in nitrogen, and hypercapnia with low levels of arterial pH (pHa) was produced for 20 minutes. In the second run the same level of hypercapnia was induced by ventilating the same cat from the above gas mixture but pHa was kept normal by a slow and continuous infusion of 1HAM (0.5 mM/ kg/min). Results of this study showed that hypercapnia increased aortic flow and induced peripheral vasodilation. Hypercapnia produced tachycardia in the presence of arterial acidosis whereas in its absence this response reversed to bradycardia. Hypercapnia increased mean arterial blood pressure (Pa) by 20% during low pHa, whereas this increase was only 10% in the absence of arterial acidosis. Therefore, it is concluded that hypercapnia in conjunction with arterial acidosis has a much stronger stimulatory influence on the CYS via different arterial chemoreceptors.

The Effect of Obidoxime on Reversal or Prevention of Paraoxon-Induced Changes in the Function of Chick Biventer Cervices Nerve-Muscle Preparation

Journal of Military Medicine, Oct 15, 2004

Study of the effects of intra-nucleus accumbens shell injections of alcohlic extract of Crocus sativus on the acquisition and expression of morphine-induced conditioned place preference in rats

Introduction: Previous studies have shown the effects of water extract of Crocus sativus on the e... more Introduction: Previous studies have shown the effects of water extract of Crocus sativus on the euphoric and behavioral properties of morphine in mice. In the present study, the effects of intra-accumbal administration of alcohol extract of Crocus sativus stigma on the acquisition and expression of morphine-induced conditioned place preference (CPP) in male Wistar rats (250-300 g) were investigated. Methods: This study was conducted on 78 male rats that were divided in 13 groups (n = 6 each group). In a pilot study, different doses of morphine (0.5, 1, 2.5, 5, 7.5 and 10 mg/kg) were injected to the animals for evaluation of the drug's ability to induce place preference. In the second phase of the experiments, the extract of the C. sativus (1, 5 and 10 µg/rat), was administered into the nucleus accumbens shell during or after induction of morphine CPP. Then, CPP was tested in the animals. One-way Analysis of Variance (ANOVA) was preformed for statistical procedure. Results: Administration of morphine (0.5, 1, 5, 7.5 and 10 mg/kg), increased the time spent in the compartment paired with morphine (i.e. conditioned place preference-CPP) (P<0.05). This increase reached significance at the dose of 10 mg/kg. Injection of the same doses of the extract (1, 5 and 10 µg/rat) 5 min before morphine (10 mg/kg) administration, caused a decrease in the time spent in drug-paired side in doses 5 and 10 µg/rat of the extract (P < 0.0001). In addition, injection of the plant extract (1, 5 and 10 µg/rat) in to the shell part of nucleus accumbens in the test day to the animals that received morphine (10 mg/kg) in the conditioning days decreased the expression of morphine CPP in the animals. This effect was statistically significant for doses 5 and 10 µg/rat of the extract (P < 0.0001). Conclusion: It may be concluded that intra-accumbens shell compartment injection of the alcoholic extract of C sativus can inhibit the acquisition and expression of morphine-induced CPP and then shift it to the aversive state in rats.

Effect of ascorbic acid supplementation on nitric oxide metabolites and systolic blood pressure in rats exposed to lead

Indian Journal of Pharmacology, 2010

A comparative study on the effect of L-arginine and morphine in induction of conditioned place preference in rat

Physiology and Pharmacology, Apr 10, 2003

It has been shown that L-arginine like the abused drugs could release dopamine from meso-cortico-... more It has been shown that L-arginine like the abused drugs could release dopamine from meso-cortico-limbic system. The purpose of the present study was to compare the effect of L-arginine with morphine as a standard abuse drug in the induction of conditioned place preference (CPP) in rat. For this purpose, male Wistar Rats (250-300 g) were used in the experiments. Five days after surgical cannulation in the ventral tegmental area (VTA), different doses of L-arginine, L-NAME or morphine were injected and conditioned biased ...

Effects of Subacute Lead Acetate Administration on Nitric Oxide and Cyclooxygenase Pathways in Rat Isolated Aortic Ring

Pharmacological Research, Jul 1, 2002

Low level exposure to lead increases blood pressure in human and rats. In this study, we investig... more Low level exposure to lead increases blood pressure in human and rats. In this study, we investigated the contribution of the nitric oxide (NO) and cyclooxygenase pathways of aortic rings of 28-day lead-treated and control rats, to the responsiveness to phenylephrine and acetylcholine. There were no differences in phenylephrine contractions between the two groups. N(ω)-nitro-l-Arginine-methyl ester (l-NAME), a NO synthase inhibitor, caused attenuation in contraction response to phenylephrine in the aortic rings of the lead-treated rats, while endothelium-denudation caused attenuation in those of controls. This may be due to either endothelium-derived vasoconstrictor(s) (such as reactive oxygen species or endothelins) or a source of NO in smooth muscle cells. There is a left-shift in acetylcholine relaxation response. Indomethacin incubation caused a left-shift in relaxation response to acetylcholine in controls but without any effect on lead-treated ones. Indomethacin incubation caused attenuation in contraction to phenylephrine in both groups. The relaxation response to sodium nitroprusside is not different between the two groups, suggesting that smooth muscle relaxation component is intact. However, the relaxation response to glyceryl trinitrate is impaired in aortic rings of lead-treated rats. It can be concluded that NO and cyclooxygenase pathways are altered in aortic rings of lead-treated rats, with possible involvement of endothelium-derived vasoconstrictors.

The effect of high intensity interval training on cardioprotection against ischemia-reperfusion injury in wistar rats

PubMed, 2015

The aims of the present study were to determine whether short term high intensity interval traini... more The aims of the present study were to determine whether short term high intensity interval training (HIIT) could protect the heart against ischemia reperfusion (IR) injury; and if so, to evaluate how long the exercise-associated protection can be lasted. Sixty-three rats were randomly assigned into sedentary (n = 15), sham (n = 7), and exercise groups (n = 41). Rats in the exercise groups performed 5 consecutive days of HIIT on treadmill: 5 min warm up with 50 % VO2max, 6×2 min with 95-105 % VO2max (about 40 to 45 m/min), 5×2 min recovery with 65-75 % VO2max (about 28 to 32 m/min), and 3 min cool down with 50 % VO2max, all at 0 % grade. Animals exposed to an in vivo cardiac IR surgery, performed at days 1, 7, and 14 following the final exercise session. Ischemia-induced arrhythmias, myocardial infarct size (IS), plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities were measured in all animals. Compared to sedentary rats, exercised animals sustained less IR injury as evidenced by a lower size of infarction and lower levels of LDH and CK at day one and day 7 post exercise. In comparison of sedentary group, IS significantly decreased in EX-IR1 and EX-IR7 groups (50 and 35 %, respectively), but not in EX-IR14 group (19 %). The exercise-induced cardioprotection disappeared 14 days following exercise cessation. There were no significant changes in ischemia-induced arrhythmia between exercised and sedentary rats. The results clearly demonstrate that HIIT protects the heart against myocardial IR injury. This protective effect can be sustained for at least one week following the cessation of the training.

Prolonged and intermittent normobaric hyperoxia induce different degrees of ischemic tolerance in rat brain tissue

Brain Research, Jun 1, 2007

Prior prolonged oxygen exposure is associated with some protection against ischemia-reperfusion (... more Prior prolonged oxygen exposure is associated with some protection against ischemia-reperfusion (IR) injury to rat brain tissue, but also with toxic effects. We sought to compare the magnitude of protection offered by prolonged and intermittent oxygen pretreatments against IR injury to the rat brain. Rats were divided into four experimental groups, each of 21 animals. The first two were exposed to 95% inspired (normobaric hyperoxia, NBHO) for 4 h/day for 6 consecutive days (intermittent NBHO) or for 24 continuous hours (prolonged NBHO). The second two groups acted as controls were exposed to 21% oxygen. After 24 h, they were subjected to 60 min of right middle cerebral artery occlusion (MCAO) followed by 24 h of reperfusion. The animals were sacrificed for assessment of infarct volume, brain edema, and blood-brain barrier (BBB) permeability, respectively. Prolonged and intermittent NBHO pretreatment reduced infarct volume by 63.3% and 73.7%, respectively, when compared to the respective NBNO groups. Intermittent NBHO (when compared to intermittent NBNO) also reduced the post-ischemic increment of brain water content significantly (81.53+/-0.8%, vs. 80.12+/-0.79%) and Evans Blue extravasation (7.49+/-2.89+/-g/g tissue vs. 3.9+/-0.79 microg/g tissue, P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001), while prolonged NBHO had no significant effect on brain water content (81.69+/-1.16% vs. 80.74+/-0.94%) and EB extravasations (6.48+/-2.42 microg/g tissue vs. 4.31+/-1.07 microg/g tissue). Intermittent hyperoxia had relatively more significant effects on brain edema and BBB protection. Although preconditioning with both prolonged and intermittent oxygen exposure protects rat brain tissue against IR injury, the intermittent hyperoxia could have relatively more protective effects in this regard.

The Role of Endothelium Derived Relaxation Factor (Edrf) in Vascular Tone Control

Razi Journal of Medical Sciences, Sep 15, 1996

Acute lead exposure and contraction of rat isolated aorta induced by D1-dopaminergic and alpha-adrenergic drugs

Archives of Iranian Medicine, Apr 1, 2006

Background/Objective: In the present study, the effect of acute lead exposure in the presence and... more Background/Objective: In the present study, the effect of acute lead exposure in the presence and absence of dopamine or alpha (α)-adrenoceptor agents on contractile response of rat isolated thoracic aorta was studied. Methods: Male Wistar rats were used in all experiments. Thoracic aorta was carefully removed, cleaned, and cut into 2-mm thick rings. The rings were mounted for measurement of isometric contractions in a tissue bath containing 10 mL of Kreb's solution at 37-38 ○ C. The following drugs were used: lead chloride, dopamine, phenylephrine, prazosin, clonidine, yohimbine, and SCH23390. One-way analysis of variance (ANOVA) and Student's t-test were used for statistical analyses. P < 0.05 was considered significant. Results: The α1-adrenoceptor antagonist (prazosin), α2-adrenoceptor antagonist (yohimbine), or dopamine D1 receptor antagonist (SCH23390), did not elicit any response. Combination of lead with dopamine, phenylephrine, or clonidine did not show any potentiation. SCH23390, prazosin, and yohimbine decreased the contraction induced by lead. SCH23390 decreased the contraction induced by dopamine, or lead plus dopamine. Prazosin reduced the contraction induced by phenylephrine or lead plus phenylephrine. Yohimbine attenuated the response induced by clonidine or lead plus clonidine. Conclusion: α1, α2, and D1 dopamine receptor mechanisms could have a role in lead-induced contraction.

Sarcoplasmic reticulum Ca2+ uptake and release in aortic smooth muscle of genetically and renal hypertensive rats

Journal of Molecular and Cellular Cardiology, May 1, 1992

Morphine Self-Administration in Rat

Trauma monthly, 2000

Praoxon-induced changes in the function of chicken biventer cervices nerve-muscle preparation and the reversal of such changes by pralidoxime

Iranian Journal of Pharmaceutical Research, Nov 20, 2010

Acute Effect of Burn Trauma to Small Skin Areas on Myocardial Ischemia-Reperfusion Injury in Rat

Introduction: It has been reported that traumas such as transverse abdominal incision before myoc... more Introduction: It has been reported that traumas such as transverse abdominal incision before myocardial ischemia result in a significantly decreased infarct size. This phenomenon is named remote preconditioning of trauma. Since small skin burn is one of most common traumas, the effect of this injury on ischemia-induced arrhythmias and infarct size was investigated in a rat model of ischemia-reperfusion injury. Methods: Twenty-four male Wistar rats were randomly assigned to 3 groups. In burn and sham groups, less than 1% of total body surface area of the dorsal skin was exposed to 100˚C and 37 ˚C water, respectively. In ischemic preconditioning group, rats were exposed to one cycle of ischemia (5 min) and reperfusion (10 min). Ischemiareperfusion injury was induced with occlusion and release of left coronary artery for 30 and 120 min, respectively. Infarct size was measured using triphenyl tetrazolium chloride staining and arrhythmias were assessed in accordance with Lambeth conventions. Results: Infarct size was significantly reduced in ischemic preconditioning group compared with the sham group (27 ± 2% vs. 50 ± 5%; P < 0.01). Infarct size in the burn group was not significantly reduced. Irreversible ventricular fibrillation was 50% of all ventricular fibrillation in the burn group, while it was 25% in the sham group, however, this difference was not significant. Conclusion: Acute minor coetaneous burn has neither protective nor harmful for the rat myocardial ischemiareperfusion injury.

Attenuation of vasoconstrictor response of knee joint blood vessels to (αl- adrenoceptor activation during chronic monoarthritis in rat: The role of nitric oxide

Physiology and Pharmacology, Oct 10, 2000

In vivo preconditioning with normobaric hyperoxia induces ischemic tolerance partly by triggering tumor necrosis factor-α converting enzyme/tumor necrosis factor-α/nuclear factor-κB

Neuroscience, May 1, 2008

Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in brain... more Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced BIT, and to explore the putative roles of tumor necrosis factor-␣ (TNF-␣) converting enzyme (TACE), TNF-␣, and nuclear factor-B (NF-B) activation in mediating this effect. Two core experimental protocols were applied to rats (experiments 1 [E1] and 2 [E2] respectively). E1 rodents comprised six subgroups, breathing room air (RA; O 2 ‫,)%12؍‬ or 95% oxygen (HO) for 4, 8, 16 h (4RA, 8RA, 16RA and 4HO, 8HO, 16HO respectively). E2 rodents were divided into subgroups, exposed to 95% inspired HO for 4 h/day for six consecutive days (intermittent hyperoxia, InHO) or for 24 continuous hours (prolonged hyperoxia, PrHO). Each of these had a control group exposed to 21% oxygen in the same chamber. Twenty-four hours after pretreatment, each group was randomly divided to receive 60 min right middle cerebral artery occlusion (MCAO-operated), sham-operation (without MCAO), or no operation (intact). After 24 h reperfusion, neurologic deficit score (NDS), brain water content, Evans Blue extravasation (as a marker of blood-brain barrier permeability), TACE expression, serum TNF-␣, and phosphor-B␣ levels were assessed in all animals, and infarct volume in the MCAO-operated subgroups. E1: Compared with the control (RA) group, infarct volume was reduced by 58.6% and 64.4% in 16 h and 24 h respectively. NDS and Evans Blue extravasation was also reduced in 16 h and 24 h. There was no statistical difference among 4 h and 8 h. E2: Preconditioning with prolonged and intermittent HO decreased NDS, infarct volume and upregulated TACE and increased phosphor-B␣ and serum TNF-␣ level significantly. Although further studies are needed to clarify the mechanisms of brain ischemic tolerance, InHO and PrHO may partly exert their effects via triggering TACE/TNF-␣/NF-B.

Decreased response of rat knee joint blood vessels to phenylephrine in chronic inflammation: involvement of nitric oxide

Experimental Physiology, 2000

The effect of chronic inflammation induced by Freund&#39;s Complete Adjuvant (FCA) on rat art... more The effect of chronic inflammation induced by Freund&#39;s Complete Adjuvant (FCA) on rat articular blood vessels and knee joint diameter was investigated. Blood flow changes in response to phenylephrine (an 1-adrenoceptor agonist) in FCA-treated and contralateral knee joints were studied over a 40 day period, using the laser Doppler flowmetery (LDF) technique. Unilateral injection of FCA (0.2 ml) increased the injected knee diameter on all days examined post-injection (P &lt; 0.001) and its maximum increase (53 +/- 2 %) was reached on day 3. After this, the diameter decreased gradually but did not return to its initial value. In control animals, topical application of 10-13-10- 7 mol phenylephrine onto the exposed joint capsule decreased blood flow dose dependently (11. 1 +/- 4.4 to 58.2 +/- 4.5 %, respectively, P &lt; 0.001). Unilateral injection with FCA attenuated the phenylephrine response in both ipsilateral and contralateral knees compared with the response of control animals (5.2 +/- 1.6 to 48.3 +/- 6.1 % and 1.9 +/- 2.2 to 45. 3 +/- 5.6 %, respectively, P &lt; 0.05). The reduction persisted for 3 weeks after FCA injection (ipsilateral for 21 days; contralateral for 30 days, P &lt; 0.001). Subsequently the response returned towards normal. To avoid the influence of 2-adrenoceptors, yohimbine (an 2-adrenoceptor antagonist) was injected (0.5 mg kg-1, I.P.) 30 min before phenylephrine application. Yohimbine blocked the vasoconstrictor effect of 10-10-10-7 mol clonidine (an 2-adrenoceptor agonist, topical application) by 44-67.7 % inhibition, respectively (P &lt; 0.001). Prazosin (an 1-adrenoceptor antagonist, 0.1 mg kg-1, I.P.) blocked the vasoconstrictor effect of phenylephrine (10-10-10-7 mol, topical application) effectively (42 to 69.8 % inhibition, respectively, P &lt; 0.001). To assess the role of nitric oxide (NO) on the observed responses, N G-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) was applied topically (0.2 micromol) 5 min before phenylephrine application. L-NAME application at 7 and 14 days after FCA injection potentiated the vasoconstrictor response in the FCA-treated knee (P &lt; 0.001) but had no significant effect on the contralateral knee. Blood pressure monitoring during phenylephrine, clonidine and L-NAME administration indicated that topical application of the drugs had no significant effect on the systemic blood pressure. These findings indicate that the vasoconstrictor response to phenylephrine was decreased in chronic inflammation and increased NO production could be involved.

The Inhibition of Carrageenan Induced Inflammation by Atropine and Substance P Antagonist in Rabbit

Trauma monthly, 2017

The pathophysiology of acute joint inflammation remains unclear. Evidence is available to suggest... more The pathophysiology of acute joint inflammation remains unclear. Evidence is available to suggest a neurally mediated component to the inflammatory process. Acute joint inflammation in the rat knee, induced by intra-articular injection of 2% carrageenan, was reduced by 44% in animals whose knee had previously been injected with 1% capsaicin, while chronic joint denervation produced a 37% reduction. These results indicate a significant neurogenic component in this model of acute joint inflammation. Substance P may be the mediator of this response as intra-articular injection of this agent provoked an acute inflammatory response. Pretreatment of the test knee with the substance P antagonist d-Pro4,d-Trp7 9 10-SP(4-11), however, resulted in a 93% reduction of the inflammatory response to carrageenan. This unexpectedly large effect suggests that this substance P antagonist blocks both neurogenic and non-neurogenic mediators of inflammation. Sympathetic efferent fibres innervating the knee joint were not found to contribute to the neurogenic component of the inflammatory process.

Effects of Fundermol Ointment on Second Degree Burns in Rats

Trauma monthly, 2000

Investigation of circulatory and tissue ACE activity during development of lead-induced hypertension

Toxicology Letters, Nov 1, 2004

Prolonged exposure to low levels of lead causes systemic hypertension. Several mechanisms have be... more Prolonged exposure to low levels of lead causes systemic hypertension. Several mechanisms have been proposed to explain lead-induced hypertension. Recently, the etiological role of the renin-angiotensin system (RAS) has been investigated in this context. This study assessed the alterations of circulatory and tissue angiotensin converting enzyme (ACE) activity during development of lead induced hypertension. Male rats were divided to two main groups: lead-treated animals which received lead acetate, 100 ppm, in drinking water for 2, 4, 6, and 8 weeks and a control group given distilled water. The ACE activity in serum and tissues was analyzed by HPLC. The blood pressure gradually increased in correlation with lead exposure with time. The study also revealed significant elevation of local and serum ACE activity in the early phase of lead treatment; however, chronic lead exposure suppressed ACE activity in serum and tissues. These results emphasize the etiological role of ACE activity in the early phase of lead-induced hypertension.

CARDIOVASCULAR RESPONSES TO HYPERCAPNIA AND VARYING LEVELS OF ARTERIAL pH IN THE ANESTHETIZED CAT

The Medical Journal of The Islamic Republic of Iran, Feb 10, 1996

Effects of acute hypercapnia on the cardiovascular system (CYS) were studied in the anesthetized ... more Effects of acute hypercapnia on the cardiovascular system (CYS) were studied in the anesthetized cat. After surgery the animal was exposed to a gas mixture of 12% CO2 and 25% O2 in nitrogen, and hypercapnia with low levels of arterial pH (pHa) was produced for 20 minutes. In the second run the same level of hypercapnia was induced by ventilating the same cat from the above gas mixture but pHa was kept normal by a slow and continuous infusion of 1HAM (0.5 mM/ kg/min). Results of this study showed that hypercapnia increased aortic flow and induced peripheral vasodilation. Hypercapnia produced tachycardia in the presence of arterial acidosis whereas in its absence this response reversed to bradycardia. Hypercapnia increased mean arterial blood pressure (Pa) by 20% during low pHa, whereas this increase was only 10% in the absence of arterial acidosis. Therefore, it is concluded that hypercapnia in conjunction with arterial acidosis has a much stronger stimulatory influence on the CYS via different arterial chemoreceptors.

The Effect of Obidoxime on Reversal or Prevention of Paraoxon-Induced Changes in the Function of Chick Biventer Cervices Nerve-Muscle Preparation

Journal of Military Medicine, Oct 15, 2004

Study of the effects of intra-nucleus accumbens shell injections of alcohlic extract of Crocus sativus on the acquisition and expression of morphine-induced conditioned place preference in rats

Introduction: Previous studies have shown the effects of water extract of Crocus sativus on the e... more Introduction: Previous studies have shown the effects of water extract of Crocus sativus on the euphoric and behavioral properties of morphine in mice. In the present study, the effects of intra-accumbal administration of alcohol extract of Crocus sativus stigma on the acquisition and expression of morphine-induced conditioned place preference (CPP) in male Wistar rats (250-300 g) were investigated. Methods: This study was conducted on 78 male rats that were divided in 13 groups (n = 6 each group). In a pilot study, different doses of morphine (0.5, 1, 2.5, 5, 7.5 and 10 mg/kg) were injected to the animals for evaluation of the drug's ability to induce place preference. In the second phase of the experiments, the extract of the C. sativus (1, 5 and 10 µg/rat), was administered into the nucleus accumbens shell during or after induction of morphine CPP. Then, CPP was tested in the animals. One-way Analysis of Variance (ANOVA) was preformed for statistical procedure. Results: Administration of morphine (0.5, 1, 5, 7.5 and 10 mg/kg), increased the time spent in the compartment paired with morphine (i.e. conditioned place preference-CPP) (P<0.05). This increase reached significance at the dose of 10 mg/kg. Injection of the same doses of the extract (1, 5 and 10 µg/rat) 5 min before morphine (10 mg/kg) administration, caused a decrease in the time spent in drug-paired side in doses 5 and 10 µg/rat of the extract (P < 0.0001). In addition, injection of the plant extract (1, 5 and 10 µg/rat) in to the shell part of nucleus accumbens in the test day to the animals that received morphine (10 mg/kg) in the conditioning days decreased the expression of morphine CPP in the animals. This effect was statistically significant for doses 5 and 10 µg/rat of the extract (P < 0.0001). Conclusion: It may be concluded that intra-accumbens shell compartment injection of the alcoholic extract of C sativus can inhibit the acquisition and expression of morphine-induced CPP and then shift it to the aversive state in rats.

Effect of ascorbic acid supplementation on nitric oxide metabolites and systolic blood pressure in rats exposed to lead

Indian Journal of Pharmacology, 2010

A comparative study on the effect of L-arginine and morphine in induction of conditioned place preference in rat

Physiology and Pharmacology, Apr 10, 2003

It has been shown that L-arginine like the abused drugs could release dopamine from meso-cortico-... more It has been shown that L-arginine like the abused drugs could release dopamine from meso-cortico-limbic system. The purpose of the present study was to compare the effect of L-arginine with morphine as a standard abuse drug in the induction of conditioned place preference (CPP) in rat. For this purpose, male Wistar Rats (250-300 g) were used in the experiments. Five days after surgical cannulation in the ventral tegmental area (VTA), different doses of L-arginine, L-NAME or morphine were injected and conditioned biased ...

Effects of Subacute Lead Acetate Administration on Nitric Oxide and Cyclooxygenase Pathways in Rat Isolated Aortic Ring

Pharmacological Research, Jul 1, 2002

Low level exposure to lead increases blood pressure in human and rats. In this study, we investig... more Low level exposure to lead increases blood pressure in human and rats. In this study, we investigated the contribution of the nitric oxide (NO) and cyclooxygenase pathways of aortic rings of 28-day lead-treated and control rats, to the responsiveness to phenylephrine and acetylcholine. There were no differences in phenylephrine contractions between the two groups. N(ω)-nitro-l-Arginine-methyl ester (l-NAME), a NO synthase inhibitor, caused attenuation in contraction response to phenylephrine in the aortic rings of the lead-treated rats, while endothelium-denudation caused attenuation in those of controls. This may be due to either endothelium-derived vasoconstrictor(s) (such as reactive oxygen species or endothelins) or a source of NO in smooth muscle cells. There is a left-shift in acetylcholine relaxation response. Indomethacin incubation caused a left-shift in relaxation response to acetylcholine in controls but without any effect on lead-treated ones. Indomethacin incubation caused attenuation in contraction to phenylephrine in both groups. The relaxation response to sodium nitroprusside is not different between the two groups, suggesting that smooth muscle relaxation component is intact. However, the relaxation response to glyceryl trinitrate is impaired in aortic rings of lead-treated rats. It can be concluded that NO and cyclooxygenase pathways are altered in aortic rings of lead-treated rats, with possible involvement of endothelium-derived vasoconstrictors.

The effect of high intensity interval training on cardioprotection against ischemia-reperfusion injury in wistar rats

PubMed, 2015

The aims of the present study were to determine whether short term high intensity interval traini... more The aims of the present study were to determine whether short term high intensity interval training (HIIT) could protect the heart against ischemia reperfusion (IR) injury; and if so, to evaluate how long the exercise-associated protection can be lasted. Sixty-three rats were randomly assigned into sedentary (n = 15), sham (n = 7), and exercise groups (n = 41). Rats in the exercise groups performed 5 consecutive days of HIIT on treadmill: 5 min warm up with 50 % VO2max, 6×2 min with 95-105 % VO2max (about 40 to 45 m/min), 5×2 min recovery with 65-75 % VO2max (about 28 to 32 m/min), and 3 min cool down with 50 % VO2max, all at 0 % grade. Animals exposed to an in vivo cardiac IR surgery, performed at days 1, 7, and 14 following the final exercise session. Ischemia-induced arrhythmias, myocardial infarct size (IS), plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities were measured in all animals. Compared to sedentary rats, exercised animals sustained less IR injury as evidenced by a lower size of infarction and lower levels of LDH and CK at day one and day 7 post exercise. In comparison of sedentary group, IS significantly decreased in EX-IR1 and EX-IR7 groups (50 and 35 %, respectively), but not in EX-IR14 group (19 %). The exercise-induced cardioprotection disappeared 14 days following exercise cessation. There were no significant changes in ischemia-induced arrhythmia between exercised and sedentary rats. The results clearly demonstrate that HIIT protects the heart against myocardial IR injury. This protective effect can be sustained for at least one week following the cessation of the training.

Prolonged and intermittent normobaric hyperoxia induce different degrees of ischemic tolerance in rat brain tissue

Brain Research, Jun 1, 2007

Prior prolonged oxygen exposure is associated with some protection against ischemia-reperfusion (... more Prior prolonged oxygen exposure is associated with some protection against ischemia-reperfusion (IR) injury to rat brain tissue, but also with toxic effects. We sought to compare the magnitude of protection offered by prolonged and intermittent oxygen pretreatments against IR injury to the rat brain. Rats were divided into four experimental groups, each of 21 animals. The first two were exposed to 95% inspired (normobaric hyperoxia, NBHO) for 4 h/day for 6 consecutive days (intermittent NBHO) or for 24 continuous hours (prolonged NBHO). The second two groups acted as controls were exposed to 21% oxygen. After 24 h, they were subjected to 60 min of right middle cerebral artery occlusion (MCAO) followed by 24 h of reperfusion. The animals were sacrificed for assessment of infarct volume, brain edema, and blood-brain barrier (BBB) permeability, respectively. Prolonged and intermittent NBHO pretreatment reduced infarct volume by 63.3% and 73.7%, respectively, when compared to the respective NBNO groups. Intermittent NBHO (when compared to intermittent NBNO) also reduced the post-ischemic increment of brain water content significantly (81.53+/-0.8%, vs. 80.12+/-0.79%) and Evans Blue extravasation (7.49+/-2.89+/-g/g tissue vs. 3.9+/-0.79 microg/g tissue, P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.001), while prolonged NBHO had no significant effect on brain water content (81.69+/-1.16% vs. 80.74+/-0.94%) and EB extravasations (6.48+/-2.42 microg/g tissue vs. 4.31+/-1.07 microg/g tissue). Intermittent hyperoxia had relatively more significant effects on brain edema and BBB protection. Although preconditioning with both prolonged and intermittent oxygen exposure protects rat brain tissue against IR injury, the intermittent hyperoxia could have relatively more protective effects in this regard.

The Role of Endothelium Derived Relaxation Factor (Edrf) in Vascular Tone Control

Razi Journal of Medical Sciences, Sep 15, 1996

Acute lead exposure and contraction of rat isolated aorta induced by D1-dopaminergic and alpha-adrenergic drugs

Archives of Iranian Medicine, Apr 1, 2006

Background/Objective: In the present study, the effect of acute lead exposure in the presence and... more Background/Objective: In the present study, the effect of acute lead exposure in the presence and absence of dopamine or alpha (α)-adrenoceptor agents on contractile response of rat isolated thoracic aorta was studied. Methods: Male Wistar rats were used in all experiments. Thoracic aorta was carefully removed, cleaned, and cut into 2-mm thick rings. The rings were mounted for measurement of isometric contractions in a tissue bath containing 10 mL of Kreb's solution at 37-38 ○ C. The following drugs were used: lead chloride, dopamine, phenylephrine, prazosin, clonidine, yohimbine, and SCH23390. One-way analysis of variance (ANOVA) and Student's t-test were used for statistical analyses. P < 0.05 was considered significant. Results: The α1-adrenoceptor antagonist (prazosin), α2-adrenoceptor antagonist (yohimbine), or dopamine D1 receptor antagonist (SCH23390), did not elicit any response. Combination of lead with dopamine, phenylephrine, or clonidine did not show any potentiation. SCH23390, prazosin, and yohimbine decreased the contraction induced by lead. SCH23390 decreased the contraction induced by dopamine, or lead plus dopamine. Prazosin reduced the contraction induced by phenylephrine or lead plus phenylephrine. Yohimbine attenuated the response induced by clonidine or lead plus clonidine. Conclusion: α1, α2, and D1 dopamine receptor mechanisms could have a role in lead-induced contraction.

Sarcoplasmic reticulum Ca2+ uptake and release in aortic smooth muscle of genetically and renal hypertensive rats

Journal of Molecular and Cellular Cardiology, May 1, 1992

Morphine Self-Administration in Rat

Trauma monthly, 2000

Praoxon-induced changes in the function of chicken biventer cervices nerve-muscle preparation and the reversal of such changes by pralidoxime

Iranian Journal of Pharmaceutical Research, Nov 20, 2010

Acute Effect of Burn Trauma to Small Skin Areas on Myocardial Ischemia-Reperfusion Injury in Rat

Introduction: It has been reported that traumas such as transverse abdominal incision before myoc... more Introduction: It has been reported that traumas such as transverse abdominal incision before myocardial ischemia result in a significantly decreased infarct size. This phenomenon is named remote preconditioning of trauma. Since small skin burn is one of most common traumas, the effect of this injury on ischemia-induced arrhythmias and infarct size was investigated in a rat model of ischemia-reperfusion injury. Methods: Twenty-four male Wistar rats were randomly assigned to 3 groups. In burn and sham groups, less than 1% of total body surface area of the dorsal skin was exposed to 100˚C and 37 ˚C water, respectively. In ischemic preconditioning group, rats were exposed to one cycle of ischemia (5 min) and reperfusion (10 min). Ischemiareperfusion injury was induced with occlusion and release of left coronary artery for 30 and 120 min, respectively. Infarct size was measured using triphenyl tetrazolium chloride staining and arrhythmias were assessed in accordance with Lambeth conventions. Results: Infarct size was significantly reduced in ischemic preconditioning group compared with the sham group (27 ± 2% vs. 50 ± 5%; P < 0.01). Infarct size in the burn group was not significantly reduced. Irreversible ventricular fibrillation was 50% of all ventricular fibrillation in the burn group, while it was 25% in the sham group, however, this difference was not significant. Conclusion: Acute minor coetaneous burn has neither protective nor harmful for the rat myocardial ischemiareperfusion injury.

Attenuation of vasoconstrictor response of knee joint blood vessels to (αl- adrenoceptor activation during chronic monoarthritis in rat: The role of nitric oxide

Physiology and Pharmacology, Oct 10, 2000

In vivo preconditioning with normobaric hyperoxia induces ischemic tolerance partly by triggering tumor necrosis factor-α converting enzyme/tumor necrosis factor-α/nuclear factor-κB

Neuroscience, May 1, 2008

Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in brain... more Recent studies suggest that intermittent and prolonged normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced BIT, and to explore the putative roles of tumor necrosis factor-␣ (TNF-␣) converting enzyme (TACE), TNF-␣, and nuclear factor-B (NF-B) activation in mediating this effect. Two core experimental protocols were applied to rats (experiments 1 [E1] and 2 [E2] respectively). E1 rodents comprised six subgroups, breathing room air (RA; O 2 ‫,)%12؍‬ or 95% oxygen (HO) for 4, 8, 16 h (4RA, 8RA, 16RA and 4HO, 8HO, 16HO respectively). E2 rodents were divided into subgroups, exposed to 95% inspired HO for 4 h/day for six consecutive days (intermittent hyperoxia, InHO) or for 24 continuous hours (prolonged hyperoxia, PrHO). Each of these had a control group exposed to 21% oxygen in the same chamber. Twenty-four hours after pretreatment, each group was randomly divided to receive 60 min right middle cerebral artery occlusion (MCAO-operated), sham-operation (without MCAO), or no operation (intact). After 24 h reperfusion, neurologic deficit score (NDS), brain water content, Evans Blue extravasation (as a marker of blood-brain barrier permeability), TACE expression, serum TNF-␣, and phosphor-B␣ levels were assessed in all animals, and infarct volume in the MCAO-operated subgroups. E1: Compared with the control (RA) group, infarct volume was reduced by 58.6% and 64.4% in 16 h and 24 h respectively. NDS and Evans Blue extravasation was also reduced in 16 h and 24 h. There was no statistical difference among 4 h and 8 h. E2: Preconditioning with prolonged and intermittent HO decreased NDS, infarct volume and upregulated TACE and increased phosphor-B␣ and serum TNF-␣ level significantly. Although further studies are needed to clarify the mechanisms of brain ischemic tolerance, InHO and PrHO may partly exert their effects via triggering TACE/TNF-␣/NF-B.

Decreased response of rat knee joint blood vessels to phenylephrine in chronic inflammation: involvement of nitric oxide

Experimental Physiology, 2000

The effect of chronic inflammation induced by Freund&#39;s Complete Adjuvant (FCA) on rat art... more The effect of chronic inflammation induced by Freund&#39;s Complete Adjuvant (FCA) on rat articular blood vessels and knee joint diameter was investigated. Blood flow changes in response to phenylephrine (an 1-adrenoceptor agonist) in FCA-treated and contralateral knee joints were studied over a 40 day period, using the laser Doppler flowmetery (LDF) technique. Unilateral injection of FCA (0.2 ml) increased the injected knee diameter on all days examined post-injection (P &lt; 0.001) and its maximum increase (53 +/- 2 %) was reached on day 3. After this, the diameter decreased gradually but did not return to its initial value. In control animals, topical application of 10-13-10- 7 mol phenylephrine onto the exposed joint capsule decreased blood flow dose dependently (11. 1 +/- 4.4 to 58.2 +/- 4.5 %, respectively, P &lt; 0.001). Unilateral injection with FCA attenuated the phenylephrine response in both ipsilateral and contralateral knees compared with the response of control animals (5.2 +/- 1.6 to 48.3 +/- 6.1 % and 1.9 +/- 2.2 to 45. 3 +/- 5.6 %, respectively, P &lt; 0.05). The reduction persisted for 3 weeks after FCA injection (ipsilateral for 21 days; contralateral for 30 days, P &lt; 0.001). Subsequently the response returned towards normal. To avoid the influence of 2-adrenoceptors, yohimbine (an 2-adrenoceptor antagonist) was injected (0.5 mg kg-1, I.P.) 30 min before phenylephrine application. Yohimbine blocked the vasoconstrictor effect of 10-10-10-7 mol clonidine (an 2-adrenoceptor agonist, topical application) by 44-67.7 % inhibition, respectively (P &lt; 0.001). Prazosin (an 1-adrenoceptor antagonist, 0.1 mg kg-1, I.P.) blocked the vasoconstrictor effect of phenylephrine (10-10-10-7 mol, topical application) effectively (42 to 69.8 % inhibition, respectively, P &lt; 0.001). To assess the role of nitric oxide (NO) on the observed responses, N G-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) was applied topically (0.2 micromol) 5 min before phenylephrine application. L-NAME application at 7 and 14 days after FCA injection potentiated the vasoconstrictor response in the FCA-treated knee (P &lt; 0.001) but had no significant effect on the contralateral knee. Blood pressure monitoring during phenylephrine, clonidine and L-NAME administration indicated that topical application of the drugs had no significant effect on the systemic blood pressure. These findings indicate that the vasoconstrictor response to phenylephrine was decreased in chronic inflammation and increased NO production could be involved.