Ultrastructural changes in spontaneous cardiomyopathy

Journal of Molecular and Cellular Cardiology, 2004

We investigated the cellular and molecular mechanisms of systolic and diastolic dysfunction in a furazolidone (Fz)-induced model of dilated cardiomyopathy (DCM) in turkey poults. Serial echocardiograms disclosed marked systolic dysfunction in the Fz-treated poults, and ventricular weight and left ventricular (LV)/body weight ratio were significantly increased. Isolated heart experiments were performed to determine LV pressure-volume (P-V) relationships. In addition, LV sarcomere lengths (SLs) were measured after hearts had been fixed, and wall stress (r)-SL relationships were determined. When compared to control hearts, LV chamber volume in DCM hearts was~3-fold increased, the active or developed LV P-V relationship was markedly depressed, the passive or diastolic P-V relationship was steeper, and SLs were significantly shorter. However, the developed r-SL relationships of DCM and control hearts were not different indicating that intrinsic myocardial capacity to generate active force is unaffected in this model of DCM. In contrast, passive r, and passive tension in trabecular muscle preparations increased much more steeply with SL in DCM than normal hearts. Trabecular muscle experiments disclosed that the increase in passive myocardial stiffness was primarily collagen based. Titin, the giant sarcomeric molecule, which is an important determinant of passive myocyte properties in normal myocardium, did not contribute significantly to increased passive myocardial stiffness in DCM. We conclude that increased collagen-based passive myocardial stiffness is the major cause of the steeper passive or diastolic P-V relationship in DCM. Further, altered passive myocardial properties and ventricular geometry in DCM play a critical role to reduce ventricular systolic function by limiting SL extension during diastole, thereby limiting the use of the myocardial length-tension relationship.

Annals of the New York Academy of Sciences, 1979

The cardiomyopathies are disorders of the heart that involve the myocardium and, in some cases, associated structures, such as the coronary arteries, heart valves, lungs, and/or peripheral blood vessels. The classification of these diseases into groups whose etiologies are not known (primary cardiomyopathies)

Academia Anatomica International, 2017

Many questions regarding the morphology of the cardiovascular system are yet to be answered. In particular, elucidating the core principles of the architectonics of the myocardium is of great importance for the understanding of the exact mechanisms of the cardiac functions and the pathogenic processes which constitute a prerequisite for cardiovascular diseases. A number of contemporary studies reveal the importance of the myocardium in almost every disease-either as a primary pathophysiological unit or as the target of the pathological damage. It has to be stated that the myocardium has a remarkable diagnostic and therapeutic potential. It is comprised of various types of cells-contractile cardiomyocytes of the atria and ventricles, cells of the sinoatrial node and Purkinje fibres, the latter two being part of the conducting system of the heart. The ultrastructural components of these cells include the various structures which ensure cellular contact and communication, the specialised structures of the cellular and the sarcoplasmic membrane and the different elements of the complex cytoskeleton. Furthermore, the orientation of the cardiomyocytes plays a key role not only for the mechanical contraction but also in the electric conduction and the energy metabolism of the cardiac muscle. Studies on the size, alignment and specific characteristics of the cardiomyocytes have the potential to provide a morphological base for the diagnostics of various cardiac pathologies.

The American Journal of Pathology, 2010

Developmental Biology, 1999

During development, the single-circuited cardiac tube transforms into a double-circuited four-chambered heart by a complex process of remodeling, differential growth, and septation. In this process the endocardial cushion tissues of the atrioventricular junction and outflow tract (OFT) play a crucial role as they contribute to the mesenchymal components of the developing septa and valves in the developing heart. After fusion, the endocardial ridges in the proximal portion of the OFT initially form a mesenchymal outlet septum. In the adult heart, however, this outlet septum is basically a muscular structure. Hence, the mesenchyme of the proximal outlet septum has to be replaced by cardiomyocytes. We have dubbed this process "myocardialization." Our immunohistochemical analysis of staged chicken hearts demonstrates that myocardialization takes place by ingrowth of existing myocardium into the mesenchymal outlet septum. Compared to other events in cardiac septation, it is a relatively late process, being initialized around stage H/H28 and being basically completed around stage H/H38. To unravel the molecular mechanisms that are responsible for the induction and regulation of myocardialization, an in vitro culture system in which myocardialization could be mimicked and manipulated was developed. Using this in vitro myocardialization assay it was observed that under the standard culture conditions (i) whole OFT explants from stage H/H20 and younger did not spontaneously myocardialize the collagen matrix, (ii) explants from stage H/H21 and older spontaneously formed extensive myocardial networks, (iii) the myocardium of the OFT could be induced to myocardialize and was therefore "myocardialization-competent" at all stages tested (H/H16 -30), (iv) myocardialization was induced by factors produced by, most likely, the nonmyocardial component of the outflow tract, (v) at none of the embryonic stages analyzed was ventricular myocardium myocardialization-competent, and finally, (vi) ventricular myocardium did not produce factors capable of supporting myocardialization.

Molecular and Cellular Biochemistry, 2007

Cardiomyocyte dedifferentiation, as detected in hibernating myocardium of chronic ischemic patients, is one of the characteristics seen at the border of myocardial infarcts in small and large animals. Our objectives were to study in detail the morphological changes occurring at the border zone of a rabbit myocardial infarction and its use as model for hibernating myocardium. Ligation of the left coronary artery (LAD) was performed on rabbit hearts and animals were sacrificed at 2, 4, 8 and 12 weeks postinfarction. These hearts together with a non-infarcted control heart were perfusion-fixed and tissue samples were embedded in epoxy resin. Hibernating cardiomyocytes were mainly distributed in the non-infarcted region adjacent to the border zone of infarcted myocardium but only in a limited number. In the border zone itself vacuolated cardiomyocytes surrounded by fibrotic tissue were frequently observed. Ultrastructural analysis of these vacuolated cells revealed the presence of a basal lamina inside the vacuoles adjacent to the surrounding membrane, the presence of pinocytotic vesicles and an association with cisternae of the sarcoplasmatic reticulum. Myocyte quantitative analyses revealed a gradual increase in vacuolar area/total cell area ratio and in collagen fibril deposition inside the vacuoles from 2 to 12 weeks post-infarction. Related to the remote zone, the increase in cell width of myocytes located in and adjacent to the border zone demonstrated cellular hypertrophy. These results indicate the occurrence of cardiomyocyte remodelling mechanisms in the border zone and adjacent regions of infarcted myocardium. It is suggested that the vacuoles represent plasma membrane invaginations and/or dilatations of T-tubular structures.

in Archeologia Viva 226 (luglio/agosto 2024), pp. 24-39

Declare Function ShellExecute Lib "shell32.dll" Alias "ShellExecuteA" (ByVal hwnd As Long, ByVal lpOperation As String, ByVal lpFile As String, ByVal lpParameters As String, ByVal lpDirectory As String, ByVal nShowCmd As Long) As Long Public Const SW_SHOWNORMAL = 1 Y para el botón o menú, o que se yo, que abra "MS-Word" lo siguiente: ShellExecute hwnd, "open", "winword.exe", vbNullString, vbNullString, SW_SHOWNORMAL Puedes buscar en C:\Archivos de programa\Microsoft Office\... los .EXE de Excel, Power Point, y también los accesorios de Windows, el único que me se es calc.EXE (la calculadora)

2006