The formation of the right and left heart ventricles from the ventricular part of the cardiac tube during embryogenesis

It has been generally assumed that the initial rudiment of the heart ventricle is divided by the longitudinal interventricular septum into the right and left ventricles. This paper presents evidence for the hypothesis that the right and the left ventricles are produced during normal development from different sequentially located segments of the cardiac tube. These segments yielding rudiments of the right and left ventricles could be detected even during early embryogenesis. This hypothesis requires a new explanation for the process of the formation of two separate outlets from the heart ventricles.     

The formation of the right and left heart ventricles from the ventricular portion of the heart tube in embryogenesis

It has been generally assumed that the initial rudiment of the heart ventricle is divided by the longitudinal interventricular septum into the right and left ventricles. This paper presents evidence for the hypothesis that the right and the left ventricles are produced during normal development from different sequentially located segments of the cardiac tube. These segments yielding rudiments of the right and left ventricles could be detected even during early embryogenesis. This hypothesis requires a new explanation for the process of the formation of two separate outlets from the heart ventricles.     

Differential expression of the cardiac ryanodine receptor in normal and arrhythmogenic right ventricular cardiomyopathy canine hearts

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a form of cardiomyopathy characterized by ventricular tachyarrhythmias and a fibrofatty infiltrate that is believed to preferentially affect the right ventricle. Mutations in the cardiac ryanodine receptor (RyR2) gene have been identified in some human families with a unique form of ARVC, ARVC2. Although the RyR2 has significant importance in excitation–contraction coupling across the ventricles, mutations in the gene encoding for it appear to have the greatest impact on the right ventricle in ARVC2. Using a canine model (boxer), the RyR2 protein and message RNA in the right ventricle, left ventricle and interventricular septum from normal dogs and dogs with ARVC were investigated by immunoblotting and real time PCR. The cardiac RyR2 message and protein expression were differentially expressed across the cardiac walls in the normal heart, with the lowest concentration expressed in the right ventricle (P < 0.05). The message and protein expression of the RyR2 were reduced in all chambers in the canine model of ARVC. We propose that the increased susceptibility of the right ventricle to ARVC may be associated with the lower baseline protein concentration of RyR2 in the normal right ventricle compared to the left ventricle and interventricular septum and that all three areas are equally affected in this canine model of ARVC. Using this naturally occurring model of canine ARVC, we may have provided new insights into the pathogenesis of this cardiomyopathy.     

Changes in myosin isozyme expression during cardiac hypertrophy in hyperthyroid rabbits

The myosin isozyme distribution in the left ventricle and in the interventricular septum of rabbits was studied after 3, 7, 11, 14 and 21 days of L-thyroxine (500 micrograms/kg/day) administration. Histochemical procedures were employed to identify V1 and V3 by their Ca2+ ATPase activity and their proportions were quantified through polyacrylamide gel electrophoresis. In the left ventricle, the subepicardium was the first to show the shift from V3 to V1, followed by the subendocardium. The intermediate region became heterogeneous by 11 days and remained so until 21 days. The right subendocardial and the intermediate regions of the interventricular septum were heterogeneous in the normal rabbit and hyperthyroidism resulted in a shift from V3 to V1 in both the right and left subendocardial regions of the septum. Like the left ventricle, the intermediate region of the interventricular septum remained heterogeneous. Localized accumulations of collagen were seen in all regions of the left ventricle and interventricular septum. From these results we conclude that in thyrotoxic myocardial hypertrophy the isozymic shift from V3 to V1 is progressive, region-specific and is directly correlated with the period of hyperthyroidism in the first 2 weeks. Prolonged hyperthyroidism results in localized accumulation of collagen which does not exhibit any regional specificity.     

Tbx5 specifies the left/right ventricles and ventricular septum position during cardiogenesis

Extensive misexpression studies were carried out to explore the roles played by Tbx5, the expression of which is excluded from the right ventricle (RV) during cardiogenesis. When Tbx5 was misexpressed ubiquitously, ventricular septum was not formed, resulting in a single ventricle. In such heart, left ventricle (LV)-specific ANF gene was induced. In search of the putative RV factor(s), we have found that chick Tbx20 is expressed in the RV, showing a complementary fashion to Tbx5. In the Tbx5-misexpressed heart, this gene was repressed. When misexpression was spatially partial, leaving small Tbx5-negative area in the right ventricle, ventricular septum was shifted rightwards, resulting in a small RV with an enlarged LV. Focal expression induced an ectopic boundary of Tbx5-positive and -negative regions in the right ventricle, at which an additional septum was formed. Similar results were obtained from the transient transgenic mice. In such hearts, expression patterns of dHAND and eHAND were changed with definitive cardiac abnormalities. Furthermore, we report that human ANF promoter is synergistically activated by Tbx5, Nkx2.5 and GATA4. This activation was abrogated by Tbx20, implicating the pivotal roles of interactions among these heart-specific factors. Taken together, our data indicate that Tbx5 specifies the identity of LV through tight interactions among several heart-specific factors, and highlight the essential roles of Tbx5 in cardiac development.     

Parasympathetic control of the heart. I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles.

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 +/- 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.     

Anatomic features of postmortem experimental ruptures of the human heart

Comparison of postmortem performed experimental cardiac ruptures with post-infarction lesions reveals uniformity of their localization. The ruptures are found to occur at places of a sharp change in the relief of the cardiac internal surface. These areas should be considered as concentrators of strain, promoting cardiac ruptures. In the left ventricle six concentrators of strain are revealed. They are: the place where the anterior part of the interventricular septum passes into the anterior wall of the left ventricle, the right edge of the papillary muscle, the left edge of the anterior papillary muscle, the left edge of the posterior papillary muscle, the right edge of the posterior papillary muscle, the place where the posterior part of the interventricular septum passes into the posterior wall of the left ventricle. Frequency of the experimental ruptures of the interventricular septum, under loading of the left ventricle, is demonstrated to depend on pressure in the right cardiac part.     

Interventricular heterogeneity in rat heart responses to hypoxia: the tuning of glucose metabolism, ion gradients, and function

The matching of energy supply and demand under hypoxic conditions is critical for sustaining myocardial function. Numerous reports indicate that basal energy requirements and ion handling may differ between the ventricles. We hypothesized that ventricular response to hypoxia shows interventricular differences caused by the heterogeneity in glucose metabolism and expression and activity of ion transporters. Thus we assessed glucose utilization rate, ATP, sodium and potassium concentrations, Na, K-ATPase activity, and tissue reduced:oxidized glutathione (GSH/GSSG) content in the right and left ventricles before and after the exposure of either the whole animals or isolated blood-perfused hearts to hypoxia. The hypoxia-induced boost in glucose utilization was more pronounced in the left ventricle compared with the right one. ATP levels in the right ventricle of hypoxic heart were lower than those in the left ventricle. Left ventricular sodium content was higher, and hydrolytic Na, K-ATPase activity was reduced compared with the right ventricle. Administration of the Na, K-ATPase blocker ouabain caused rapid increase in the right ventricular Na(+) and elimination of the interventricular Na(+) gradients. Exposure of the hearts to hypoxia made the interventricular heterogeneity in the Na(+) distribution even more pronounced. Furthermore, systemic hypoxia caused oxidative stress that was more pronounced in the right ventricle as revealed by GSH/GSSG ratios. On the basis of these findings, we suggest that the right ventricle is more prone to hypoxic damage, as it is less efficient in recruiting glucose as an alternative fuel and is particularly dependent on the efficient Na, K-ATPase function.     

A 2D finite element model of the interventricular septum under normal and abnormal loading

The interventricular septum is the structure that separates the left and right ventricles of the heart. Under normal loading conditions, it is concave to the left ventricle, but under abnormal loading the septum flattens and occasionally inverts. In the past, the septum has frequently been modelled as integral to the left ventricle with the effects of pressure from the right ventricle being ignored. Under abnormal loading, the septum has been described as behaving equivalent to a "flapping sail". There has been no consideration of structural behaviour under these conditions. A 2-D plane stress FE model of the septum was used to investigate the difference in structural behaviour of the septum during diastole between normal and abnormal loading. The biaxial stress patterns that develop are distinctively disparate. Under normal loading, the septum behaves much like a thick-walled cylinder subject to internal and external pressure, with the resulting stresses being circumferential tension and radial compression, both varying with radius. These stresses are very low throughout most of diastole. However, under abnormal loading, the septum behaves in an arch-like fashion, with high compressive stresses almost circumferential in direction, combined with radial compression. We conclude that right ventricular pressures cause bending effects in the wall of the heart, and that under abnormal loading, the compressive stresses that develop in the septum may lead to an understanding of certain, previously unexplained, pathological conditions.     

Intramural chronotopography of myocardial depolarization in the heart ventricles of the pig (Sus scrofa domesticus)

Multichannel synchronous cardioelectrotopography is used to analyze the sequence of myocardial depolarization in the ventricles of the pig heart. Formation of early depolarization areas has been established in subendocardium of interventricular septum and in the base of papillary muscles of the left ventricle; of multiple foci-in the thickness of myocardial walls; of areas of late depolarization-in subepicardium of the dorsolateral side of the left ventricle. In pig heart ventricles, as compared with other ungulates (reindeer and sheep) there are revealed differences in location of areas of the early and late depolarization areas and the breakthrough of excitation wave onto subepicardium.     

A 2D Finite Element Model of the Interventricular Septum Under Normal and Abnormal Loading

Abstract

The interventricular septum is the structure that separates the left and right ventricles of the heart. Under normal loading conditions, it is concave to the left ventricle, but under abnormal loading the septum flattens and occasionally inverts. In the past, the septum has frequently been modelled as integral to the left ventricle with the effects of pressure from the right ventricle being ignored. Under abnormal loading, the septum has been described as behaving equivalent to a “flapping sail”. There has been no consideration of structural behaviour under these conditions. A 2-D plane stress FE model of the septum was used to investigate the difference in structural behaviour of the septum during diastole between normal and abnormal loading. The biaxial stress patterns that develop are distinctively disparate. Under normal loading, the septum behaves much like a thick-walled cylinder subject to internal and external pressure, with the resulting stresses being circumferential tension and radial compression, both varying with radius. These stresses are very low throughout most of diastole. However, under abnormal loading, the septum behaves in an arch-like fashion, with high compressive stresses almost circumferential in direction, combined with radial compression. We conclude that right ventricular pressures cause bending effects in the wall of the heart, and that under abnormal loading, the compressive stresses that develop in the septum may lead to an understanding of certain, previously unexplained, pathological conditions.     

Reflection of distribution of the epicardial ventricular potential on the dog body surface during electrical stimulation of the myocardium]

Electrical pacing of the apex, base, and free wall of the heart right and left ventricles, as well as the left ventricle's interventricular septum revealed that localisation of the ectopic focus determined the sequence of ventricular depolarisation, the site formation, and the pathway of displacement of the areas' positive and negative potentials and their extrema on the thoracic surface. Time of the mutual movement (inversion) of positive and negative zones on the body surface was found to depend on the pacing site in the wall of ventricles.     

金钱豹和猪獾冠状动脉的解剖

为了阐明金钱豹(Panthera pardus)和猪獾(Arctonyx collaris)心冠状动脉的分支分布特征及血供情况,为心脏生物学及动物学研究提供结构基础资料,利用血管铸型和组织透明方法观察研究了金钱豹与猪獾心左、右冠状动脉的分支分布.结果表明,金钱豹和猪獾的心均由左右冠状动脉营养.金钱豹左冠状动脉分为室间隔支、前降支和旋支.前降支又分出左室上支、左室中支和左室下支.右冠状动脉沿途分出右室前支、右室后下支和右室后上支.猪獾左冠状动脉分为前降支和旋支.前降支又分出室间隔支和左室前支,旋支又分出左缘支和左室后支.其右冠状动脉沿途分出右室前支、右缘支和右室后支.金钱豹和猪獾心的室间隔均由发自左冠状动脉的独立的室间隔支营养,二者左右冠状动脉在膈壁的分布属于均衡型.     

Impaired left ventricular filling due to right-to-left ventricular interaction in patients with pulmonary arterial hypertension

The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 +/- 13 vs. 41 +/- 10 ml/m(2) (P < 0.001), 46 +/- 14 vs. 61 +/- 14 ml/m(2) (P < 0.001), and 216 +/- 90 vs. 541 +/- 248 ml/s (P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume (r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate (r = 0.64, P < 0.001) and left ventricular end-diastolic volume (r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.     

Morphological study of the atrioventricular conduction system and Purkinje fibers in yak

We studied the morphology of the atrioventricular conduction system (AVCS) and Purkinje fibers of the yak. Light and transmission electron microscopy were used to study the histological features of AVCS. The distributional characteristics of the His‐bundle, the left bundle branch (LBB), right bundle branch (RBB), and Purkinje fiber network of yak hearts were examined using gross dissection, ink injection, and ABS casting. The results showed that the atrioventricular node (AVN) of yak located in the right side of interatrial septum and had a flattened ovoid shape. The AVN of yak is composed of the slender, interweaving cells formed almost entirely of the transitional cells (T‐cells). The His‐bundle extended from the AVN, and split into left LBB and RBB at the crest of the interventricular septum. The LBB descended along the left side of interventricular septum. At approximately the upper 1/3 of the interventricular septum, the LBB typically divided into three branches. The RBB ran under the endocardium of the right side of interventricular septum, and extended to the base of septal papillary muscle, passed into the moderator band, crossed the right ventricular cavity to reach the base of anterior papillary muscle, and divided into four fascicles under the subendocardial layer. The Purkinje fibers in the ventricle formed a complex spatial network. The distributional and cellular component characteristics of the AVCS and Purkinje fibers ensured normal cardiac function.