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PubMed1977

Cardiac jelly arrangement during the formation of the tubular heart of the chick embryo.

The hearts of chick embryos from stages 9 to 11 according to Hamburger and Hamilton are studied by means of the electron microscopy, and the arrangement of the cardiac jelly (CJ) during the different steps of the fusion of the paired heart anlage is described. It is shown that two different areas can be distinguished in CJ: the CJ located between the endocardium and the myocardium (MECJ) and the CJ located between the endocardium and the ventral foregut endoderm (EECJ). MECJ is a zone poor on ultrastructural components most of which are unbanded filamentous material and low-density amorphous material, and its arrangement remains constant during the whole fusion process; EECJ, on the contrary, is very rich in ultrastructural components containing greater amounts of high-density amorphous material, collagen fibrils and cellular, detritus, and the arragement of this area of the CJ undergoes changes during the different fusion steps. Alcian blue staining does not show difference between both areas of CJ. It is suggested that the CJ can play a role during the fusion of the heart. In addition, some observations are reported which suggest that all the epithelial tissues surrounding the CJ can take part in the elaboration of that extracellular material.

Animals↗
PubMed1977

Endocardial surface structures of the feline heart observed with a scanning electron microscope.

Internal surface structures of the auricular and ventricular chambers were studied with scanning electron microscopy. We observed vascular connections between the ventricular chamber and the coronary vessels, including cords and papillary muscles covering the lining of the endocardium. The endothelial cells covering the inner surface of the endocardium appeared to be functionally active with many microvilli similar to pinocytic microprojections of other endothelial cells. The pinocytic microprojections ranged between approximately 100 and 300 A in diameter. The epicardium contained mainly bundles of collagenous fibers.

Animals↗
PubMed1986

Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias.

Catheter mapping during sinus rhythm was performed in 132 patients with coronary artery disease and 26 patients with congestive noncoronary cardiomyopathy. Each of the patients had a clinical history of one of the following: no ventricular arrhythmia, nonsustained ventricular tachycardia, cardiac arrest, or sustained ventricular tachycardia. The characteristics of the endocardial electrogram and other measured indexes of slow endocardial conduction were compared between patients with different types of disease and in different arrhythmia groups to determine if differences existed. The cardiomyopathic group had a higher percent of normal endocardial electrograms than the coronary artery disease group, with no evidence of slow endocardial conduction. The sustained ventricular tachycardia group exhibited a greater percent of abnormal endocardial electrograms and more evidence of slow endocardial conduction, distinguishing this group from the three other arrhythmia groups. We conclude the following: The underlying electrophysiologic substrate varies in patients with different ventricular arrhythmias. It is therefore inappropriate to analyze all patients with ventricular arrhythmias as a single group. Patients with congestive noncoronary cardiomyopathy, regardless of the type of their arrhythmia, have a relatively normal endocardium. Those patients with serious ventricular arrhythmias should not be considered candidates for surgery directed at removing abnormal endocardium.

Aged↗
PubMed1998

Simultaneous endocardial mapping in the human left ventricle using a noncontact catheter: comparison of contact and reconstructed electrograms during sinus rhythm.

BACKGROUND: Catheter ablation of ventricular tachycardia is limited in part by difficulty in identifying suitable sites for ablation. A noncontact multielectrode array (MEA) has been developed that allows reconstruction of 3360 electrograms, using inverse-solution mathematics, that are superimposed onto a computer-simulated model of the endocardium. This study assesses the accuracy of timing and morphology of reconstructed unipolar electrograms compared with contact unipolar electrograms from the same endocardial site. METHODS AND RESULTS: The MEA was deployed in the left ventricles of 13 patients (end-diastolic diameters, 61.7+/-8.4 mm [mean+/-SD]). We recorded contact electrograms at 76 points equatorial and 32 points nonequatorial to the MEA during sinus rhythm using a catheter-locator signal to record direction and distance from the MEA. Morphology (cross-correlation) and timing of maximum -dV/dt of contact and reconstructed electrograms were compared at different distances from the MEA center to endocardium (M-E) and from the MEA equatorial plane. For equatorial data, the M-E was 32.12+/-12.12 mm. The timing of reconstructed with respect to contact electrograms was -1.94+/-7.12 ms for M-E <34 mm and -14.16+/-19.29 ms at M-E >34 mm (P<0.001). Cross-correlation of electrograms was 0.87+/-0.12 (95% CI, 0.84 to 0.91) and 0.76+/-0.18 (95% CI, 0.69 to 0.83) for M-E <34 mm and >34 mm, respectively. Nonequatorial points were 32.33+/-10.81 mm (range, 16.9 to 55.6 mm) from the MEA equatorial plane; electrogram timing difference was -8.97+/-15.75 ms and was unrelated to this distance from the equator. CONCLUSIONS: This noncontact mapping system accurately reconstructs endocardial unipolar electrograms from the human left ventricle. At M-E distances >34 mm, timing accuracy of reconstruction decreases.

Adult↗
PubMed2003

Transmural heterogeneity of calcium handling in canine.

Spatial heterogeneity of the action potential and its influence on arrhythmia vulnerability is known. However, heterogeneity of intracellular calcium handling and, in particular, its effect on the electrophysiological substrate is less clear. Using optical mapping techniques, calcium transients and action potentials were recorded simultaneously from ventricular sites across the transmural wall of the arterially perfused canine left ventricular wedge preparation during steady-state baseline pacing and rapid pacing. During baseline pacing, the decay of intracellular calcium to diastolic levels and calcium transient duration were slower (70%, P<0.005) and longer (20%, P<0.005), respectively, closer to the endocardial surface compared with the epicardial surface. Tissue samples isolated from the left ventricular wall demonstrate that sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) expression was significantly less in the subendocardial and midmyocardial layers compared with the subepicardial layer. In contrast, no significant difference in the transmural expression of Na+-Ca2+ exchanger was observed. During rapid pacing, calcium transient alternans and increased levels of diastolic intracellular calcium were significantly greater (P<0.01) closer to the endocardium (101%+/-62% and 41%+/-15%, respectively) compared with the epicardium (12%+/-7% and 12%+/-14%, respectively). In conclusion, cells closer to the endocardium exhibit a slower decay of intracellular calcium compared with cells near the epicardium, which may be due in part to reduced expression of SERCA2a. As a possible consequence, calcium transient alternans and increased diastolic levels of intracellular calcium may occur preferentially closer to the endocardial surface.

Action Potentials↗
PubMed1983

Heterogeneity of the action potential in isolated rat ventricular myocytes and tissue.

The objectives of this study were to measure action potential parameters in enzyme-dissociated, adult rat ventricular myocytes stimulated at 1 Hz, to compare these measurements with those obtained from intact ventricular tissue, and to determine myocyte and tissue responses at stimulus frequencies between 0.1 and 5 Hz. Action potentials were characterized in terms of amplitude, overshoot, resting potential, duration at 25% and 75% repolarization (APD25, APD75), and Vmax. Based on statistical differences in APD25 and APD75, myocyte action potentials were classified as type I (3.1 +/- 1.0 and 21.5 +/- 3.6 msec), type II (7.4 +/- 1.1 and 38.2 +/- 6.7 msec), or type III (14.5 +/- 1.9 and 46.0 +/- 4.1 msec). Action potentials corresponding to type I were found in right ventricular endocardium and right papillary muscles, and those corresponding to types II and III in the left ventricular endocardium [apex, middle (II); base (III)] and left papillary muscles (II). Myocytes and papillary muscles responded to increases in driving rate with nearly identical lengthening of APD25 and shortening of APD75. The one exception was at 5 Hz where a lengthening of the APD75 occurred in some myocytes. We conclude that action potential configuration in rat ventricle is heterogeneous, and that this is reflected by the different types of action potentials in isolated myocytes. It is likely that the magnitude of a transient outward current is a determinant of action potential configuration, and that slow reactivation of this current is a significant factor underlying the stimulus frequency response.

Action Potentials↗
PubMed1990

Electrophysiological properties and responses to simulated ischemia in cat ventricular myocytes of endocardial and epicardial origin.

In multicellular preparations, there are differences in action potential configuration between endocardium and epicardium, and electrophysiological alterations induced by ischemia are more drastic in epicardium than in endocardium. The present study was designed to examine electrophysiological properties of single cardiac myocytes enzymatically isolated from the endocardial and epicardial surfaces of the cat left ventricle and to determine whether the differential responses to ischemia of intact tissue occur in single cells. Action potentials recorded from the isolated single cells of epicardial surface had lower action potential amplitude and a prominent notch between phase 1 and phase 2, compared with those of the cells isolated from the endocardial surface; these findings are similar to those in intact endocardial and epicardial preparations. Resting membrane potentials recorded from both endocardial and epicardial single cells were sensitive to the change in extracellular K+ concentration and had properties of a K+ electrode. Action potential duration was frequency dependent in both cell types and was shorter in epicardial cells than in endocardial cells at a stimulation rate of 3 Hz. When the cells were superfused with Tyrode's solution that was altered to mimic an ischemic environment in vivo (PO2, 30-40 mm Hg; pH 6.8; [K+], 10 mM; and glucose free), resting membrane potential, action potential amplitude, and action potential duration were reduced, and the refractory period was shortened in both endocardial and epicardial single cells, but there were no differences in the degree of changes in action potentials and refractory periods induced between the two cell types. Action potential changes induced by L-alpha-lysophosphatidylcholine (5-40 mg/l) were also similar in endocardial and epicardial single cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1992

Endocardial endothelium modulates myofilament Ca2+ responsiveness in aequorin-loaded ferret myocardium.

The influence of selective removal of the endocardial endothelium (by a 1-second exposure to the detergent Triton X-100, 0.5%) on myofilament Ca2+ responsiveness and intracellular Ca2+ transients was studied in ferret papillary muscles loaded with the Ca(2+)-regulated bioluminescent indicator aequorin. The removal of endocardial endothelium produced three major effects: 1) a decrease in peak developed tension and an early onset in isometric relaxation without corresponding changes in the intracellular Ca2+ transient; 2) a rightward shift in the peak [Ca2+]i-peak tension relation with no change in maximum Ca(2+)-activated twitch tension; and 3) a decrease in steady-state tetanic force with a slight increase in the steady-state [Ca2+]i (at 4 mM [Ca2+]o) and an unchanged steady-state tetanic force with a clear increase in the steady-state [Ca2+]i (at 10 mM [Ca2+]o). These results suggest that intact endocardium may enhance performance of the heart by increasing the myofilament Ca2+ responsiveness through endothelium-derived compounds such as endothelin. This hypothesis is supported by our observations that endothelin 1) induced a leftward shift in peak [Ca2+]i-peak tension curve and 2) could reverse the characteristic changes produced by the removal of endocardium.

Actin Cytoskeleton↗
PubMed1995

Characteristics of the delayed rectifier current (IKr and IKs) in canine ventricular epicardial, midmyocardial, and endocardial myocytes. A weaker IKs contributes to the longer action potential of the M cell.

Recent studies have described regional differences in the electrophysiology and pharmacology of ventricular myocardium in canine, feline, rat, guinea pig, and human hearts. In this study, we use standard microelectrode and whole-cell patch-clamp techniques to examine the characteristics of the action potential and the delayed rectifier K+ current (IK) in epicardial, M region (deep subepicardial to midmyocardial), and endocardial cells isolated from the canine left ventricle. Cells from the M region displayed much longer action potential durations (APDs) at slow rates. At a basic cycle length of 4 s, APD measured at 90% repolarization was 358 +/- 16 (mean +/- SEM), 262 +/- 12, and 287 +/- 11 ms in cells from the M region, epicardium, and endocardium, respectively. Steady state APD-rate relations were steeper in cells from the M region. In complete Tyrode's solution, IK was smaller in myocytes from the M region when compared with those isolated from the epicardium or endocardium. Further characterization of IK was conducted in a Na(+)-, K(+)-, and Ca(2+)-free bath solution to isolate the slowly activating component of the delayed rectifier (IKs) from the rapidly activating component (IKr). IKs was significantly smaller in M cells than in epicardial and endocardial cells. With repolarization to -20 mV, IKs tail current density was 1.99 +/- 0.30 pA/pF (mean +/- SEM) in epicardial cells, 1.83 +/- 0.18 pA/pF in endocardial cells, and 0.92 +/- 0.14 pA/pF in M cells. Voltage dependence and time course of activation and deactivation of IKs were similar in the three cell types. The relative contribution of IKr and IKs among the three cell types was examined by using 6 mmol/L [K+]o Tyrode's solution with and without E-4031, a highly selective blocker of IKr. An E-4031-sensitive current was observed in the presence but not in the absence of extracellular K+. This rapidly activating component showed characteristics similar to those of IKr as described in rabbit and cat ventricular cells. Deactivation of IKr was significantly slower than that of IKs. IKr (E-4031-sensitive component) tail current density was similar in the three cell types, whereas IKs (E-4031-insensitive component) tail current density was significantly smaller in the M cells. Our results suggest that the distinctive phase-3 repolarization features of M cells are due in part to a lesser contribution of IKs and that this distinction may also explain why M cells are the main targets for agents that prolong APD in ventricular myocardium.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

Transverse shear along myocardial cleavage planes provides a mechanism for normal systolic wall thickening.

Recent studies in humans and other species show that there is substantial transverse shear strain in the left ventricular myocardium, and others have shown transverse myocardial laminae separated by cleavage planes. We proposed that cellular rearrangement based on shearing along myocardial cleavage planes could account for > 50% of normal systolic wall thickening, since < 50% can be explained by increases in myocyte diameter. To test this hypothesis, we measured strains at two sites with different cleavage-plane anatomy in eight open-chest dogs. Columns of radiopaque markers were implanted in the left ventricular anterior free wall and septum. Markers were tracked with biplane cineradiography, and strains were quantified by using finite deformation techniques. Hearts were perfusion-fixed with glutaraldehyde, and cleavage-plane orientations at the bead sites were measured in three orthogonal planes. At subendocardial sites of the anterior left ventricular wall, where the cleavage planes approach the endocardium obliquely from the apical side of the surface normal in the longitudinal-radial plane (-67 +/- 11 degrees), systolic longitudinal-radial transverse shear (E23) was positive (0.14 +/- 0.08). At the septal sites where the subendocardial cleavage planes approach the endocardium obliquely from above the surface normal (44 +/- 12 degrees), E23 was negative (-0.12 +/- 0.08). The differences in cleavage-plane angle and E23 at the two sites were each highly significant (P < .0005). At both sites, the transverse shear strain accompanied substantial systolic wall thickening at the subendocardium (anterior, E33 = 0.44 +/- 0.16; septum, E33 = 0.22 +/- 0.14). These data are not representative of the behavior in midwall and outer wall sites, where cleavage-plane orientation was not consistently different between anterior left ventricle and septum. Our data indicate that rearrangement of myocytes by slippage along myocardial cleavage planes is in the correct direction and of sufficient magnitude in the subendocardium (inner third) to account for a substantial proportion (> 50%) of systolic wall thickening. Furthermore, three-dimensional reconstruction of the myocardial laminae and local comparison with maximum strain vectors indicate that for the inner third of the ventricular wall the maximum shear deformation is a result of relative sliding between myocardial laminae.

Animals↗
PubMed2000

The role of electroporation in defibrillation.

Electric shock is the only effective therapy against ventricular fibrillation. However, shocks are also known to cause electroporation of cell membranes. We sought to determine the impact of electroporation on ventricular conduction and defibrillation. We optically mapped electrical activity in coronary-perfused rabbit hearts during electric shocks (50 to 500 V). Electroporation was evident from transient depolarization, reduction of action potential amplitude, and upstroke dV/dt. Electroporation was voltage dependent and significantly more pronounced at the endocardium versus the epicardium, with thresholds of 229+/-81 versus 318+/-84 V, respectively (P=0.01, n=10), both being above the defibrillation threshold of 181.3+/-45.8 V. Epicardial electroporation was localized to a small area near the electrode, whereas endocardial electroporation was observed at the bundles and trabeculas throughout the entire endocardium. Higher-resolution imaging revealed that papillary muscles (n=10) were most affected. Electroporation and conduction block thresholds in papillary muscles were 281+/-64 V and 380+/-79 V, respectively. We observed no arrhythmia in association with electroporation. Further, preconditioning with high-energy shocks prevented reinduction of fibrillation by 50-V shocks, which were otherwise proarrhythmic. Endocardial bundles are the most susceptible to electroporation and the resulting conduction impairment. Electroporation is not associated with proarrhythmic effects and is associated with a reduction of vulnerability.

Action Potentials↗
PubMed2005

Anatomic relations between the esophagus and left atrium and relevance for ablation of atrial fibrillation.

BACKGROUND: Esophageal injury is a potential complication after intraoperative or percutaneous transcatheter ablation of the posterior aspect of the left atrium. Understanding the spatial relations between the esophagus and the left atrium is essential to reduce risks. METHODS AND RESULTS: We examined by gross dissection the course of the esophagus in 15 cadavers. We measured the minimal distance of the esophageal wall to the endocardium of the left atrium with histological studies in 12 specimens. To measure the transmural thickness of the atrial wall, we sectioned another 30 human heart specimens in the sagittal plane at 3 different regions of the left atrium. The esophagus follows a variable course along the posterior aspect of the left atrium; its wall was <5 mm from the endocardium in 40% of specimens. The posterior left atrial wall has a variable thickness, being thickest adjacent to the coronary sinus and thinnest more superiorly. Behind is a layer of fibrous pericardium and fibrofatty tissue of irregular thickness that contains esophageal arteries of 0.4+/-0.2-mm external diameters. CONCLUSIONS: The nonuniform thickness of the posterior left atrial wall and the variable fibrofatty layer between the wall and the esophagus are risk factors that must be considered during ablation procedure. Esophageal arteries and vagus nerve plexus on the anterior surface of the esophagus may be affected by ablative procedures.

Adult↗
PubMed1974

Regional myocardial blood flow in awake dogs.

The objectives of this study were to test the hypothesis in awake dogs that during control conditions endocardial vessels are maximally dilated and to determine whether variables introduced by general anesthesia and thoracotomy modify distribution of myocardial blood flow or impair capacity for augmentation of flow in response to a coronary vasodilator stimulus. Myocardial blood flow was measured in relatively small, 2-3 g, left ventricular epicardial and endocardial samples by using 7-10-mum radioisotope-labeled microspheres during control conditions and during infusion of adenosine in dosages which produced maximum increases in coronary blood flow. Measurements were made initially in awake resting animals and were repeated after pentobarbital anesthesia, thoracotomy, and pericardiotomy. Blood flow (mean+/-SEM) in the epicardium and endocardium, respectively, was 0.75+/-0.06 and 0.83+/-0.06 during control conditions and 4.98+/-0.28 and 4.49+/-0.27 cm(3)/min/g during adenosine. These data demonstrate considerable capacity for vasodilation in both myocardial layers and thus refute the hypothesis that endocardial vessels are maximally dilated during control conditions. During control conditions blood flow within epicardial and endocardial layers was essentially homogeneous around the circumference of the left ventricle. In contrast to previous studies in anesthetized animals, however, transmural gradients were present in most regions, i.e., endocardium: epicardium ratio (endo/epi) 1.06-1.16. During adenosine, circumferential epicardial flows were homogeneous; however, circumferential endocardial flows were inhomogeneous and increased less than epicardial flows, endo/epi 0.81-0.99.Anesthesia, thoracotomy, and pericardiotomy increased epicardial and endocardial flow, mean values 1.08+/-0.10 and 1.11+/-0.08 cm(3)/min/g, respectively. Transmural gradients remained in only papillary muscle regions. Adenosine increased epicardial flow comparably before and after anesthesia. Although adenosine increased endocardial flow three- to fourfold after anesthesia, the increase was considerably less than epicardial flow, i.e., endo/epi 0.63-0.78.

Adenosine↗
PubMed1999

Evaluation of left atrial wall elasticity using acoustic microscopy.

Left atrial wall elasticity is one of the important factors regulating left atrial stiffness and functions. The authors evaluated left atrial wall elasticity by measuring the sound speed through the left atrial wall, based on the hypothesis that high elasticity tissues will yield larger sound speed values through the tissue, and examined age-associated changes in left atrial wall elasticity. Left atrium specimens were obtained from 30 normal subjects (age, 15-95 years) at autopsy. An acoustic microscope, operating at 450 MHz, was used to measure the sound speed in the endocardium and the myocardium of the left atrium. The sound speeds in endocardium and myocardium demonstrated significant correlation with age (r = 0.74, p<0.0001 and r = 0.47, p<0.01, respectively). These findings indicate that left atrial wall elasticity increased with advancing age. These changes may lead to deterioration of left atrial compliance and eventual left atrial failure in older subjects.

Adolescent↗
PubMed2005

Characterization of Nfatc1 regulation identifies an enhancer required for gene expression that is specific to pro-valve endocardial cells in the developing heart.

Nfatc1 is an endocardial transcription factor required for development of cardiac valves. Herein, we describe identification and characterization of a tissue-specific enhancer in the first intron of murine Nfatc1 that activates a heterogenic promoter and directs gene expression in a subpopulation of endocardial cells of the developing heart: the pro-valve endocardial cells. This enhancer activity begins on embryonic day (E) 8.5 in endocardial cells at the ventricular end of the atrioventricular canal, intensifies and extends from E9.5 to E11.5 in endocardium along the atrioventricular canal and outflow tract. By E12.5, the enhancer activity is accentuated in endocardial cells of forming valves. Sequential deletion analysis identified that a 250 bp DNA fragment at the 3' end of the intron 1 is required for endocardial-specific activity. This region contains two short conserved sequences hosting a cluster of binding sites for transcription factors, including Nfat and Hox proteins. Electrophoresis mobility shift and chromatin immunoprecipitation assays demonstrated binding of Nfatc1 to the Nfat sites, and inactivation of Nfatc1 downregulated the enhancer activity in pro-valve endocardial cells. By contrast, mutation of the Hox site abolished its specificity, allowing gene expression in non pro-valve endocardium and extracardiac vasculature. Thus, autoregulation of Nfatc1 is required for maintaining high Nfatc1 expression in pro-valve endocardial cells, while suppression through the Hox site prevents its expression outside pro-valve endocardial cells during valve development. Our data demonstrate the first autonomous cell-specific enhancer for pro-valve endocardial cells and delineate a unique transcriptional mechanism that regulates endocardial Nfatc1 expression within developing cardiac valves.

Animals↗
PubMed2005

Bmp2 is essential for cardiac cushion epithelial-mesenchymal transition and myocardial patterning.

Cardiac cushion development provides a valuable system to investigate epithelial to mesenchymal transition (EMT), a fundamental process in development and tumor progression. In the atrioventricular (AV) canal, endocardial cells lining the heart respond to a myocardial-derived signal, undergo EMT, and contribute to cushion mesenchyme. Here, we inactivated bone morphogenetic protein 2 (Bmp2) in the AV myocardium of mice. We show that Bmp2 has three functions in the AV canal: to enhance formation of the cardiac jelly, to induce endocardial EMT and to pattern the AV myocardium. Bmp2 is required for myocardial expression of Has2, a crucial component of the cardiac jelly matrix. During EMT, Bmp2 promotes expression of the basic helix-loop-helix factor Twist1, previously implicated in EMT in cancer metastases, and the homeobox genes Msx1 and Msx2. Deletion of the Bmp type 1A receptor, Bmpr1a, in endocardium also resulted in failed cushion formation, indicating that Bmp2 signals directly to cushion-forming endocardium to induce EMT. Lastly, we show that Bmp2 mutants failed to specify the AV myocardium with loss of Tbx2 expression uncovering a myocardial, planar signaling function for Bmp2. Our data indicate that Bmp2 has a crucial role in coordinating multiple aspects of AV canal morphogenesis.

Animals↗
PubMed1988

Embryonic vascular development: immunohistochemical identification of the origin and subsequent morphogenesis of the major vessel primordia in quail embryos.

The development of the embryonic vasculature is examined here using a monoclonal antibody, QH-1, capable of labelling the presumptive endothelial cells of Japanese quail embryos. Antibody labelling is first seen within the embryo proper at the 1-somite stage. Scattered labelling of single cells appears ventral to the somites and at the lateral edges of the anterior intestinal portal. The dorsal aorta soon forms a continuous cord at the ventrolateral edge of the somites and continues into the head to fuse with the ventral aorta forming the first aortic arch by the 6-somite stage. The rudiments of the endocardium fuse at the midline above the anterior intestinal portal by the 3-somite stage and the ventral aorta extends craniad. Intersomitic arteries begin to sprout off of the dorsal aorta at the 7-somite stage. The posterior cardinal vein forms from single cells which segregate from somatic mesoderm at the 7-somite stage to form a loose plexus which moves mediad and wraps around the developing Wolffian duct in later stages. These studies suggest two modes of origin of embryonic blood vessels. The dorsal aortae and cardinal veins apparently arise in situ by the local segregation of presumptive endothelial cells from the mesoderm. The intersomitic arteries, vertebral arteries and cephalic vasculature arise by sprouts from these early vessel rudiments. There also seems to be some cell migration in the morphogenesis of endocardium, ventral aorta and aortic arches. The extent of presumptive endothelial migration in these cases, however, needs to be clarified by microsurgical intervention.

Animals↗
PubMed1995

Cloche, an early acting zebrafish gene, is required by both the endothelial and hematopoietic lineages.

Endothelial and hematopoietic cells appear synchronously on the extra-embryonic membranes of amniotes in structures known as blood islands. This observation has led to the suggestion that these two ventral lineages share a common progenitor. Recently, we have shown in the zebrafish, Danio rerio, that a single cell in the ventral marginal zone of the early blastula can give rise to both endothelial and blood cells as well as to other mesodermal cells (Stainier, D. Y. R., Lee, R. K. and Fishman, M. C. (1993). Development 119, 31-40; Lee, R. K. K., Stainier, D. Y. R., Weinstein, B. M. and Fishman, M. C. (1994). Development 120, 3361-3366). Here we describe a zebrafish mutation, cloche, that affects both the endothelial and hematopoietic lineages at a very early stage. The endocardium, the endothelial lining of the heart, is missing in mutant embryos. This deletion is selective as evidenced by the presence of other endothelial cells, for example those lining the main vessels of the trunk. Early cardiac morphogenesis proceeds normally even in the absence of the endocardium. The myocardial cells form a tube that is demarcated into chambers, beats rhythmically, but exhibits a reduced contractility. This functional deficit is likely due to the absence of the endocardial cells, although it may be a direct effect of the mutation on the myocardial cells. Cell transplantation studies reveal that the endothelial defect, i.e. the endocardial deletion, is a cell-autonomous lesion, consistent with the possibility that cloche is part of a signal transduction pathway. In addition, the number of blood cells is greatly reduced in cloche mutants and the hematopoietic tissues show no expression of GATA-1 or GATA-2, two key hematopoietic transcription factors that are first expressed during early embryogenesis. These results show that cloche is involved in the genesis and early diversification of the endothelial and blood lineages, possibly by affecting a common progenitor cell population.

Animals↗