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PubMed1996

Endothelial isoform of nitric oxide synthase in rat heart increases during development.

BACKGROUND: Although nitric oxide seems important to cardiovascular function, the ontogenesis of this chemical messenger in the heart is unknown. To investigate this issue, we determined the distribution of nitric oxide synthase (NOS) in the rat heart at different stages during development. METHODS: Immunohistochemistry and the NADPH-diaphorase reaction were used to localize NOS activity-specifically, the endothelial isoform (eNOS) and neuronal isoform (bNOS)-in fetal (14- and 18-day gestation), neonatal (0-, 3-, and 6-day gestation), 12-day-old, 1-month-old, and mature adult Fischer 344 rat hearts. RESULTS: There was sparse eNOS immunoreactivity in the endocardium of the youngest fetal hearts; antibody to eNOS did not localize any vessels within the noncompact myocardium at this stage. By the eighteenth day of embryonic development (e18), eNOS was present not only in endocardium but also in the intima of numerous small vessels within the compact myocardium. In the neonatal rat heart, vascular eNOS predominated, with extensive reaction product in arteries, veins, and numerous capillary size vessels within the myocardium; the endocardium also contained eNOS immunoreactivity. A similar distribution was maintained throughout the remainder of development. Only rare bNOS-immunoreactive neurons were detected in hearts at the three oldest ages. CONCLUSIONS: (1) At e14, eNOS is confined to the endocardium of the developing rat heart; (2) as the myocardium becomes compact, vascular eNOS predominates over endocardial eNOS; (3) at birth, there is extensive eNOS in a distribution similar to the mature pattern; and (4) there is very little bNOS-immunoreactive neural tissue in the rat heart at any stage.

Aging↗
PubMed1998

[Early clinical results with transnasal esophageal echocardiography].

UNLABELLED: Currently undergoing a clinical trial a new miniaturized monoplane ultrasound probe potentially enhances the practicability of perioperative transesophageal echocardiography (TEE) without loss of echocardiographic quality. METHODS: In the present prospective study, the nasally inserted miniaturized TEE probe was tested in 12 ventilated patients and compared with a conventional TEE probe. Echocardiographic quality was tested by two independent investigators by analyzing the percentage of the endocardium contour detection (< 50%, 50-75%, 75-100%) in the left ventricular short- and long-axis views. RESULTS: In 11 patients, more than 50% of endocardium were visualized continuously with both probes. Although the nasal TEE probe was inferior to conventional TEE in detecting lateral endocardium, automated endocardium detection compared well with both methods. Inter- and intraobserver variability in manual measurements of the left ventricular cross-sectional area was below 5% on average and differed non-significantly with regard to the method. In 2 patients, continuous monitoring was aggravated by repeated loss of contact between the miniaturized TEE probe and mucosa. CONCLUSIONS: In comparison with conventional TEE, the miniaturized TEE probe provides practicability advantages without significant loss of information for cardiovascular monitoring.

Adult↗
PubMed1986

Intramural activation of the human ventricle: findings in normal and abnormal myocardial segments in patients with coronary artery disease.

To define the intramural electrical activation of normal and abnormal myocardial segments in patients with coronary artery disease, mapping was performed using a plunge electrode with 10 electrodes 1 mm apart. Five transmural bipolar electrograms (40 to 500 Hz) were recorded from 79 sites in 13 patients at the time of open-heart surgery. The results were correlated with ventriculography. In 64 sites with normal contraction, activation spread from endocardium to epicardium in 20.5 +/- 2 msec, and no electrograms were abnormal. Activation time did not differ between the different anatomic segments. In the eight hypokinetic sites, activation spread from endocardium to epicardium in 22.2 +/- 2 msec, and no electrograms were abnormal. In the seven sites with akinesis or dyskinesis, abnormal electrograms were noted and were concentrated towards the endocardium. In four patients, the 40% to 80% of electrograms closest to the endocardium were abnormal, while in three patients all transmural electrograms were abnormal. The variable depth of electrically abnormal tissue should be considered in operations and ablative procedures for ventricular arrhythmias.

Adult↗
PubMed1993

Semicarbazide protection from in vivo oxidant injury of vascular tissue by allylamine.

Allylamine is a specific cardiovascular toxin that causes vascular and myocardial lesions. Previous studies showed that allylamine-induced chronic lesions are markedly reduced by semicarbazide, an inhibitor of semicarbazide-sensitive amine oxidase (SSAO), and that allylamine is metabolized to the aldehyde, acrolein, by SSAO. We hypothesized that inhibitors of SSAO might reduce the acute cardiovascular toxicity of allylamine. To test our hypothesis, we fed 150 mg/kg allylamine to semicarbazide-pretreated (3 h; 98 mg/kg) rats. Animals were sacrificed 1 h after allylamine treatment. Aorta, epicardium, and endocardium were assayed for SSAO, glutathione peroxidase, catalase, thiol status and lipid peroxidation. SSAO activity was decreased significantly in aorta, epicardium and endocardium. Activity was 30-times higher in aorta than in epicardium and endocardium. A striking decrease in malonaldehyde level (lipid peroxidation) was found in aorta of pretreated rats as compared to allylamine-only treated rats. The reduction of free-SH content in aortic mitochondria was also attenuated in pretreated rats. Changes were not so marked in epicardium and endocardium. These results suggest that in vivo pretreatment with semicarbazide at least partially protects aortic mitochondria from allylamine toxicity. The mechanism can be explained on the basis of the fact that semicarbazide inhibits acrolein formation in allylamine-treated rats.

Allylamine↗
PubMed2004

A computational study of the interaction between coronary blood flow and myocardial mechanics.

An anatomically based computational model of coronary blood flow, coupled to cardiac mechanics, is verified with experimental data and used to investigate the mechanisms by which myocardial contraction inhibits coronary blood flow. From finite deformation mechanics solutions the regional variation in intramyocardial pressure (IMP) exerted on coronary vessels embedded in the ventricular wall is calculated. This pressure is then coupled to a haemodymanic model of vascular blood flow to predict the spatial-temporal characteristics of perfusion throughout the myocardium. The calculated IMP is shown to vary approximately linearly between ventricular pressure at the endocardium and atmospheric pressure at the epicardium through the diastolic loading and isovolumic contraction phases. During the ejection and isovolumic relaxation phases IMP values rise slightly above ventricular pressure. The average radius of small arterial vessels embedded in the myocardium decreases during isovolumic contraction (18% at left ventricular endocardium) before increasing during ejection (10% at left ventricular endocardium) due to a rise in inflow pressure. Embedded venous vessels show a reduction in radius through both phases of contraction (35% at left ventricular endocardium). Calculated blood flows in both the large epicardial and small myocardial vessels show a 180 degrees phase difference between arterial and venous velocity patterns with arterial flow occurring predominantly during diastole and venous flow occurring predominantly during systole. These results indicate that the transmission of ventricular cavity pressure through the myocardium is the dominant mechanism by which coronary blood flow is reduced during the isovolumic phase of contraction. In the ejection phase of contraction myocardial stiffening plays a more significant role in inhibiting blood flow.

Biomechanical Phenomena↗
PubMed1992

Potential cellular mechanisms of hydrogen peroxide-induced cardiac arrhythmias.

The electrophysiologic effects of hydrogen peroxide on the isolated guinea pig right ventricular free wall were studied using simultaneous recordings of action potentials from the epicardium and the endocardium. Exposure to hydrogen peroxide caused a time- and concentration-dependent change in action potential characteristics. Action potential durations at 50 and 90% of repolarization (APD50 and APD90, respectively) were significantly prolonged by hydrogen peroxide in both the epicardium and the endocardium. Although prolongation occurred at lower concentrations (0.5 mM) in the epicardium, increases in APD in response to higher concentrations of hydrogen peroxide (1 or 4 mM) were maintained for a longer period of time in the endocardium. In addition, hydrogen peroxide (1 or 4 mM) caused significant depolarization in the epicardium after 10 min, although this effect was observed only in the endocardium exposed to 4 mM hydrogen peroxide. Ventricular arrhythmias were observed in 5 of 7, 6 of 7, and 7 of 7 preparations exposed to 0.5, 1, and 4 mM hydrogen peroxide, respectively. The most frequently observed electrophysiologic abnormalities were associated with increased automaticity. Coupled beats, including clearly identifiable early and delayed depolarizations, were also observed. Verapamil (2 microM) and amiloride (0.1 mM) reduced both the incidence and the duration of hydrogen peroxide-induced arrhythmias but did not influence the effects on APD. This study is the first demonstration of hydrogen peroxide-mediated transmural dispersion in APD that could play an important role in the development of ventricular arrhythmias. In addition, our results demonstrate that hydrogen peroxide can induce ventricular arrhythmias through several cellular mechanisms, including increased automaticity, coupled beats, and triggered activity.

Action Potentials↗
PubMed1990

Pharmacological analysis of established ventricular fibrillation.

1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.

Animals↗
PubMed2005

Sinus node revisited in the era of electroanatomical mapping and catheter ablation.

OBJECTIVE: To study the architecture of the human sinus node to facilitate understanding of mapping and ablative procedures in its vicinity. METHODS: The sinoatrial region was examined in 47 randomly selected adult human hearts by histological analysis and scanning electron microscopy. RESULTS: The sinus node, crescent-like in shape, and 13.5 (2.5) mm long, was not insulated by a sheath of fibrous tissue. Its margins were irregular, with multiple radiations interdigitating with ordinary atrial myocardium. The distances from the node to endocardium and epicardium were variable. In 72% of the hearts, the whole nodal body was subepicardial and in 13 specimens (28%) the inner aspect of the nodal body was subendocardial. The nodal body cranial to the sinus nodal artery was more subendocardial than the remaining nodal portion, which was separated from the endocardium by the terminal crest. In 50% of hearts, the most caudal boundaries of the body of the node were at least 3.5 mm from the endocardium. When the terminal crest was > 7 mm thick (13 hearts, 28%), the tail was subepicardial or intramyocardial and at least 3 mm from the endocardium. CONCLUSIONS: The length of the node, the absence of an insulating sheath, the presence of nodal radiations, and caudal fragments offer a potential for multiple breakthroughs of the nodal wavefront. The very extensive location of the nodal tissue, the cooling effect of the nodal artery, and the interposing thick terminal crest caudal to this artery have implications for nodal ablation or modification with endocardial catheter techniques.

Adult↗
PubMed2004

Functional and transmural modulation of M cell behavior in canine ventricular wall.

Previous studies have demonstrated a discrete population of midmyocardial (M) cells in the ventricular myocardium having excessive action potential duration (APD) prolongation during long activation cycle lengths (CL) and under the influence of APD-prolonging agents. However, M cells have not been found in other studies. Existing explanations for the discrepancies appear inadequate. We hypothesized that instead of being a discrete group, M cell behavior is functional and conditionally expressed. We mapped APDs on the cut-exposed transmural surfaces of arterially perfused ventricular wedges from 26 dogs during Na+ current modification with anemone toxin II (ATX-II). Compared with the endocardium, APDs were not statistically different in the parallel layer having the longest mean APD (APDL) and were significantly shorter in the epicardium in the 26 wedges before ATX-II. ATX-II (> or =5 nmol/l) prolonged APD heterogeneously (midmyocardium > endocardium > epicardium). The differences increased at longer CLs. ATX-II (20.0 nmol/l) shifted the APD(L) layer to 32 +/- 6.2% (6 wedges, CL: 4,000 ms) of the transmural thickness from the (sub)endocardium (8.6 +/- 7.2%, 26 wedges, ATX-II free). We detected the presence of M cell behavior (significantly longer APDs in the APDL layer than in the endocardium and epicardium, P < or = 0.04, CL: 4,000 ms) in the 18 wedges having > or =5 nmol/l ATX-II but not (P >0.36) in the other 18 wedges having < or =2.5 nmol/l ATX-II. Both the position of the APDL layer and presence of M cell-like behavior were modulated by ATX-II. The dynamic spatial modulation indicates that M cell behavior is functional and only becomes manifest under suitable conditions.

Action Potentials↗
PubMed1995

Effect of coronary artery reperfusion on transmural myocardial remodeling in dogs.

BACKGROUND: The effects of reperfusion after coronary occlusion on transmural remodeling of the ischemic region early and late after nontransmural infarction must importantly affect the recovery of regional function. Accordingly, analysis of local volume and three-dimensional strain was performed using a finite element method to determine regional remodeling. Systolic and remodeling strains were measured using radiographic imaging of three columns (approximately 1 cm apart) of four to six gold beads implanted across the left ventricular posterior wall in 6 dogs. METHODS AND RESULTS: After a control study, infarction was produced by 2 to 4 hours of proximal left circumflex coronary artery occlusion followed by reperfusion. Follow-up studies were performed at 2 days, 3 weeks, and 12 weeks with the dogs under anesthesia and in closed-chest conditions. Biplane cineradiography was performed to obtain the three-dimensional coordinates of the beads. At 2 days, end-systolic strains were akinetic with loss of normal transmural gradients of shortening and thickening. Remodeling strains (RS) were determined by use of a nonhomogeneous finite element method by referring the end-diastolic configuration during follow-up studies to its control state at matched end-diastolic pressures and heart rates. Tissue volume at 2 days increased substantially, more at the endocardium (30 +/- 7%) than at the epicardium (5 +/- 12%, P < .01); the increase was associated with an average RS in the wall-thickening direction of 0.18 +/- 0.15 (P < .01) with all other RS near zero. At 12 weeks systolic function partially recovered, with normal wall thickening in the epicardium (radial strain, 0.081 +/- 0.056 [control] versus 0.113 +/- 0.088 [12 weeks]) but with dysfunction in the endocardium (0.245 +/- 0.108 [control] versus 0.111 +/- 0.074 [P < .01] [12 weeks]). This inability of the inner wall to recover function may be related to increased transmural torsional shear and negative longitudinal-radial transverse shear in the inner wall. Volume loss occurred at 12 weeks in the endocardium (-36 +/- 16%) corresponding to transmural gradients in longitudinal RS and both transverse shear RS. Negative longitudinal RS was greater at the endocardium (-0.20 +/- 0.10) than at the epicardium (-0.06 +/- 0.05, P < .01). CONCLUSIONS: These results indicate the presence of marked subendocardial edema 2 days after reperfusion following 2 to 4 hours of coronary occlusion. At 3 months after reperfusion, however, there was volume loss in the inner wall due to shrinkage along the myofiber direction with reduced transmural function and loss of longitudinal shortening, while both tissue volume and function recovered completely in the outer wall.

Animals↗
PubMed2004

Estimated global transmural distribution of activation rate and conduction block during porcine and canine ventricular fibrillation.

We quantified ventricular fibrillation (VF) activation rate, conduction block, and organization transmurally in pigs and dogs, whose transmural Purkinje distribution differ. In six pigs and five dogs, 75 to 100 plunge needles, containing four electrodes for the right ventricle (RV) and six electrodes for the left ventricle (LV) and septum, were inserted in vivo. Six VF episodes were electrically initiated and allowed to last for 47 to 180 seconds. From the FFT power spectra, dominant frequency (DF), an estimate of activation rate, and incidence of double peaks (DPI), an estimate of conduction block, were calculated every 8 ms at each electrode. DF was highest at the epicardium and lowest at the endocardium, whereas DPI was highest at the endocardium and lowest at the epicardium for the entire LV and the RV base in both pigs and dogs for the first 70 seconds of VF. This distribution changed little throughout the first 3 minutes of VF in pigs but reversed in dogs by 2 minutes of VF. In conclusion, estimated activation rates and conduction block incidence during VF are not uniformly distributed transmurally. During the first minute of VF, the faster activating LV base epicardium exhibits less estimated block than the slower endocardium, raising the possibility that faster activating epicardium generates wavefronts that drive the endocardium early during VF. Constancy of this pattern in pigs but its reversal by 2 minutes in dogs is consistent with the hypothesis that activation during later VF is driven by Purkinje fibers.

Animals↗
PubMed1993

Regional myocardial capillary erythrocyte transit time in the normal resting heart.

A major determinant of oxygen transport to the myocardium is the time spent by the erythrocytes (red blood cells [RBCs]) traversing the microcirculation. Although it has been shown that the myocardium has regional differences in blood volume, blood flow, metabolism, and sensitivity to ischemic injury, the regional distribution of RBC transit times through the myocardial capillaries has not been previously measured. The present study was designed to measure the regional myocardial capillary RBC transit time by a new technique to determine whether there are regional differences in the capillary RBC transit time in the normal resting heart. Anesthetized open-chest male New Zealand White rabbits (3.0-3.7 kg, n = 8) were studied. Regional myocardial blood volume was determined using chromium-51-labeled RBCs, and regional blood flow was measured using a reference flow technique and a left atrial injection of 15-microns-radiolabeled (gadolinium-153, 10-20 muCi) microspheres. Capillary blood volume was determined by multiplying the regional blood volume by the histologically determined fraction of the total blood volume that was in the capillaries. Capillary RBC transit time was calculated as the quotient of capillary blood volume and blood flow. The myocardial capillary blood volume was the same in the endocardium and the epicardium (4.67 +/- 0.67 ml/100 g for endocardium versus 4.52 +/- 0.70 ml/100 g for epicardium, p = NS), whereas myocardial blood flow tended to be greater in the endocardium (6.09 +/- 0.73 ml/sec per 100 g for endocardium versus 5.47 +/- 0.75 ml/sec per 100 g for epicardium), although this was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Homocyst(e)ine impairs endocardial endothelial function.

Homocyst(e)ine injured vascular endothelium and modulated endothelial-dependent vascular function. Endothelium plays an analogous role in both the vessel and the endocardium. Therefore, we hypothesized that homocyst(e)ine modulated endocardial endothelium (EE) dependent cardiac function. The ex vivo cardiac rings from normal male Wistar-Kyoto rats were prepared. The contractile responses of left and right ventricular rings were measured in an isometric myobath, using different concentrations of CaCl2. The response was higher in the left ventricle than right ventricle and was elevated in endocardium without endothelium. The half effective concentration (EC50) and maximum tension generated by homocyst(e)ine were 10(6) and 5-fold lower than endothelin (ET) and angiotensin II (AII), respectively. However, in endothelial-denuded endocardium, homocyst(e)ine response was significantly increased (p<0.005, compared with intact endothelium) and equal to the response to ET and AII. To determine the physiological significance of ET, AII, homocyst(e)ine, and endothelial nitric oxide in EE function, cardiac rings were pretreated with AII (10(-10) M) or ET (10(-13) M) and then treated with homocyst(e)ine (10(-8) M). Results suggested that at these concentrations AII, ET, or homocyst(e)ine alone had no effect on cardiac contraction. However, in the presence of 10(-10) M AII or 10(-13) M ET, the cardiac contraction to homocyst(e)ine (10(-8) M) was significantly enhanced (p<0.01, compared with without pretreatment) and further increased in the endocardium without endothelium. The pretreatment of cardiac ring with the inhibitor of nitric oxide, Nomega-nitro-L-arginine methyl ester (L-NAME), increased contractile response to homocyst(e)ine. These results suggested that homocyst(e)ine impaired EE-dependent cardiac function and acted synergistically with AII and ET in enhancing the cardiac contraction.

Angiotensin II↗
PubMedDate not supplied

Cardiac and aortic lesions in chronic experimental poisoning with mercury vapors.

The nature of the toxic influence of mercury and its effect on the cardio-vascular system are not well understood. In chronic poisoning with metallic mercury and its compounds, circulatory disorders have been observed in patients. The problem whether metallic mercury damages the endocardium and myocardium directly or indirectly through vascular changes or vegetative system stimulation remains unsolved. A study was undertaken in which a group of experimental rabbits was exposed to the chronic action of mercury vapors by inhalation and compared with a control group. Before the experiment and towards its end, ECG were taken and 24-hr urinary excretion of mercury was determined in both groups. After 3 months the animals were autopsied, and fragments of myocardium, papillary muscles, endocardium and ascending aorta were taken for histopathologic investigation. In the poisoned animals, the ECG tracings showed bradycardia. Morphologic lesions had the character of thrombosis in small and medium-caliber blood vessels, necrotic foci, thickening of the endocardium of the papillary muscles and perivalvular region and endothelial proliferation with inflammatory foci. The results indicate that, besides influencing the vegetative system, mercury vapor damages the endocardium directly and produces vascular lesions resulting in myocardial changes.

Animals↗
PubMed1996

[Infarction exclusion technique for postinfarction ventricular septal defect].

A new technique for post-infarction ventricular septal defect is accomplished by suturing a single patch to healthy endocardium excluding the infarcted area from the high left ventricular pressure. We have used this infarction exclusion technique for 3 cases since 1994. Three patients developed cardiogenic shock before operation and were managed initially with an intra-aortic balloon pump. All patients were urgently operated using this technique, at the same time, CABG operation was performed in 2 cases from the finding of preoperative coronary angiography. All of the patients survived. The first patient had a residual shunt (L-R; 30%), which spontaneously resolved in one month after the operation. In this method, a two-dimensional plane patch has to be sutured to healthy endocardium like a three-dimensional dome. Consequently the edge of the patch has wrinkles, which cause a residual shunt easily at the suture line. So from the second case, previously prepared circular conic patch, which had been made from a plane circular patch, was sutured to the left ventricular endocardium. At the suture line, this conic patch was well fitted to the endocardium, and the patients had no residual shunt. Though this method has the advantage to retain left ventricular function and volume, the technique must be improved to prevent residual shunt after operation.

Aged↗
PubMed1998

Production of the transforming growth factor-beta binding protein endoglin is regulated during chick heart development.

The early embryonic heart consists of two cell types. The cells form an inner epithelial tube of endocardium within an outer tube of myocardium separated by a cell-free extracellular matrix. A crucial process in heart development is the production of cushion mesenchyme in the atrioventricular (AV) canal and outflow tract (OT). Cushion mesenchyme differentiates from the endocardium in response to signaling molecules produced by the adjacent myocardium. In chicken hearts, both transforming growth factor-beta3 (TGF-beta3) and TGF-beta2 are present and have been identified as being important in the production of cushion mesenchyme. We were interested in how the signals from these two similar molecules may be differentiated during early heart development. To this end, we examined the expression of endoglin, a TGF-beta receptor molecule, in the developing chick heart. Endoglin is typically located on endothelial cell layers and binds tightly to TGF-beta1 and TGF-beta3 but not well to TGF-beta2. We show that during the formation of the primitive heart tube, endoglin is found at relatively high levels in both presumptive myocardium and endocardium. However, as myocardium differentiates and development proceeds, endoglin expression is progressively reduced. At stage 20 in the heart, endoglin expression is most readily seen in the AV canal and the OT. This pattern of expression is similar to the reported TGF-beta3 expression patterns in the heart.

Animals↗
PubMed1999

Bulbus arteriosus of the Antarctic teleosts. II. The red-blooded Trematomus bernacchii.

The structure of the bulbus arteriosus of the Antarctic teleost, Trematomus bernacchii, has been studied by light, scanning, and transmission electron microscopy. The wall of the bulbus arteriosus is divided into endocardial, subendocardial, middle and external layers. The endocardial endothelium covers the inner surface of the bulbus wall and invaginates into the subendocardium to form solid epithelial cords that show secretory activity. The subendocardial tissue is divided into finger-like ridges. Ridge cells located under the endocardium appear in niches limited by collagen fibers and thin cell extensions. Away from the endocardium ridge cells cluster into small groups, show some of the characteristics of smooth muscle cells, and appear enmeshed in a filamentous meshwork that lacks collagen and elastin fibers. The middle bulbus layer is formed by typical smooth muscle cells that are enmeshed in a filamentous meshwork similar to that observed in the ridges. The ridges and the middle layer appear to be formed by the same cell type, smooth muscle, with a gradient of differentiation from the endocardium toward the middle layer. In the absence of elastin fibers the filamentous meshwork should confer elastic properties to the bulbus wall. The stretching of the meshwork along the main axis of the middle layer cells, and between different cellular layers, suggests the existence of tensile stress and, hence, the involvement of smooth muscle cells in bulbus wall dynamics. The external layer is formed by numerous cellular types embedded in a collagenous matrix. Among these cellular types, myofibroblasts, macrophages, granulocytes, lymphocytes, dendrite-like cells, degenerating cells, and plasma cells can be recognized. The subepicardial tissue appears to be a specialized site involved in the production of the humoral immune response and displays many of the morphological characteristics of a germinal center. The outer limiting layer of the bulbus, the visceral pericardium, is formed by epithelial cells that show desmosomes and tight junctions. This suggests a close control of permeability with respect to the pericardial fluid.

Animals↗
PubMed1989

Endocardial surface and atrial morphological changes during development and aging.

Light, scanning, and transmission electron microscopic observations related to morphological changes of the right atrium as well as the atrial endocardium during development (15th embryonic day and 1 day old) and aging (560 days old) in the Syrian hamster were described and correlated. From the fetus to the adult, the atrial endocardium differentiates in parallel with, or in response to, the subjacent proliferating myocytes in the atrial wall and the trabeculae. Simultaneously, the atrium compartmentalizes grossly into a main chamber and an appendicular region. There is a progressive differentiation from a rudimentary, open chamber with primitive mural ridges in the fetal atria to a distinct, separate, atrial main chamber and appendage with a dense network of trabeculae in the adult. The fetal and neonatal endocardial, endothelial cells are convex with a central nuclear bulging and attenuated cytoplasmic extensions; the adult endocardium shows a squamous endothelium. Two cell surface specializations were observed in all age groups: microvilli and blebs or cytoplasmic protrusions. The general atrial morphology and surface endocardial changes were correlated with growth and the role of the endocardial endothelium as a barrier which controls metabolic exchanges, including the transport of atrial natriuretic factor, between the myocytes and the blood. This endothelial function appears to be essential in the fetal and neonatal age groups since no blood vessels are detected in these groups.

Aging↗