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PubMed1983

Elastica-positive material in the atrial endocardium. Light and electron microscopic identification.

The elastic layer of the endocardium is studied in various laboratory animals (mouse, rat, rabbit, cat, and dog) and in man. Coarse elastica-positive fibers form a tightly woven layer in the endocardium of the left atrium; the elastic layer consists of loosely arranged delicate fibers in the endocardium of the right atrium. Electron microscopy shows the elastic material to consist of homogeneous elastin (E) and of elastic fiber microfibrils (EFM). Elastic material in the endocardium of the left atrium is mainly formed of E with few EFM present. By contrast, the portion of EFM predominated that of E in elastic fibers from the right atrium, where some elastica-positive fibers even appear as pure bundles of microfibrils. This was also observed in human material obtained from aged individuals (8th decennium). It is concluded that EFM are not only progenitors of E but represent an independent fibrous component of the connective tissue.

Aged↗
PubMed1998

An autocrine function for transforming growth factor (TGF)-beta3 in the transformation of atrioventricular canal endocardium into mesenchyme during chick heart development.

Transformation of atrioventricular canal endocardium into invasive mesenchyme is a critical antecedent of cardiac septation and valvulogenesis. Previous studies by Potts et al. (Proc. Natl. Acad. Sci. USA 88, 1510-1520, 1991) showed that treatment of atrioventricular canal endocardial and myocardial cocultures with TGFbeta3 antisense oligodeoxynucleotides blocked mesenchyme formation. Based on this observation, we sought to: (i) identify the target tissue of TGFbeta3 antisense oligos in this transformation bioassay, and (ii) more clearly define the mechanism of TGFbeta3 function in atrioventricular canal mesenchyme formation. In situ hybridization and immunohistochemistry showed little or no TGFbeta3 mRNA or protein in the atrioventricular canal myocardium or endocardium prior to mesenchyme formation (stage 14; paraformaldehyde fixation). However, by stage 18 transforming atrioventricular canal endocardial cells and mesenchyme as well as myocardium were positive for both TGFbeta3 mRNA and protein. In culture bioassays, atrioventricular canal endocardial monolayers pretreated with antisense phosphorothioate oligodeoxynucleotides to TGFbeta3 did not transform into invasive mesenchyme in response to cardiocyte conditioned medium: the subsequent addition of exogenous TGFbeta3 protein relieved this inhibition. Control cultures without pretreatment or those receiving missense oligos generated similar numbers of invasive mesenchyme in response to cardiocyte conditioned medium. Direct addition of TGFbeta3 protein to atrioventricular canal endocardial monolayers in the absence of cardiocyte conditioned medium resulted in loss of cell:cell associations and stimulated cellular hypertrophy, but did not engender invasive mesenchyme formation or alter endocardial proliferation after 24 h of culture. Similar results were obtained with TGFbeta2 protein, either alone or in combination with TGFbeta3. The results of this study indicate that: (i) atrioventricular canal endocardium expresses TGFbeta3 in response to a myocardially derived signal other than TGFbeta3, (ii) atrioventricular canal endocardial TGFbeta3 functions in an autocrine fashion to elicit selected characteristics necessary for cushion tissue formation, and (iii) TGFbeta3 alone or in combination with TGFbeta2 is insufficient to transform atrioventricular canal endocardium into invasive mesenchyme in culture.

Animals↗
PubMed1998

Ischemic preconditioning and arrhythmogenesis in the rabbit heart: effects on epicardium versus endocardium.

The goals of this study were: (1) to determine if preconditioning protects against arrhythmias and contractile dysfunction, and if protection for these two endpoints occurs in parallel; and (2) to investigate the anti-arrhythmic action of preconditioning by examining its effect on electrical activity in epicardium v endocardium. We monitored ECGs, epicardial and endocardial monophasic action potentials (MAP), left-ventricular developed presssure (LVDP) and end-diastolic pressure (EDP) in isolated rabbit hearts. Hearts were subjected to a 30-min test ischemia and 45 min of reperfusion. Preconditioning cycles (PC) consisted of 1-4 ischemic episodes (5 min each separated by 10 min of reperfusion) administered 30 min before the test protocol. The test ischemia caused ventricular fibrillation (VF) in 42% of non-PC hearts. One PC totally suppressed VF (0%). The incidence of VF was 30% in 2 PC, 72% in 3 PC and 47% in 4 PC hearts. A large rise in EDP occurred in non-PC and 1 PC hearts, and this rise was prevented by 2, 3 or 4 PC. None of the protocols improved post-ischemic recovery of LVDP or EDP. The test ischemia generated a large dispersion in MAP duration between epicardium and endocardium (39ms), but this dispersion was markedly reduced after 1 PC (14ms). In conclusion, our results demonstrate that 1 PC completely protects against ischemia-induced VF in rabbit hearts, whereas 2 or more PC are required to prevent the ischemia-induced rise in EDP. Thus, preconditioning against arrhythmias and contractile dysfunction does not occur in parallel. Our data also suggest that 1 PC may exert its anti-arrhythmic effect through reduction of the substrate for reentrant arrhythmias during ischemia (dispersion of repolarization) via effects on MAP changes in endocardium.

Action Potentials↗
PubMed1980

Ultrastructure of atrial endocardium and myocardium in three species of gadidae (Teleostei).

The atrial endocardium and myocardium in three teleost species Gadiculus thori J. Smith, Melanogrammus aeglefinus (L.) and Onos cimbrius L. of the family Gadidae are described. The myocardial cells contain few myofibrils and a moderately developed sarcoplasmic reticulum and are connected by short nexuses. G. thori has many atrial specific granules in some of the myocardial cells facing the endocardium. Such cells contain little contractile material. The endocardium is composed of tall cells (10 micrometer) with basal extensions, protrusions of the surface and sometimes cytoplasmic bridges between adjacent cells. The endocardial cells contain bristle-coated vesicles, a well developed agranular endoplasmic reticulum, and many moderately dense bodies (MDB). MDB are membrane-bounded, contain tubules, granules and often fibres, and have different amounts of amorphous material and variable electron density. These bodies appear to fuse in a characteristic manner. Ultrahistochemical tests show that the granules in MDB probably contain catecholamines.

Animals↗
PubMed1987

Intercellular gaps in the early development of chick mural endocardium. A TEM study.

Embryonic chick hearts stages 15 to 21 according to the Hamburger-Hamilton series (1951) were subjected to TEM and light-microscopical examination to investigate ventricular mural endocardium during early trabeculation. Serial sectioning of consecutively-aged embryos indicated an invagination of the endocardial layer which lines the intertrabecular and intermuscular spaces. During the proceeding development, frequently occurring approaches and contacts between mural endocardium and myocardium could be observed. At all stages examined, the cardiac jelly appeared as an acellular, at particular sites very attenuated matrix. The intercellular gaps of the endocardium could not be correlated to the invagination and the endothelialization of the intertrabecular spaces.

Animals↗
PubMed1989

Rate dependence of action potential duration and refractoriness in canine ventricular endocardium differs from that of epicardium: role of the transient outward current.

Previous studies have provided evidence for an important contribution of the transient outward current to the electrical activity of canine ventricular epicardium, but not endocardium. The present study examines the characteristics of action potential duration and refractoriness in these two tissue types. The time and rate dependence of changes in action potential duration and refractoriness observed in epicardium were significantly more accentuated than in endocardium. The restitution of action potential duration in epicardium paralleled the restitution of phase 1 amplitude of the action potential in this tissue. The correlation between phase 1 amplitude and action potential duration recorded from a large number of epicardial and endocardial preparations was significant under both steady state and restitution conditions. 4-Aminopyridine, a transient outward current blocker, decreased the time dependence of phase 1 amplitude and concomitantly decreased the time dependence of action potential duration in epicardium. 4-Aminopyridine abbreviated the action potential duration of epicardium at slow stimulation rates but had little effect or prolonged it at fast rates or after premature stimulation. (The availability of a transient outward current is relatively small after premature stimulation.) The data support the hypothesis that the prominent presence of a transient outward current in epicardium, but not endocardium, contributes to the differences in the time and rate dependence of action potential duration and refractoriness in the two tissue types. The results also demonstrate the effect of an outward current to prolong the action potential and the effect of an outward current blocker to abbreviate the action potential.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed2001

Increased von Willebrand factor in the endocardium as a local predisposing factor for thrombogenesis in overloaded human atrial appendage.

OBJECTIVES: We investigated immunoreactive von Willebrand factor (vWF), a platelet adhesion molecule, in the endocardial endothelium and its relationship to thrombogenesis in the human atrial appendage. BACKGROUND: Intra-atrial thrombogenesis is generally thought to be induced by blood stasis in the atrial appendage involved with atrial fibrillation (AF). Little attention has been paid to alterations of the endocardial endothelium on which the thrombus develops. METHODS: Atrial appendage tissue was obtained at heart surgery or at autopsy from AF and non-AF cardiac patients and from noncardiac patients. Immunohistochemistry for endothelial cell markers including vWF, CD31, CD34 and endothelial nitric oxide synthase (eNOS) and platelet glycoprotein Ib/IX or IIb/IIIa was performed and semiquantitatively graded. RESULTS: In contrast to the apparent immunostaining for CD31, CD34 and eNOS, only focal or little immunoreactive vWF was seen in the endocardium of noncardiac patients. Immunoreactive vWF in the endocardial endothelium was increased in most cardiac patients, particularly in the left, but not in the right, atrial appendage of patients with mitral valvular disease, irrespective of whether AF was present. Platelet adhesion/thrombus formation in the endocardium was found in limited sites in which the overlying endothelium was deficient in eNOS and CD34. When warfarin-treated cases were excluded, there was a significant correlation between the immunohistochemical grade for vWF and the degree of platelet adhesion/thrombus formation in the endocardium. CONCLUSIONS: Immunoreactive vWF in the endocardial endothelium was increased in overloaded human atrial appendage, which may be a local predisposing factor for intraatrial thrombogenesis.

Adult↗
PubMed1989

Endocardium of the left ventricle in volume-loaded canine heart. A histological and ultrastructural study.

To investigate the effects of volume loading of the heart, the endocardium was studied histologically and ultrastructurally. Thirteen adult female beagle dogs were used. An arterio-venous shunt was constructed between the right common carotid artery and the right external jugular vein in nine animals to induce a volume load. Four animals were used as controls. All were kept for 6-12 months. Heart weight, relative heart weight (heart weight/body weight), cardiac output index, stroke volume index and volumes of both ventricles in the experimental animals were significantly larger than in the controls. Shunted blood volume was significantly correlated with heart weight. The endocardium of the left ventricle in the experimental animals showed elastofibrosis and was significantly thicker than in the controls. In 5 hearts, it was more than 20 microns thick and its endothelial cells showed many long microvilli with a very thick basement membrane (1.5-2.0 microns). The thickness of the endocardium was significantly correlated with the heart weight, relative heart weight and cardiac output index, within 1%, 5% and 5% risk, respectively. These endocardial changes were thought to be induced by hemodynamic changes in the left ventricle of the volume-loaded heart, probably being correlated with changes in cardiac function and morphology.

Animals↗
PubMed1996

The role of the endocardium in the facilitatory effect of bradykinin on electrically-induced release of noradrenaline in rat cardiac ventricle.

1. The present investigation was undertaken to study the role of bradykinin in noradrenaline release from the ventricle of the rat induced by electrical stimulation. Slices of the left ventricle of adult Wistar rats with or without endocardium were previously loaded with 0.2 microM [3H]-noradrenaline and washed out before electrical stimulation was applied. 2. Bradykinin (0.1-100 nM) concentration-dependently increased tritium release evoked by electrical stimulation (EC50 = 3.5 (1.2-10.2) nM; n = 12). The angiotensin converting enzyme inhibitor, captopril (1 microM), which per se had no effect on tritium release, caused a marked enhancement of the bradykinin facilitatory effect, shifting the concentration-response curve of bradykinin to the left by about one log unit. The compound Hoe 140, a selective inhibitor of B2-bradykinin receptors, competitively antagonized the effect of bradykinin, indicating the involvement of these receptors in the action of bradykinin. 3. In endocardium-free ventricle, bradykinin had no effect either in the absence or in the presence of captopril. 4. These results show that: (1) bradykinin is able to facilitate noradrenaline release evoked by electrical stimulation of the rat ventricle through activation of B2-bradykinin receptors located on endocardial cells; (2) this action of bradykinin which is markedly potentiated by the inhibition of the angiotensin-converting enzyme seems to be exerted through the release of some factor which is formed in the endocardium and diffuses into the myocardium where it acts.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Comparison of biaxial mechanical properties of excised endocardium and epicardium.

A complete understanding of cardiac mechanics requires knowledge of the mechanical properties of each of the tissues that comprise the heart, Data and constitutive relations are available for the nonlinear multiaxial behavior of epicardium and noncontracting myocardium, but there have been no comparable results for endocardium. In this paper, we present biaxial mechanical data for endocardium and epicardium excised from the same bovine hearts. The data reveal that these two membranes behave differently; endocardium exhibits a greater stiffness in the low-strain range. Moreover, quantification of endocardial behavior requires a seven-parameter, polynomial-exponential pseudostrain-energy function w, whereas epicardium can be described by a four-parameter exponential w. Comparison of our current findings with previous results on canine epicardium reveals further that canine and bovine epicardium behave similarly, although the latter is more extensible. Thus there appear to be marked species differences.

Animals↗
PubMed1990

Eosinophils from hypereosinophilic patients damage endocardium of isolated feline heart muscle preparations.

Persistent eosinophilia in humans is often associated with endocardial damage to the heart, but a causal relation has not been established. We investigated the effect of eosinophils and eosinophil supernatants obtained from eight hypereosinophilic patients on the contractile performance and endocardial morphology of isolated, electrically stimulated cat papillary muscle preparations (n = 16). All these eosinophil suspensions contained high proportions of "hypodense" or "activated" cells. Eosinophils (5-15 x 10(6) ml organ bath) or eosinophil culture supernatants (prepared by overnight incubation at 37 degrees C) when added to papillary muscles produced acute changes in contractile behavior of these muscles identical to the previously reported effects of selective endocardial damage: a reduction in time to peak isometric twitch tension causing a reduction in peak isometric tension but with no significant reduction in rate of tension development or in maximum unloaded shortening velocity. All of these muscle preparations showed severely damaged endocardium at scanning electron microscopy. Addition of eosinophils from hypereosinophilic patients to muscles with selectively damaged endocardium (by previous transient [1-second] exposure to 1% Triton X-100) produced no further change in contractile performance. No significant change in contractile performance or endocardial morphology of papillary muscles (n = 16) was observed after addition of eosinophils (7.5-10 x 10(6] or neutrophils (8-15 x 10(6] from normal subjects or of cell-free culture medium. Thus, activated human eosinophils produce specific morphological and functional changes suggestive of specific damage to endocardium of isolated feline cardiac muscle.

Adult↗
PubMed1988

Transient outward current prominent in canine ventricular epicardium but not endocardium.

Previous studies have denied the presence of a transient outward current (Ito) in ventricular myocardium of dog, sheep, and calf. Using conventional microelectrode techniques, we provide evidence for a significant contribution of Ito to epicardial, but not endocardial, activity of canine ventricular myocardium. The epicardial action potential when compared with that of endocardium shows a smaller phase 0 amplitude, a much more prominent phase 1, and a phase 2 amplitude that is greater than that of phase 0. Epicardial action potentials, unlike those of endocardium, display a "spike and dome" morphology that becomes progressively more accentuated at slower stimulation rates. Using the restitution of phase 1 amplitude as a marker for the process responsible for the spike and dome phenomenon, we were able to delineate two exponential components: 1) a slow component that recovers with a time constant of 350-570 msec and 2) a fast component with a time constant of 41-85 msec. The slow component was largely abolished by 1-5 mM 4-aminopyridine, an Ito blocker. The fast component was diminished by 4-aminopyridine, but it was also inhibited by ryanodine and by Sr2+ replacement of Ca2+, which are interventions known to inhibit the Ca2+-activated component of Ito. Following 4-aminopyridine and Sr2+ or ryanodine treatment, the epicardial responses more closely resembled those of endocardium. In summary, the data demonstrate a marked heterogeneity of active membrane properties in canine ventricular muscle. These observations may aid in understanding the basis for rate-dependent changes in the T wave of the ECG, supernormal conduction in ventricular muscle, the greater sensitivity of epicardium to ischemia, and the rate dependence of some cardiac arrhythmias.

4-Aminopyridine↗
PubMedDate not supplied

[Comparative study of the space constant of electrotonic decay in the endocardium and epicardium of the rabbit right atrium].

The distribution of the electronic potential in the endocardium and epicardium of the rabbit right atrium was studied. The distribution of the electronic potential was studied by the method of intracellular polarization of cardiac fibers via a suction electrode perfused from the inside with a KCl isotonic solution. The space constant of electronic decay along and across cardiac fibers in the endocardium and epicardium of rabbit right atrium was measured. It was shown that the space constant of electronic potential decay in rabbit the right atrium endocardium in the areas of ordered arrangement of trabecules both along (lambda x = 2117 +/- 653 microns) and across (lambda y = 394 +/- 212 microns) the fiber was higher (p < 0.001) than that in epicardium (lambda x and lambda y equal to 1361 +/- 486 microns and 212 +/- 63 microns, respectively). The values lambda x and lambda y do not significantly differ between separate areas of the epicardium. The degree of electrotonic anisotropy in all the structures investigated was almost the same, its value ranging from 2 to 17.

Algorithms↗
PubMed1986

[Metastatic cancer of the endocardium].

16 cases of metastatic cancer in the endocardium collected from 2,050 autopsy cases in Baptist Medical Center, Missouri, USA from 1961 to 1983 are reported. There were 484 malignant tumors and 68 metastatic cancers in the heart, in which 16 involved the endocardium comprising 0.8% of the total autopsies during the same period, 3.3% of the malignant tumors and 23.5% of the metastatic cancer in the heart. Primary sites of these 16 cases are as follows: malignant melanoma 6 cases, lung cancer 2, thyroid carcinoma 2, rectal cancer 2, breast, liver, kidney and skin 1 case each. Metastatic cancer in the endocardium is rare. Diagnosis is commonly made by occurrent findings during autopsy. The primary lesions, metastatic sites and pathological and clinical features are discussed.

Adenocarcinoma↗
PubMed1984

The early changes induced by isoproterenol in the endocardium and adjacent myocardium.

The acute phase of isoproterenol cardiotoxicity in the rat heart was studied by both scanning and transmission electron microscopy. The endocardium and immediate adjacent myocardium of the left ventricle and septum were chosen for examination because this area should be less affected by myocardial underperfusion. The initial damage, which was mainly to the endocardium, was well defined by 30 minutes; this damage consisted of endocardial cell contraction and separation with activated platelets adhering to the exposed subendocardium. Myocardial cell changes were present at 1 hour and always included those cells adjacent to the endocardium; frequently the damage did not extend to involve the deeper tissue layers. Polymorphonuclear leukocytes were present but not in large numbers before three hours. These results suggest that myocardial ischemia due to the action of isoproterenol is not a major factor in isoproterenol cardiotoxicity.

Animals↗
PubMed1982

[Difference of the shortening characteristics between left ventricular endocardium and epicardium as measured by radiopaque markers in experimental dogs].

This study was performed to clarify the difference of shortening characteristics between left ventricular epicardium and endocardium. Four to five pairs of radiopaque markers (lead beads, phi 0.3- 0.8 mm) were implanted just beneath the epicardium and endocardium, respectively in eight open-chest dogs. After the pericardium and thorax were closed, biplane cine-roentgenograms were obtained. The spatial distance (segment length) between any two of the markers was calculated using a digitizer-computer-plotter system. Left ventricular wall thickness (Th) was measured as a distance between epicardial and endocardial markers. The maximum left ventricular thickness (Thmax) was 9.4 +/- 3.4 mm (mean +/- SD), the minimum (THmin) 8.4 +/- 3.1 mm, and a percent increase of wall thickness [(Thmax-Thmin)/Thmin] was 12.7 +/- 6.5%. The value of epicardial segment length divided by endocardial segment length as normalized by each length at R wave of ECG was 1.088 +/- 0.071 at the end of systole and 0.979 +/- 0.016 at end diastole, indicating that endocardial segment shortened and distended more than epicardial segment during systole and diastole, respectively. Epicardial segment began to shorten 3 +/- 26 msec earlier and distend 4 +/- 50 msec earlier than endocardial one. This study revealed a small but consistent difference in the amount of shortening and its initiation and termination between the epicardium and endocardium.

Angiocardiography↗
PubMed1993

Endocardium modulates myocardial contractile performance in isolated guinea pig papillary muscles.

Selective removal of endocardium by 1-s immersion of the muscle into 0.5% Triton X-100 resulted in a significant reduction of PT (peak isometric twitch tension) at 1.25 mmol.L-1 [Ca2+]o over the stimulation frequency from 0.2 to 2.0 Hz (3.2 +/- 0.2 vs 4.4 +/- 0.4 mN/mm2 at 1 Hz, P < 0.01), while +dT/dtmax was unaltered. Tension-[Ca2+]o relation was shifted in accordance to [Ca2+]o, but with no significant change on PT at high [Ca2+]o compared with endocardium-intact muscles. TPT (time to peak isometric tension) and RT1/2 (half isometric relaxation time) were typically shortened at all [Ca2+]o or various stimulation frequencies (TPT: 203 +/- 18 vs 265 +/- 37 ms; RT1/2: 77 +/- 10 vs 108 +/- 26 ms, at 1.25 mmol.L-1 and 1 Hz, P < 0.01). Stimulation duration-threshold curve was slightly shifted to the left, yet no change in ERP (effective refractory period) was found. The data demonstrated that endocardium was an important modulator of myocardial contractile performance.

Animals↗
PubMed1982

Sequelae of atriotomy and ventriculotomy on the endocardium, conduction system and coronary arteries.

The endocardium was analyzed in all four chambers of 99 hearts with various types of congenital heart defects in which surgical repair was performed more than 6 weeks before death. The findings were compared with those of normal hearts in similar age groups. In some cases the endocardium was microscopically examined. This study revealed that in many cases all four chambers had fibroelastosis of the endocardium (diffuse regardless of the type of surgery done previously). These data suggest that diffuse fibroelastosis can occur as a result of surgical intervention and may be related to blocked lymphatic drainage. Sudden death in some patients long after surgery for congenital heart disease and the failure of the chambers to regress to normal size in some cases after total surgical repair may be related to fibroelastosis of the chambers. The sinoatrial node may be injured in atriotomy and in the performance of the Mustard procedure. Ventriculotomy may injure the right bundle branch. Ventriculotomy may also injure the coronary supply to the right ventricle or rarely the anterior descending coronary artery.

Adolescent↗