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At least 19 recordsLinked to original sources
PubMed1991

Factors released from endocardium of the ferret and pig modulate myocardial contraction.

1. In isolated heart muscle preparations, selective removal of the endocardium results in a characteristic and unusual negative inotropic effect. Possible mechanisms for this effect were investigated in this study. 2. In endocardium-intact preparations of ferret papillary muscle, 8-bromo-cyclic GMP, sodium nitroprusside, atrial natriuretic peptide (ANP) and substance P each induced changes in contractile behaviour similar to selective endocardial removal, and each significantly elevated myocardial cyclic GMP levels. Substance P failed to elevate myocardial cyclic GMP levels following removal of endocardium or in the presence of haemoglobin, suggesting that it may act by releasing endothelium-derived relaxing factor (EDRF) from endocardium. However, there was no change in myocardial cyclic GMP levels following endocardium removal alone. 3. In cascade bioassay experiments, it was confirmed that porcine cultured endocardial cells released an unstable humoral agent whose effects on an endothelium-denuded pig coronary artery were indistinguishable from EDRF. 4. The negative inotropic effects of endocardium removal were reversed in bioassay experiments where an endocardium-denuded papillary muscle was exposed to the effluent from a column of porcine cultured endocardial cells on microcarrier beads. This demonstrates for the first time the release of a 'contraction prolonging factor' from endocardium, the tonic release of which would explain the negative inotropic effect of endocardium removal. 5. It is concluded that elevation of ferret papillary muscle cyclic GMP (as for example with EDRF) produces changes in contractile performance similar to those induced by endocardium removal. We also demonstrate that superfused porcine cultured endocardial cells release a humoral agent (provisionally named 'endocardin') which causes reversal of the changes in mechanical properties seen after endocardial removal.

Animals↗
PubMed1991

Sodium channel block produces opposite electrophysiological effects in canine ventricular epicardium and endocardium.

Using microelectrode techniques we compared the effects of tetrodotoxin (TTX, 2-3 microM), DL-propranolol (1-3 micrograms/ml), and flecainide acetate (10-15 microM) on isolated canine ventricular epicardial (epicardium) and endocardial (endocardium) tissues. Propranolol, TTX, and flecainide decreased Vmax and phase 0 amplitude in a use-dependent manner in both tissues. The effects of propranolol were slow to develop and wash out. TTX and propranolol always abbreviated action potential duration in endocardium. Action potential duration was abbreviated by 23.8 +/- 5.6 msec after propranolol (1 microgram/ml, basic cycle length [BCL] = 1,000 msec) and 10.8 +/- 12.9 msec after TTX (2 microM, BCL = 1,000 msec). In epicardium, the reduction of phase 0 and 1 amplitudes led to a slowing of the second action potential upstroke and an increase in the amplitude of phase 2. This accentuation of the notch resulted in a paradoxical prolongation of the epicardial action potential. Action potential duration was prolonged 34.4 +/- 11.3 msec after 4 hours of exposure to propranolol (1 microgram/ml, BCL = 1,000 msec), 11.1 +/- 6.3 msec after 15 minutes of exposure to TTX (2 microM, BCL = 1,000 msec), and 19.9 +/- 8.2 msec after 25-45 minutes of exposure to flecainide (15 microM, BCL = 500 msec). With stronger sodium block, phase 1 terminated at more negative potentials, the second upstroke often failed to appear, and an all-or-none repolarization ensued causing a marked abbreviation of the epicardial action potential. In some epicardial preparations, we observed marked abbreviation at some sites but prolongation at other sites after sodium blockade with flecainide. The dispersion of repolarization was often attended by reentrant activity. The differential response of epicardium and endocardium to sodium blockade was not observed when the preparations were pretreated with 4-aminopyridine or ryanodine, agents known to diminish the transient outward current and epicardial notch. Acceleration-induced prolongation of refractoriness was observed after sodium blockade in epicardium but not in endocardium. Postrepolarization refractoriness also occurred in epicardium but not in endocardium after TTX, propranolol, or flecainide exposure. The data indicate that propranolol, TTX, and flecainide, via their action to block sodium current, may exert opposite effects on action potential duration and refractoriness in cells spanning the ventricular wall. The presence of the transient outward current in epicardium but not in endocardium appears to contribute importantly to these differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1975

Intercellular junctions of rat endocardium.

The ultrastructure of the intercellular junctions of rat endocardium has been characterized following lanthanum exposure in vitro and uranyl acetate staining en bloc. The interendothelial clefts of the endocardium run either a relatively straight or convoluted course and posses one or two loci where the plasma membranes are in close apposition or form punctate fusions. Elongate restrictions, that exhibit hexagonal arrays of subunits following lanthanum immersion (gap junctions), are also present in the intercellular endocardial clefts. The occurrence of interendothelial clefts of endocardium lacking occlusive foci can account for the permeability properties of ventricular endocardium, where the direction of diffusion of macromolecules has been attributed to pressure gradients between ventricular cavity and myocardium. The relationship of gap junctions to possible electrical phenomena within the endocardium is also discussed.

Animals↗
PubMed1991

Laser-induced fluorescence emission: I. The spectroscopic identification of fibrotic endocardium and myocardium.

UNLABELLED: Laser-induced fluorescence has been developed as a guidance system for laser angioplasty. Laser ablation has been used for resection of arrhythmogenic ventricular scar. We have investigated the use of laser-induced fluorescence for the detection of fibrotic and ischemic changes in endocardium and myocardium. Fluorescence emission spectra from human necropsy specimens were correlated with histologic examination. Normalized fluorescence intensity detected from both the endocardial and the myocardial surfaces of the fibrotic ventricular specimens was significantly higher than that of corresponding normal specimens at 440 to 475 nm. Fibrotic endocardium could be identified by a fluorescence emission intensity ratio less than 1.5 for wavelength ratio 375/450nm. Acutely infarcted endocardium was recognizable by a ratio of 1.5 to 2.0. The specificity and sensitivity of detection of scarred endocardium was 70 and 100%, respectively. Fibrotic myocardium was also consistently identified by fluorescence spectroscopy. CONCLUSION: Fluorescence emission spectroscopy can differentiate normal and fibrotic endocardium and myocardium, in vitro. This technique may be useful for guidance during laser ablation of arrhythmogenic ventricular scar.

Capillaries↗
PubMed1975

[Compensatory-adaptive changes in the endocardium in functional overload of the heart].

In experiments on 46 dogs a structural rearrangement of the endocardium of the left atrium in the process of development of the chronic compensated cardial insufficiency was studied. Dynamics of changes, caused by hypertrophy of the subendothelial layer of the endocardium and its subsequent differentiation, which led to hyperelastosis of the endocardium, as well as hypertrophy and hyperplasia of the smooth-muscle elements of the endocardium were revealed. Analysis of the data obtained, from the functional point of view, enabled the authors to consider the described rearrangement of the endocardium as one of the mechanisms of cardiac compensation.

Acute Disease↗
PubMed1991

Origins and patterning of avian outflow tract endocardium.

Outflow tract endocardium links the atrioventricular lining, which develops from cardiogenic plate mesoderm, with aortic arches, whose lining forms collectively from splanchnopleuric endothelial channels, local endothelial vesicles, and invasive angioblasts. At two discrete sites, outflow tract endocardial cells participate in morphogenetic events not within the repertoire of neighboring endocardium: they form mesenchymal precursors of endocardial cushions. The objectives of this research were to document the history of outflow tract endocardium in the avian embryo immediately prior to development of the heart, and to ascertain which, if any, aspects of this history are necessary to acquire cushion-forming potential. Paraxial and lateral mesodermal tissues from between somitomere 3 (midbrain level) and somite 5 were grafted from quail into chick embryos at 3-10 somite stages and, after 2-5 days incubation, survivors were fixed and sectioned. Tissues were stained with the Feulgen reaction to visualize the quail nuclear marker or with antibodies (monoclonal QH1 or polyclonals) that recognize quail but not chick cells. Many quail endothelial cells lose the characteristic nuclear heterochromatin marker, but they retain the species-specific epitope recognized by these antibodies. Precursors of outflow tract but not atrioventricular endocardium are present in cephalic paraxial and lateral mesoderm, with their greatest concentration at the level of the otic placode. Furthermore, the ventral movement of individual angiogenic cells is a normal antecedent to outflow tract formation. Cardiac myocytes were never derived from grafted head mesoderm. Thus, unlike the atrioventricular regions of the heart, outflow tract endocardial and myocardial precursors do not share a congruent embryonic history. The results of heterotopic transplantation, in which trunk paraxial or lateral mesoderm was grafted into the head, were identical, including the formation of cushion mesenchyme. This means that cushion positioning and inductive influences must operate locally within the developing heart tubes.

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↗
PubMed1991

Role of the endocardium in the inotropic action of UD-CG-212 CL.

UD-CG-212 CL is a metabolite of pimobendan (UD-CG-115 BS), a non-glycosidic, non-adrenergic positive inotropic agent. In the present study we investigated the effect of UD-CG-212 CL on cat papillary muscles in the presence or absence of an intact endocardial endothelium. The endocardium was damaged by a very short detergent treatment. We demonstrated that, in muscles with an intact endocardial endothelium, UD-CG-212 CL induced a moderate, but significant inotropic effect resembling the changes induced by adrenoceptor agonists. Addition of an alpha- and or beta-blocker reduced this positive inotropic effect. The effect induced by UD-CG-212 CL, was completely abolished after the endocardial endothelium was damaged. We conclude that the endocardium played a modulatory role in the action of UD-CG-212 CL through the release of various factors with inotropic activity.

Adrenergic alpha-Antagonists↗
PubMed1990

Effects of multipolar electrode radiofrequency energy delivery on ventricular endocardium.

This study examined the effects of radiofrequency energy applied in a bipolar fashion with single as compared with multiple sequential applications at the canine endocardium. In this closed-chest model, radiofrequency energy (750 kHz) was delivered between two adjacent poles of an electrode catheter. Single applications were performed at distinct sites in the left (n = 30) and right ventricles (n = 29) of 13 normal dogs. A multiple sequential technique, which enlarges the ablated endocardial surface, was applied in the left (n = 13) and right ventricles (n = 4) of seven normal dogs and six dogs with remote myocardial infarction. Single applications (199 +/- 200 joules) resulted in lesions with a volume of 0.12 +/- 0.06 cm3 (range 0.03 to 0.31 cm3) and an endocardial surface area of 0.29 +/- 0.15 cm2 (range 0.06 to 0.63 cm2). Changes at the catheter/tissue interface led to a rise in impedance, restricting further enlargement of the necrosis. Sequential delivery of radiofrequency energy between poles 1 and 2, 2 and 3, and 3 and 4 of a quadripolar electrode catheter repeated 9 to 11 times in slightly different positions allowed a cumulative energy of 6571 +/- 3857 joules to be applied to the endocardium, resulting in a lesion volume of 0.84 +/- 0.38 cm3, with an endocardial lesion surface area of 3.7 +/- 1.2 cm2 (range 2.9 to 5.1 cm2). Histologically, all radiofrequency lesions were restricted to the endocardium/subendocardium with a small border zone of injury. Aggressive stimulation techniques did not induce ventricular tachycardia in any of the dogs before and 19 +/- 11.4 days after multiple sequential ablations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Repolarization differences between guinea pig atrial endocardium and epicardium: evidence for a role of Ito.

It has long been known that ventricular epicardial action potential duration (APD) is shorter than endocardial, and recent evidence suggests that a larger transient outward current (Ito) in epicardium is responsible for the difference. To evaluate possible corresponding regional variations in atrial tissue, we studied guinea pig atrial epicardial and endocardial action potentials using standard microelectrode techniques. Epicardial APD was consistently shorter than endocardial, but the difference was greatly diminished by rapid pacing or early premature activation, situations in which Ito availability should be limited. 4-Aminopyridine (4-AP), at concentrations (0.5 mM) producing specific Ito blockade, increased APD significantly in atrial epicardium without affecting endocardium. The effect of 4-AP on APD was most marked at slow rates, at which Ito would be greatest, and was negligible at rapid rates or during premature activation, during which Ito would be largely inactivated. At larger concentrations (5 mM) 4-AP caused an equalization of epicardial and endocardial APD. The equimolar substitution of strontium for calcium did not affect APD at slow rates and increased APD (particularly in endocardium) at rapid rates, suggesting that the Ito underlying endocardial-epicardial differences was unlikely to be calcium dependent. We conclude that epicardial-endocardial differences in APD, well documented in ventricular tissue, can also occur in atrial tissue and that the underlying ionic mechanisms appear to be similar.

4-Aminopyridine↗
PubMed1992

Permeability of rat atrial endocardium, epicardium, and myocardium to large molecules. Stretch-dependent effects.

Atrial distension, which stimulates atrial natriuretic peptide secretion by atrial myocytes, also stretches nonmuscle cells. In a noncontracting in vitro preparation of combined right and left atria we demonstrated by electron microscopy that, at 37 degrees C, transition from zero pressure to a physiological distending pressure of 5.1 mm Hg rapidly rendered atrial endocardial endothelium permeable to the macromolecular probes horseradish peroxidase (HRP; M(r), approximately 40,000) and wheat germ agglutinin-HRP (M(r), approximately 70,000); each probe was introduced at the atrial cavitary endocardial surface. Stretch-dependent permeabilization was also demonstrable in spontaneously contracting atria, was reversed by removing the distending pressure, and was unaffected by varying external Ca2+ concentration from 0.2 to 1.4 mM or by experimental perturbations that markedly decrease ANP secretory rates. Although transendocardial HRP and wheat germ agglutinin-HRP passage required stretch, native ferritin (M(r), = 500,000) could traverse unstretched endocardium. Probes were detected in noncoated endocardial vesicles and intercellular junctions between endocardial cells, but the relative contributions of vesicular transcytosis and paracellular diffusion could not be determined. Although HRP entered plasmalemmal caveolae of myocytes in stretched atria, myocytes did not internalize HRP by fluid-phase endocytosis. Distending pressure also caused apparent flow reversal in thebesian blood vessels, with retrograde transfer of HRP across the endocardium into the myocardium. HRP and ferritin presented at the external surface of the epicardium (visceral pericardium) were endocytosed by mesothelial cells, entered junctions between mesothelial cells, and readily crossed the epicardium of both stretched and unstretched preparations.

Animals↗
PubMed1991

Catheter ablation of the atrioventricular junction using a helical microwave antenna: a novel means of coupling energy to the endocardium.

Catheter ablation with either direct current defibrillator discharges or radiofrequency energy produces tissue injury via current flow from an electrode into the adjacent myocardium. In order to affect tissue at a distance, excessive power density may be produced at the electrode-tissue interface with the possibility of explosive gas formation or coagulum formation. A novel microwave catheter was developed with a helical antenna distally. This coil, although not in direct contact with the endocardium, radiates an electromagnetic field into the tissue that, in turn, causes thermal injury. The utility of this system for ablation was assessed in six dogs. The antenna catheter was introduced percutaneously and positioned so as to record the largest His electrogram. Microwave power (50 watts at 2,450 MHz) was applied for 114 +/- 118 seconds. Complete AV block was produced in all six animals with 1.8 +/- 1.2 applications. There was no ventricular ectopy or change in blood pressure during microwave ablation. One dog died 6 days after ablation. The remaining five dogs had persistent, complete AV block during 6 weeks of follow-up. Pathological analysis at 6 weeks revealed a large (mean 2.8 x 4.7 mm) fibrovascular scar in the region of the AV junction. Percutaneous microwave ablation of the endocardium appears feasible. By radiating an electromagnetic field without direct contact, this system can produce large lesions without being limited by desiccation of tissue and impedance rise.

Animals↗
PubMed1978

Starch granulomata of the endocardium.

Two cases of granuloma of the endocardium following cardic catherterisation are described. In each case the granuloma consisted essentially of macrophages associated with intracellular and extracellular starch granules, derived presumably from the glove powder used at operation. No previous cases of this condition have been found in the literature.

Adult↗
PubMed1978

Permanent cardiac pacing with electrodes of a new type of fixation in the endocardium.

To improve electrode construction the following main problems have been considered: (1) reliable initial fixing in the endocardium, and (2) reducing the area of contact surface and improving threshold values. In this article we have described three original electrodes: 1) an endocardial electrode with a multi-edged tip (contact area 28 mm2), which gives high electric field strength and low thresholds; 2) a spreading tip electrode, which was created on the basis of morphological data. The tissues grow into the spread spaces of this tip and ensure better stability (contact area 17.8 mm2); and 3) a double-screw-in electrode which differs from the other corkscrew types. The contact end (surface area--10.4 mm2) consists of two sickle-shaped hooks. The sickle handle is 0.7 mm in length which prevents further hook penetration in the wall of the heart. It was found that a multi-edged electrode and electrodes supplied with a fixation device are, in terms of energy consumption, more effective compared to electrodes with spherical or cylindrical tips of the same area of contact surface. The double-screw-in endocardial electrode has useful features: reliable fixation and a small contact surface area and, therefore, a low threshold value. Thirty-five double-screw-in electrodes were inserted into an atrial position and 28 into a ventricular position. We have not observed any displacement of such electrodes during the past two years.

Cardiac Pacing, Artificial↗
PubMed1975

Freeze-drying from tertiary butanol in the preparation of endocardium for scanning electron microscopy.

The scanning electron microscope appearances and shrinkage of blocks of canine endocardium prepared by freeze-drying directly, by freeze-drying after replacing tissue water with tertiary butanol (2-methyl propan-2-ol) and by critical point drying were compared. All three methods demonstrated endothelial cells which showed nuclear prominences, microvilli and intercellular boundaries. The microvilli varied in size and number from dog to dog but were generally less well defined in specimens freeze-dried from water. Shrinkage due to t-butanol dehydration was significantly less than that which occurred in ethanol in the critical point drying method. Overall the reduction in surface area was significantly less in specimens freeze-dried directly at -65 C (6.8%) than in those dried from t-butanol at -20 C (15.4%) and those prepared bly critical point drying (22.1%). However the amount of shrinkage observed in t-butanol treated tissue was not significantly different from that which was critical point dried. It was not possible to distinguish between comparable samples prepared by these two methods on the basis of their scanning electron microscopic appearances. Thus the relative simplicity and convenience of the t-butanol method, together with its saving of time, its use of standard freeze-drying equipment and the avoidance of ice-crystal artefact justify its consideration as an alternative method of preparing wet biological tissue for scanning electron microscopy.

Animals↗
PubMed1975

The ultrastructure of the sensory end-organs (baroreceptors) in the atrial endocardium of young mini-pigs.

Light and electron microscopical studies on pig hearts have confirmed the presence in the right and the left atrial endocardium of distinct circumscribed, unencapsulated end-organs (baroreceptors) associated with 4-9 mum thick nerve fibres. The myelin sheath terminates before the entrance of the nerve into the end-organ. The regular presence of thin axon profiles containing clusters of small agranular vesicles, both around the thick nerve fibre and in the periphery of the end-organs, suggests a double innervation. The thick fibre arborizes inside an aggregate of Schwann-like cells to form a large number of terminals which are considered to be the mechano-sensitive receptors of the organ. In addition to the nervous structures and the Schwann-like cells the organs contain a varying number of connective tissue fibrils. The terminals are covered by a basement membrane but are partly or completely devoid of Schwann cell covering. Most of the space inside the terminals is occupied by tightly packed mitochondria. Glycogen granules are regularly present, sometimes abundant. SER occurs widely, frequently forming complexes with glycogen granules. These complexes may be highly organized as parallel or concentric structures, suggesting a close connection between SER and glycogen metabolism in the terminals. The terminals are regularly furnished with small protrusions containing numerous 30-100 nm clear vesicles which resemble pinocytotic vesicles. In addition, a few 80 nm dense-cored vesicles are found. The occurrence of numerous cyto-segresomes and lipofuscin-like bodies suggests a lively turnover of organelles in the terminals.

Animals↗
PubMed1990

Does endocardium modulate myocardial contractile performance?

It is now clear that the endocardium releases at least two agents which exert opposing effects on myocardial contraction. One appears to be endothelium-derived relaxing factor (EDRF), as in vascular endothelium, but the identity of the other is unknown. The mechanism by which these agents exert their characteristic but opposing effects on the duration of contraction likewise remains unknown. It is unlike that of other inotropic interventions and merits further investigation. Alterations in the time of onset of relaxation have important implications for diastolic filling.

Animals↗
PubMed1978

Metastatic tumors of the endocardium: report of three cases.

Because of their apparent rarity and the tendency of clinicians to lump indicative signs and symptoms under the heading of metastatic disease, metastatic tumors of the endocardium are seldom mentioned in the literature, in the three cases presented herein, endocardial metastases were evident at autopsy. In one case of malignant melanoma, clinical evidence for endocardial involvement was present in life. This article also presents a case of endocardial involvement by Wilms' tumor and a case of endocardial involvement by hypernephroma with pulmonry tumor emboli.

Adenocarcinoma↗