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PubMed1999

Localization of distant urogenital system-, central nervous system-, and endocardium-specific transcriptional regulatory elements in the GATA-3 locus.

We found previously that neither a 6-kbp promoter fragment nor even a 120-kbp yeast artificial chromosome (YAC) containing the whole GATA-3 gene was sufficient to recapitulate its full transcription pattern during embryonic development in transgenic mice. In an attempt to further identify tissue-specific regulatory elements modulating the dynamic embryonic pattern of the GATA-3 gene, we have examined the expression of two much larger (540- and 625-kbp) GATA-3 YACs in transgenic animals. A lacZ reporter gene was first inserted into both large GATA-3 YACs. The transgenic YAC patterns were then compared to those of embryos bearing the identical lacZ insertion in the chromosomal GATA-3 locus (creating GATA-3/lacZ "knock-ins"). We found that most of the YAC expression sites and tissues are directly reflective of the endogenous pattern, and detailed examination of the integrated YAC transgenes allowed the general localization of a number of very distant transcriptional regulatory elements (putative central nervous system-, endocardium-, and urogenital system-specific enhancers). Remarkably, even the 625-kbp GATA-3 YAC, containing approximately 450 kbp and 150 kbp of 5' and 3' flanking sequences, respectively, does not contain the full transcriptional regulatory potential of the endogenous locus and is clearly missing regulatory elements that confer tissue-specific expression to GATA-3 in a subset of neural crest-derived cell lineages.

Animals↗
PubMed1980

A method to analyze the motion of the endocardium during contraction.

Regional segmental wall motion analysis assumes a linear or radial grid system. In this study, motion patterns of points on the canine endocardium were evaluated. Radiopaque endocardial and epicardial markers were inserted along the anterior and posterior descending coronary arteries. Postoperative cine radiography showed that the endocardial markers did not move along either linear or radial grids. The endocardial and epicardial markers were shown to have different patterns of movement.

Animals↗
PubMedDate not supplied

Presence of contractile-type smooth muscle cells in the endocardium.

A smooth muscle layer exists in the parietal endocardium. Notwithstanding previous pioneer work, little has been known on the phenotypes of these smooth muscles. In humans as in animals, smooth muscles show two distinct phenotypes, the 'synthetic' and 'contractile' states, which can be differentiated on the basis of the expression of two types of myosin heavy chain isoforms, SM1 and SM2. In this study, using SM1- and SM2-specific monoclonal antibodies, we performed immunohistochemical examinations to determine the phenotype of the endocardial smooth muscles. We report here that the endocardial smooth muscles have the contractile phenotype.

Antibodies, Monoclonal↗
PubMed1997

Effects of quinidine on repolarization in canine epicardium, midmyocardium, and endocardium: I. In vitro study.

BACKGROUND: The antiarrhythmic action of quinidine is associated with a slowing of conduction and prolongation of repolarization. The latter effect has no consistent correlation with quinidine actions on action potential duration (APD) in isolated tissue experiments. To enhance our understanding of the mechanisms of quinidine action, we studied its effect on APD in canine epicardial, midmyocardial, and endocardial tissues. METHODS AND RESULTS: Standard microelectrode techniques were used to study the effects of quinidine 2.5 to 20 micromol/L on APD in ventricular epicardial, endocardial, and transmural (M-cell) slabs at cycle lengths (CLs) from 300 to 4000 ms. Qualitatively different time courses of actions and concentration- and rate-dependent effects were seen in M cells compared with the others. In endocardium and epicardium, quinidine induced monotonic and concentration-dependent APD prolongation at all CLs. In contrast, the effects of quinidine in M cells varied from prolongation to shortening, depending on duration of superfusion, concentration, and CL. Experiments with E4031 and TTX suggested that in M cells, quinidine-induced APD lengthening was attributable to block of delayed rectifier potassium current and APD shortening was due to inhibition of TTX-sensitive steady-state sodium current. CONCLUSIONS: In vitro, there is a significant difference of quinidine effects in M cells versus epicardial and endocardial cells that appears to reflect differences in the contributions of specific ion channels to the APD at the three sites. The differences may influence the actions of quinidine on repolarization of the heart in situ and determine both the proarrhythmic and antiarrhythmic actions of the drug.

Action Potentials↗
PubMed1997

Effects of quinidine on repolarization in canine epicardium, midmyocardium, and endocardium: II. In vivo study.

BACKGROUND: In the companion article, we report a significant difference in quinidine effects on the action potential duration between surface (epicardial and endocardial) cells and midmyocardial cells (M cells) of canine left ventricle in vitro. This article considers two questions raised by the previous study: (1) Are the complex quinidine effects in vitro reflected in its actions on the heart in situ? (2) What are the cellular determinants of quinidine effects on QT interval in ECG? METHODS AND RESULTS: We used plunge and surface electrodes to measure activation-recovery intervals (ARIs) of bipolar electrograms obtained from epicardium, endocardium, and midmyocardium (3, 5, and 9 mm from epicardium) of canine left ventricle in conditions of AV block and right ventricular pacing. Quinidine was infused continuously; its plasma level increased from 1.6+/-0.1 microg/mL at 30 minutes to 7.6+/-0.7 microg/mL at 180 minutes. At cycle lengths (CLs) from 300 to 1500 ms, there was no ARI gradient across the ventricular wall before and during quinidine infusion. At a CL of 300 ms, therapeutic concentrations of quinidine prolonged ARIs and QT intervals. At a CL of 1500 ms, ARIs were significantly prolonged at low quinidine concentrations. With an increase of quinidine concentration, this effect subsided and disappeared. CONCLUSIONS: In situ, quinidine-induced prolongation of repolarization is uniform in all myocardial layers and follows the pattern observed in M cells in vitro. The ability of quinidine in therapeutic concentrations to prolong repolarization at rapid heart rates can contribute to its antiarrhythmic efficacy.

Animals↗
PubMed1999

Validation of a new noncontact catheter system for electroanatomic mapping of left ventricular endocardium.

BACKGROUND: Improvements in cardiac mapping are required to advance our understanding and treatment of arrhythmias. This study validated a new noncontact multielectrode array catheter and accompanying analysis system to provide electroanatomic mapping of the entire left ventricular (LV) endocardium during a single beat. METHODS AND RESULTS: A 9F 64-electrode balloon array catheter with an inflated size of 1.8x4.6 cm was used to simultaneously record electrical potentials generated by the heart and locate a standard electrophysiology (EP) catheter within the same chamber. By use of the recorded location of the EP-catheter tip, LV geometry was determined. Array potentials served as inputs to a high-order boundary-element method to produce 3360 potential points on the endocardial surface translatable into electrograms or color-coded activation maps. Three methods of validation were used: (1) driven electrodes in an in vitro tank were located; (2) waveforms generated from the array catheter were compared with catheter contact waveforms in canine LV; and (3) sites of local LV endocardial activation were located and marked with radiofrequency lesions. Tank testing located a driven electrode to within 2.33+/-0.44 mm. Correlation of timing and morphology of computed versus contact electrograms was 0.966. Radiofrequency lesions marked 17 endocardial pacing sites to within 4.0+/-3.2 mm. CONCLUSIONS: This new system provides anatomically accurate endocardial isopotential mapping during a single cardiac cycle. The locator component enabled placement of a separate EP catheter to any site within the mapped chamber.

Animals↗
PubMedDate not supplied

Sarcomatous pleural mesothelioma metastatic to left ventricular endocardium.

A 71-year-old man, a cigarette smoker with long-term asbestos exposure, developed multifocal malignant sarcomatous pleural mesothelioma that metastasized to the left ventricular endocardium without invading pericardium, myocardium, or the contiguous pulmonary vein. This is the first reported case of malignant pleural mesothelioma to metastasize in such a manner.

Aged↗
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↗
PubMed1999

[Papillary fibroelastoma of the endocardium].

Six cases of papillary fibroelastoma of the endocardium were presented. All cases appeared as incidental findings at autopsy. Grossly, they were verrucous or tuft-like growths less than 1 cm in size on cardiac valves. Histologically, they consisted of a fibrocollagenous stalk and multiple papillary fronds with typical zonal architecture: central dense hyaline core containing elastic fibers surrounded by a layer of myxoid matrix and covered by hyperplastic endothelial cells. At the surface of papillary fronds there were foci of fibrin deposition. Histogenesis of papillary fibroelastomas is unclear, they are considered variously as primary benign tumours, hamartomas or organized thrombi.

Aged↗
PubMed2002

[Semiautomatic algorithm for tracing an outline of the endocardium in newborns].

Visual assessment of the endocardial outline is too subjective and the results do not provide enough support for reliable analysis. The main problem that hinders echocardiographic diagnosis in measurements of ventricular size and shape during subsequent cycles of cardiac function lies in difficulties in obtaining precise delineation of endocardial margins. A new, semiautomatic algorithm for tracing endocardial outlines of newborns that were detectable in echocardiographic images is presented. The material consisted of 1920 historical echograms of newborns with selected congenital heart defects (total anomalous pulmonary venous return--TAPVR, hypoplastic left heart syndrome--HLHS, and transposition of the great arteries--TGA) and control group. The algorithm was successfully used in the analysis of 384 images of heart chambers (right and left ventricles) of newborns in systole and diastole. The results were subjected to a statistical analysis and revealed that semiautomatic algorithms can give consistent, repeatable, good quality results, and image analysis methods can be an efficient, additional tool for the quantitative interpretation of echocardiograms of the endocardium in newborns.

Algorithms↗
PubMedDate not supplied

[Pathomorphology of the endocardium and myocardium in the heart injury].

Light, polarization, luminescent microscopy, phase contrast, special staining methods and scanning electron microscopy were used for studying sections and fragments of the endocardium and myocardium from 123 patients who had died of heart contusion and ischemic heart disease and from 50 rats with experimental heart contusion. The morphological classification of heart contusion and differential-diagnostic table of myocardial alterations due to contusion of the heart and ischemic heart disease are proposed to facilitate pathomorphological diagnosis of heart contusion. The classification of pathomorphological signs in heart contusion is presented.

Adolescent↗
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↗
PubMed1987

[Morphologic features of the endothelial lining of the blood vessels and endocardium].

The endothelial lining (EL) of ventricular endocardium and coronary arteries of a dog, minipig and humans, as well as that of the abdominal aorta of a rat and superior vena cava (minipig) was studied using luminescent microscope in the reflected light after staining of the non-fixed tissue with thioflavine-T and argentation. Marked heterogeneity of the endotheliocytes was shown to be both specific and depending on the localization of the cells in the cardiovascular system. Comparative analysis of EL in different animal species and in man, as well as in different parts of the CVS, indicated the relationship between the cellular morphologic features and local hemodynamics.

Animals↗
PubMed1981

[Permeability characteristics of the endocardium and the myocardial capillaries to horseradish peroxidase in fetal and postnatal rats].

After intravenous or intracardial application of horseradish peroxidase (HRP) at the myocardial capillaries of fetal, juvenile and adult rats a fast transport of the tracer into the interstite can be observed. In the fetal cases the transport takes place especially through the interendothelial junctions, in the postnatal cases a considerably amount of the peroxidase traversed also by plasmalemmal vesicles. In adults the T-tubules of the myocytes are labelled already after 15 min of circulation. From fetal stages up to adults the junctions of the endocardium are well permeable to HRP. After a short circulation time we found large deposits of reaction product in the subendocardial space. The reasons for the different permeability of fetal heart and skeletal muscle capillaries were discussed.

Aging↗
PubMed1989

Analysis of the endocardium and cardiac jelly in truncal development in the cardiac lethal mutant axolotl Ambystoma mexicanum.

Recessive mutant gene c in axolotls results in a failure of the heart to function because of abnormal embryonic induction processes. The myocardium in this mutant lacks organized sarcomeric myofibrils. The present study was undertaken to determine if developmental abnormalities were evident in other areas of the heart besides the myocardium. A detailed comparative survey of the structure of developing normal and mutant hearts, including the endocardium, its cellular derivatives, and the extracellular matrix, known as cardiac jelly, showed that in the mutant there are fewer than the normal number of endocardial cells lining the heart lumen, the number of mesenchyme cells is reduced, and the cardiac jelly area is greatly enlarged in the posterior part of the truncus adjacent to the ventricle.

Ambystoma↗
PubMed1977

Trichinosis causing extensive ventricular mural endocarditis with superimposed thrombosis. Evidence that severe eosinophilia damages endocardium.

Clinical and morphologic observations are described in a 46 year old woman with fatal trichinosis. Attention is called to the occurrence of extensive ventricular endocardial damage with superimposed thrombosis; Evidence is presented to indicate that the most likely cause of the endocardial damage is the associated eosinophilia. The mechanism by which eosinophils damage endocardium, however, remains obscure.

Coronary Disease↗