Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENDOCARDIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1995

Effects of brief and prolonged ischemia on eicosanoid synthesis in dog and rat hearts.

We compared the effects of brief and prolonged myocardial ischemia on tissue prostaglandin synthesis. Regional ischemia was induced in dogs and maintained for 5 or 30 minutes. Isolated rat hearts were subjected to global ischemia in a working heart preparation for periods of 5 or 20 minutes. De novo synthesis of prostaglandins PGE2 and PGF2 alpha was measured in endocardial and epicardial explants from hearts subjected to transient ischemia. After 5 minutes of coronary ligation, PGE2 production by the ischemic canine endocardium increased by 68%, compared with non-ischemic tissue, and PGF2 alpha levels rose by 29%. In isolated rat hearts, 5-minute ischemia increased endocardial rate of PGE2 synthesis (13.2 +/- 1.7 pmol/g/h, as compared with 6.7 +/- 0.5 under normoxic conditions). Ischemic stimulation of eicosanoid production by the endocardium was no longer apparent after 30-minute regional or 20-minute global ischemia. In contrast, the epicardium showed significant changes only after 30-minute ischemia and only with respect to PGF2 alpha (12.0 +/- 6.2 in the ischemic vs 7.1 +/- 3.2 pmol/g/h in the non-ischemic tissue). Ischemia-induced differences in prostaglandin production were attenuated in the presence of arachidonic acid or aspirin.

Animals↗
PubMed1996

[New method for automatic tracking of the endocardial boundary in clinical use].

This study attempted to detect the left ventricular endocardial boundary in six healthy men (volunteers) using a newly developed computerized two-dimensional echocardiography method. Automatic detection of the left ventricular endocardium was achieved by; sampling of pictures, noise reduction of the pictures, filtering, decision of the early loop, detection of the left ventricular endocardial boundary, smoothing the boundary, and correction of the boundary. This process requires only 2-3 sec. Areas of the short-axis cross-sections in systolic and diastolic phases of one cardiac cycle were obtained and the percent change rate of these areas on a cardiac cycle were calculated. These were compared with the results obtained by the manual method. The boundary of the left ventricular endocardium detected by the computerized method almost coincided with that found by the manual method. Areas and the change rates obtained were correlated with those by the manual method (areas: r = 0.86, % change rate of area: r = 0.94). This new method is suitable for clinical use.

Adult↗
PubMed1997

Thrombin augments vascular cell-dependent migration of human mast cells: role of MGF.

Recent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine- (HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 +/- 344 cells [100 +/- 11.4%] vs. MGF, 100 ng/ml: 8806 +/- 1019 [291 +/- 34%] vs. HAUEC: 9703 +/- 1506 [320.8 +/- 49.8%] vs. HUTMEC: 8950 +/- 1857 [295.9 +/- 61.4%] vs. HSMEC: 9965 +/- 2018 [329.4 +/- 66.7%] vs. HUVEC: 9487 +/- 1402 [313.6 +/- 46.4%], p < 0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

Blotting, Northern↗
PubMed1997

Fibronectins are essential for heart and blood vessel morphogenesis but are dispensable for initial specification of precursor cells.

The underlying mechanisms of lethal cardiovascular defects associated with the fibronectin-null (FN.null) mutation in mouse embryos were investigated by lineage analysis of myocardial, endocardial, and endothelial cells. A wide variation in phenotype was observed on two genetic backgrounds. In the less severe class (C57/BL6 background), FN.null embryos display a defective heart. Myocardial cells express the specific marker MF-20 and are correctly localized in the anterior trunk region, but myocardial organization is disrupted, resulting in a bulbous heart tube. Endocardial cells express the specific marker platelet-endothelial cell adhesion molecule-1 (PECAM-1) and are localized within the myocardium, but the endocardium appears collapsed. Endothelial cells of two vascular beds are specified, but the aortae are distended and lack contact with the surrounding mesenchyme, while no vessels form in the yolk sac. Defects in the more severe class suggest that FNs are essential earlier in development on the 129/Sv background. Myocardial and endocardial cells are specified, but morphogenesis of the myocardium and endocardium does not occur. Aortic endothelial cells are specified and localized normally, but remain scattered. Yolk sac endothelial cells resemble those of the less severe class. We conclude that FNs are essential for organization of heart and blood vessels, but are dispensable for cellular specification in the appropriate regions within the embryo.

Animals↗
PubMed1997

Superior-septal approach for transmitral mapping and cryoablation of ventricular tachycardia.

A superior-septal approach was used for mapping and cryoablation of the left ventricular endocardium over the mitral annulus in a patient with ventricular tachycardia associated with an inferior myocardial infarction without a ventricular aneurysm. This approach provides an excellent view of the mitral valve, and allows safe, adequate mapping and cryoablation of the left ventricular endocardium without the necessity of a ventriculotomy.

Aged↗
PubMed1989

Mucopolysaccharidosis I presenting with endocardial fibroelastosis of infancy.

We describe two female infants with Hurler syndrome (mucopolysaccharidosis I) whose deaths are attributed to cardiac failure with associated, autopsy-confirmed endocardial fibroelastosis. One infant had confirmed alpha-L-iduronidase deficiency in cultured dermal fibroblasts, and the other infant had histologic evidence of tissue mucopolysaccharide accumulation at autopsy and a sibling with confirmed alpha-L-iduronidase deficiency and the Hurler syndrome phenotype. Clear cells ("Hurler" cells) were identified within the myocardium and endocardium of both infants. We propose that the ventricular mural accumulation of mucopolysaccharides induced extensive proliferation of elastic or collagen fibers within the endocardium. Cardiac failure may precede recognition of clinical and roentgenographic features of Hurler syndrome. Our findings and a literature review suggest that certain heritable storage disorders, including mucopolysaccharidosis I, should be considered when infants have clinical electrocardiographic and echocardiographic findings consistent with endocardial fibroelastosis or have autopsy-documented endocardial fibroelastosis.

Endocardial Fibroelastosis↗
PubMed1997

Vagal afferent innervation of the atria of the rat heart reconstructed with confocal microscopy.

We have used confocal microscopy to analyze the vagal afferent innervation of the rat heart. Afferents were labeled by injecting 1,1'-dioleyl-3,3,3',3'-tetramethylindocarbocyanine methanesulfonate (DiI) into the nodose ganglia of animals with prior supranodose de-efferentations, autonomic ganglia were stained with Fluoro-gold, and tissues were examined in whole mounts. Distinctively different fiber specializations were observed in the epi-, myo-, and endocardium: Afferents to the epicardium formed complexes associated with cardiac ganglia. These ganglia consisted of four major ganglionated plexuses, two on each atrium, at junctions of the major vessels with the atria. Ganglionic locations and sizes (left > right) were consistent across animals. In addition to principal neurons (PNs), significant numbers of small intensely fluorescent (SIF) cells were located in each of these plexuses, and vagal afferents provided dense pericellular varicose endings around the SIF cells in each ganglionic plexus, with few if any terminations on PNs. In the myocardium, vagal afferents formed close contacts with cardiac muscles, including conduction fibers. In the endocardium, vagal fibers formed "flower-spray" and "end-net" terminals in connective tissue. With three-dimensional reconstruction of confocal optical sections, a novel polymorphism was seen: Some fibers had one or more collaterals ending as endocardial flower sprays and other collaterals ending as myocardial intramuscular endings. Some unipolar or pseudounipolar neurons within each cardiac ganglionic plexus were retrogradely labeled from the nodose ganglia. In conclusion, vagal afferents form a heterogeneity of differentiated endings in the heart, including structured elements which may mediate chemoreceptor function, stretch reception, and local cardiac reflexes.

Afferent Pathways↗
PubMed1999

Expression of the Mf1 gene in developing mouse hearts: implication in the development of human congenital heart defects.

The transcription factor FKHL7 gene has recently been associated with the anterior segment dysgenesis disorder of the eye known as Axenfeld-Rieger anomaly (ARA). A growing body of evidence indicates that mutations in FKHL7 cause not only defects in the anterior segment of the eye but defects in the heart valves and septa as well. In order to evaluate its contribution to normal heart septation and valve formation, expression of the mouse homologue Mf1 in embryonic hearts was analyzed by in situ hybridization. A weak but significant level of Mf1 expression could be detected in the endocardium of mouse embryos as early as day 8.5 post-conception (p.c.). Mf1 expression was undetectable in the hearts of day 9.5 p.c. embryos, but by day 10.5-11 p.c., Mf1 transcripts could be found again in the endocardium of both the atrium and ventricle and a relatively strong signal was observed in the dorsal portion of the septum primum, in what appeared to be the spinal vestibule. At day 13 p.c. when aortic and pulmonary trunks are separated, relatively more Mf1 transcripts were detected in the leaflets of aortic, pulmonary, and venous valves, the ventral portion of the septum primum, as well as in the single layer of cells on the edges of the atrioventricular cushion tissues. Surprisingly, there was no signal detected in the developing interventricular septum. At day 15 p.c., overall Mf1 signals were greatly decreased. However, significant levels of expression could still be observed in the atrial septum, the tricuspid valve, the mitral valve, and in the venous valve but not in the interventricular septum. The temporal and spatial expression patterns of the Mf1 gene in developing mouse hearts suggest that Mf1 may play a critical role in the formation of valves and septa with the exception of the interventricular septum. This is further supported by our studies showing that mutations in the FKHL7 gene were associated with defects in the anterior segment of the eye as well as atrial septal defects or mitral valve defects. Dev Dyn 1999;216:16-27.

Animals↗
PubMed1984

Echocardiographic assessment of left ventricular diastolic function in a normal population and a group of patients with myocardial hypertrophy.

In order to study left ventricular diastolic function, digitized M-mode echocardiograms of the free wall endocardium were analyzed. A population of 117 healthy individuals was compared with a group of 22 patients with myocardial hypertrophy due to aortic stenosis (AS), and a group of 21 with hypertrophic cardiomyopathy (HCMP). The time constant Te of endocardial retraction in normals (66 +/- 13 ms) differed significantly from Te in the patients (AS, 105 +/- 23 ms, p less than 0.001; HCMP, 113 +/- 31 ms, p less than 0.001). Peak velocity of endocardial retraction (peak neg. dEnd/dt, in the normals 8.6 +/- 2.7 s-1) did not differ between normals and patients (AS, 7.0 +/- 2.3 s-1; HCMP, 7.3 +/- 2.4 s-1). Fractional shortening (FS) of the internal diameter, a parameter of left ventricular systolic function, tended to be higher in the AS patients than in the normal group, but was on the average significantly increased in the group of HCMP. However, most patients in the hypertrophic groups had FS within normal limits +/- 2 SD. The discrepancy between normal or supernormal systolic function and a pathological prolonged time constant Te in myocardial hypertrophy demonstrates the importance of diastolic parameters in left ventricular characterization. Te is a useful parameter of left ventricular diastolic function which can be provided noninvasively from echocardiographic M-mode curves of the free wall endocardium.

Adolescent↗
PubMed2005

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy.

In the present investigation the relationship between the sympathetic nervous system and the endocardial levels of receptor binding sites for natriuretic peptides and the plasma content of atrial natriuretic peptide were analyzed in rats. In order to destruct the cardiac sympathetic nerve terminals, chemical sympathectomy with 6-hydroxydopamine was made in parallel with intravenous measurements of blood pressure and heart frequency. By use of immunohistochemical and enzyme-linked-immunosorbent techniques the expression of tyrosine hydroxylase-positive sympathetic nerve terminals and plasma levels of pro-atrial natriuretic peptide were determined, respectively. The occurrence of receptor binding sites for natriuretic peptides was examined by in vitro receptor autoradiography. In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers. Interestingly, this was found in parallel with a significant decrease of systolic and diastolic blood pressure and increased plasma levels of pro-atrial natriuretic peptide in the treated group of rats. These findings, together with those in previous studies, give support to an idea that one part of the blood pressure-decreasing effects, seen in patients treated with beta-adrenergic blockade, might be through a reduction of the natriuretic clearance receptor C, then giving rise to increased levels of atrial natriuretic peptide.

Animals↗
PubMed1987

Laser catheter ablation of simulated ventricular tachycardia.

Catheter-directed laser injury of the left ventricular endocardium for ablation of ventricular tachycardia was studied in a canine model of simulated ventricular tachycardia. Bipolar plunge electrodes were placed at thoracotomy into the left ventricular endocardium in nine anesthetized dogs. Ventricular tachycardia was simulated by pacing at 200 beats per minute. After four days of recovery, catheter-directed neodymium:yttrium-aluminum-garnet laser injury was produced at the site of earliest recorded electrical activation during pacing tachycardia as detected by endocardial catheter mapping. Immediately after laser injury and again five days after injury, pacing tachycardia was attempted. Failure to pace after laser injury was defined as successful arrhythmia ablation. In 3/9 (33%) experiments, the laser-injured tissue surrounded the tachycardia source (pacing wires), and pacing-simulated ventricular tachycardia was prevented. When the laser injury did not involve the tachycardia source, 6/9 animals, due to limitations of the mapping system, pacing was not prevented. One animal developed sustained ventricular tachycardia during laser injury, with conversion to sinus rhythm by lidocaine. One animal, without recognized ventricular arrhythmia, died five days after laser injury. No unusual findings were noted at autopsy. These preliminary data suggest that catheter-directed laser-induced injury can ablate arrhythmia sources. Further studies are indicated in a more physiologic model, and the safety and risks of the procedure need further evaluation.

Animals↗
PubMed1989

Transmural metabolite distribution in regional myocardial ischemia as studied with 31P NMR.

Phosphorus-31 nuclear magnetic resonance (31P NMR) has been applied to study the canine heart prior to and during regional myocardial ischemia induced by partial flow reduction in the left anterior descending coronary artery (LAD). NMR data were acquired in a transmural fashion by restricting the signal to a column perpendicular to the heart wall using B0 gradients and obtaining spectroscopic spatial resolution along the third dimension using the B1 gradient and adiabatic excitation. With this approach, transmural spectra were accumulated in five separate voxels spanning the wall of the left ventricle from the epicardium to the endocardium. In the normal canine myocardium the levels of high-energy phosphates CP and ATP were relatively constant throughout the left ventricular wall, with only minor evidence of free inorganic phosphate in any of the transmural voxels. However, during sustained partial occlusion of the LAD, significant regional differences between the epi- and the endocardium were noted. The data demonstrate the importance of studying cardiac bioenergetics with transmural differentiation.

Animals↗
PubMedDate not supplied

Prenatal diagnosis of endocardial fibroelastosis.

In a case of fetal heart failure caused by endocardial fibroelastosis, prenatal echocardiography clearly demonstrated a thickened endocardium. We therefore suggest that an abnormal endocardium may be detected in utero by ultrasound, thus representing an important clue in the differential diagnosis of fetal nonimmune hydrops and in the evaluation of pregnancies at risk for endocardial fibroelastosis.

Adult↗
PubMed1994

Localization of transcription factor GATA-4 to regions of the mouse embryo involved in cardiac development.

To clarify the role of transcription factor GATA-4 in mammalian development, we have determined the pattern of expression of GATA-4 in early postimplantation mouse embryos. Using in situ hybridization and immunohistochemistry, we find that GATA-4 RNA and protein are expressed in cells associated with heart development. Intraembryonic expression of GATA-4 RNA is first apparent in coelomic epithelial cells of the primitive streak embryo (approximately 7.0-7.5 days postcoitum). During formation and bending of the heart tube (approximately 8 days postcoitum), GATA-4 RNA and protein are expressed in endocardium, myocardium, and embryonic structures containing precardiac mesoderm such as the septum transversum and intraembryonic coelomic epithelium. By the onset of cardiac septation (approximately 9 days postcoitum), abundant GATA-4 RNA expression is evident in endocardium, endocardial cushion tissue, and myocardium. Expression of GATA-4 by the myocardium continues through gestation and after birth. The temporal and spacial patterns of GATA-4 expression support a role for this factor in the regulation of cardiac differentiation, analogous to the established role of transcription factor GATA-1 in the regulation of hematopoiesis.

Animals↗
PubMed2000

Patterning the embryonic heart: identification of five mouse Iroquois homeobox genes in the developing heart.

We isolated cDNAs of mouse Iroquois-related homeobox genes Irx1, -2, -3, -4, and -5 and characterized their patterns of expression in the developing heart. Irx1 and Irx2 were found to be expressed specifically in the ventricular septum from the onset of its formation onward. In fetal stages, the expression of both genes appeared to gradually become confined to the myocardium of the atrioventricular bundle and bundle branches of the forming ventricular conduction system. Irx3 was found to be expressed specifically in the trabeculated myocardium of the ventricles. Irx4 expression was observed in a segment of the linear heart tube and the atrioventricular canal and ventricular myocardium including the inner curvature after looping, resembling the pattern of MLC2V. Transcripts for Irx5 were detected specifically in the endocardium lining the ventricular and atrial working myocardium that also expressed von Willebrand factor, but were absent from the endocardium of the endocardial cushions, i.e., the atrioventricular canal, inner curvature, and outflow tract. The spatiodevelopmental pattern of Irx5 matched that of ANF, a marker for the forming working myocardium of the chambers. Taken together, all members of the Irx gene family were found to be expressed in highly specific patterns in the developing mouse heart, suggesting a critical role in the specification of the distinct components of the four-chambered heart.

Amino Acid Sequence↗
PubMed1990

Protective effects of phosphatidylcholine against mechanisms of ischemia and reperfusion-induced arrhythmias in isolated guinea pig ventricular tissues.

The effects of exogenous phosphatidylcholine (PC) on some potential mechanisms of ischemia and reperfusion-induced arrhythmias were tested using the superfused right ventricular free wall of the guinea pig. Exposure of the preparation to simulated "ischemia" (hypoxia, acidosis, glucose deprivation and hyperkalemia) resulted in several electrophysiological derangements, including a marked depolarization of the maximum diastolic potential (MDP) in both endocardium and epicardium, shortening of the action potential duration (APD), and prolongation of the transmural conduction time followed by transmural conduction block. In a few preparations, coupled beats were also observed. Reperfusion was associated with arrhythmic activity in all preparations. Both the characteristics and the severity of reperfusion-associated arrhythmias were dependent upon the duration of the preceding "ischemia". In hearts exposed to ischemic conditions for 40 min, transmural conduction block persisted until 45 min of reperfusion and no electrical activity was present in the epicardium during this time. However, both coupled beats as well as abnormal automaticity were observed in the endocardium. When the period of "ischemia" was reduced to 20 min, recovery from transmural conduction block occurred sooner and coupled beats and abnormal automaticity were detected in both epicardial and endocardial layers. Superfusion with PC during both "ischemia" and reperfusion (PC1 group), or during reperfusion only (PC2 group), significantly altered the response of the preparations to reperfusion. Following 40 min "ischemia", preparations treated with PC recovered from transmural conduction block more rapidly (PC1 group, 4 min, P less than 0.05; PC2 group, 23 min, ns), compared to control.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

Nicorandil and cardiovascular performance in anaesthetized pigs with a concentric coronary artery stenosis.

The present investigation compares the systemic and regional haemodynamics in nicorandil-treated and solvent-treated pigs with a concentric stenosis around the left anterior descending coronary artery. The stenosis per se led to a decrease in mean arterial blood pressure, cardiac output, stroke volume, maximum rate of rise in left ventricular pressure and transmural (more marked in the endocardium than in the epicardium) blood flow to and myocardial wall motion in the post-stenotic segment. Infusions of nicorandil (15 and 30 micrograms.kg-1.min-1, intravenously) decreased arterial blood pressure, cardiac output and the maximum rate of rise in left ventricular blood pressure. There was a tendency for epicardial blood flow in the non-stenotic segment to increase but blood flow to the ischaemic myocardium (epicardium as well as endocardium) was further compromised. Using the postsystolic wall thickening as an index for the viability of the myocardium and the Bretschneider formula for myocardial oxygen demand and the calculated myocardial oxygen consumption, we found that nicorandil further compromised the oxygen balance but did not jeopardize the viability of the myocardium. Regionally, nicorandil decreased renal blood flows but enhanced blood flows to the brains and adrenals. It is concluded that nicorandil lacks beneficial effects on the ischaemic myocardium in pigs with a concentric coronary artery stenosis. Apparently, the potential adverse effect (decrease in coronary perfusion pressure) of nicorandil outweighs its potential salutary effects (coronary vasodilatation and decrease in myocardial oxygen consumption due to peripheral vasodilatation.

Anesthesia↗
PubMed1980

Development of mouse semilunar valves.

The development of the semilunar valves of the great arteries of the mouse is studied by light and scanning electron microscopy. The earliest anlage of the valves is observed at day 11.5 of gestation, as three pairs of tubercles protruding towards the lumen of the truncus arteriosus. These early cusps consist of a core of mesenchymal tissue covered by the endocardium. From day 12.5 to 14 a process of excavation takes place in the arterial face of the cusps resulting in the achievement of their final shape. Our observations suggest that the excavation process is produced by a selective growth of the free edges of the cusps. Numerous pieces of evidence are reported suggesting that the selective growth of the cusps is due to an inductive interaction between the endocardium of the arterial face of the cusps and the underlying mesenchyme. The histogenesis of the cusps takes place very late in development and possibly continues into the postnatal period. The results are compared with studies made in other vertebrates.

Animals↗