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 325 records · Page 18Linked to original sources
PubMed2000

Nicorandil attenuates both temporal and spatial repolarization alternans.

T-wave alternans (TWA) on the electrocardiogram have been frequently associated with long QT syndrome (LQTS) and abrupt rate change. The present study investigated the effect of the potassium channel opener nicorandil on the repolarization alternans at the endocardium and the epicardium in the left ventricle. Electrocardiogram and transmural monophasic action potentials from the endocardium and the epicardium were simultaneously recorded in Langendorff-perfused guinea pig hearts. The hearts were paced at a basic cycle length (BCL) of 240 ms and the cycle length (CL) was abruptly shortened to 170 ms to induce repolarization alternans. Disopyramide and nicorandil were used to increase or attenuate repolarization alternans, respectively. Repolarization alternans were numerically expressed as the sum of the absolute difference between consecutive monophasic action potential durations at 90% repolarization (MAPD90) in the first 10 beats. In the control hearts, the MAPD90 alternans were 78.6 +/- 14.9 ms at the endocardium, and 49.8 +/- 58 ms at the epicardium (P = .03 endocardium vs epicardium). Disopyramide (2 microg/mL) increased the MAPD90 alternans to 186.6 +/- 30.6 ms at the endocardium and 116.4 +/- 16.5 ms at the epicardium, and enhanced the difference of repolarization alternans between the endocardium and the epicardium (transmural dispersion) from 28.8 +/- 11.3 ms to 70.2 +/- 18.7 ms (P = .02 vs controls). Nicorandil (400 ng/mL) suppressed the MAPD90 alternans to 79.6 +/- 16.3 ms at the endocardium and 56.0 +/- 11.8 ms at the epicardium, and attenuated the transmural dispersion to 23.6 +/- 6.0 ms (P = .02 vs disopyramide-administrated hearts). Our results suggest that nicorandil attenuates both temporal (beat-to-beat) and spatial (between the endocardium and the epicardium) repolarization alternans induced by the combination of cycle length changes and disopyramide administration.

Animals↗
PubMed1998

Regional electrophysiological effects of hypokalaemia, hypomagnesaemia and hyponatraemia in isolated rabbit hearts in normal and ischaemic conditions.

OBJECTIVE: The aims of this study were to establish an isolated working heart model for electrophysiological recordings from the epicardium and endocardium and to examine regional effects of changes in ion concentrations in normal and ischaemic conditions. METHODS: Monophasic action potential duration (MAPD90), effective refractory period (ERP) and conduction delay were measured simultaneously in the epicardium and endocardium of rabbit hearts paced at 3.3 Hz, subjected to 30 min of regional ischaemia and 15 min of reperfusion. The hearts were exposed before and throughout ischaemia and reperfusion to hypokalaemia (K+ = 2 mM), hypomagnesaemia (Mg2+ = 0.5 mM) or hyponatraemia (Na+ = 110 mM). RESULTS: In the control hearts, no regional electrophysiological differences were seen before ischaemia, but ischaemia-induced MAPD90 shortening and postrepolarisation refractoriness were greater in the epicardium than in the endocardium and conduction delay increased only in the epicardium. Hypokalaemia shortened ERP in the epicardium (but not endocardium) and increased conduction delay in all areas before ischaemia, but it had no effects during ischaemia. During reperfusion hypokalaemia increased the incidence of recurrent tachyarrhythmias. Hypomagnesaemia had no effect before ischaemia, increased epicardial (but not endocardial) MAPD90 shortening during ischaemia, although it had no pro-arrhythmic action. Hyponatraemia increased conduction delay in all areas before ischaemia and produced asystole or severe bradycardia in all hearts. During ischaemia, hyponatraemia decreased ERP shortening and inducibility of arrhythmias in the epicardium (but not endocardium). CONCLUSIONS: We conclude that the more pronounced effect of ischaemia upon the epicardium than the endocardium can be explained by the contact of the endocardium with intracavitary perfusate. We also conclude that changes in ion concentrations may have differential regional electrical effects in normal or ischaemic conditions.

Animals↗
PubMed1994

Human endocardial innervation and its relationship to the endothelium: an immunohistochemical, histochemical, and quantitative study.

OBJECTIVE: The endocardium contains an extensive neural plexus, the composition and function of which are unclear. The aim of this study was to characterise the innervation of the endocardium in terms of the relative density and distribution of its autonomic and sensory nerve subpopulations and to assess the relationship between these nerves and endocardial endothelial cells. METHODS: Immunohistochemical, histochemical, confocal, and quantitative image processing techniques were applied to whole mount preparations of human postmortem endocardium obtained within 24 h of death. RESULTS: The overall distribution of nerve fibres and fascicles was demonstrated using antisera to the general neural marker protein gene product 9.5 (PGP 9.5). Nerves displaying acetylcholinesterase activity represented the main nerve subpopulation, occupying 9-18% of the quantified field area. Neuropeptide Y immunoreactive nerves formed the most numerous peptide containing nerve subpopulation identified, occupying 5-19% and 2-7% of the field area in the ventricle and atrial endocardium respectively and having similar distribution patterns to tyrosine hydroxylase immunoreactive nerves. Nerves showing immunoreactivity for somatostatin, vasoactive intestinal polypeptide, and substance P were detected at a lower density, occurred more frequently in the ventricular than atrial endocardium, and showed a similar distribution in the right and left sides of the heart. Combined peptide immunofluorescence and acetylcholinesterase staining, of the same preparation, indicated that putative sympathetic and sensory nerve subpopulations could be distinguished from presumed parasympathetic, acetylcholinesterase positive, nerves. The relationship between immunostained nerves and endothelial cells was assessed using confocal microscopy. Varicose nerve fibres were detected within 0.2 micron of overlying endothelial cells in the right ventricle and between 0.4-0.6 micron in the left ventricle. CONCLUSIONS: The heterogeneous population of nerve fibres demonstrated in the human endocardium may influence the known interaction between endocardial endothelial cells and the myocardium.

Adolescent↗
PubMed1999

Modulation of endocardial natriuretic peptide receptors in right ventricular hypertrophy.

Natriuretic peptide (NP) receptors (NPRs) located at the endocardial endothelium are suggested to be involved in regulating myocardial contractility. However, the characteristics and modulation of NPRs in relation to cardiac failure are not well defined. This study examined the properties of NPRs in ventricular endocardium using quantitative receptor autoradiography, RT-PCR, Southern blot analysis, and activation of particulate guanylyl cyclase (GC) by NPs. In control rats, specific 125I-labeled rat atrial NP (rANP)(1-28) binding sites were localized in right (RV) and left ventricular (LV) endocardium. Binding affinities of 125I-rANP(1-28) were remarkably higher in RV than LV endocardium. Radioligand binding at these sites was mostly inhibited by des[Gln18,Ser19,Gly20,Leu21, Gly22]ANP(4-23), a specific NP clearance receptor ligand. mRNAs for all three recognized NPRs were detected in endocardial cells by RT-PCR and confirmed by Southern blot analysis. Production of cGMP by particulate GC in endocardial cell membranes was stimulated by NPs with a rank order of potency of C-type NP(1-22) >> brain NP (BNP)(1-26) > ANP(1-28). We also examined the modulation of these NPRs during cardiac hypertrophy induced by monocrotaline (MCT). In MCT-treated rats with pulmonary hypertension, specific (125)I-rANP(1-28) binding to hypertrophied RV endocardium almost disappeared and cGMP production by NPs was significantly decreased. In rats with pulmonary hypertension, plasma levels of ANP and BNP were increased by fivefold compared with controls. The results indicate that there is a differential distribution of NPRs in the cardiac chambers, with the most abundant binding sites in RV endocardium, that NPR-B is the predominant GC-coupled NPR in ventricular endocardium, and that endocardial NPRs are downregulated with ventricular hypertrophy. Downregulation of NPRs may be associated with an increment of endogenous NP production caused by mechanical overload in hypertrophied ventricle.

Animals↗
PubMed2002

Transmural reentry triggered by epicardial stimulation during acute ischemia in canine ventricular muscle.

Ischemia depresses tissue excitability more rapidly in the ventricular epicardium than in the endocardium. We hypothesized that this would provide the substrate for transmural reentry originating in the epicardium. We mapped transmural conduction in isolated and perfused wedges taken from canine left ventricles during global ischemia while pacing alternately between the epicardium and endocardium. Ischemia reduced conduction velocity more in the epicardium than in the endocardium. We observed that the epicardial-initiated activation penetrated the ventricular wall transmurally while failing to conduct laterally along the epicardium, then conducted laterally along the endocardium and midmyocardium, and reentered the epicardium in 9 of 16 wedges during epicardial stimulation after 600 +/- 182 s of ischemia. Endocardial stimulation applied immediately before or after the epicardial stimulation initiated activation that spread quickly along the endocardium and then transmurally to the epicardium without reentry in six of the nine wedges. The transmural asymmetric conduction was not observed in four separate wedges after the endocardium was removed. Therefore, ischemia-induced transmural gradient of excitability provided the substrate for reentry during epicardial stimulation.

Acute Disease↗
PubMed1980

Effects of aging on hydroxyproline in human heart muscle.

Hydroxyproline concentration in the NaCl-soluble, TCA-soluble, and residual fractions of heart muscle was chemically determined in 40 autopsy subjects (25 men and 15 women), to study the effects of aging. In the left ventricle, the total hydroxyproline content of the endocardium and papillary muscle increased significantly in relation to age; the increase was greatest in the TCA-soluble fraction, followed by the residual fraction. Statistical analysis revealed that hydroxyproline in the residual fraction increased from the epicardium to the endocardium and then to the papillary muscle. Significant negative correlations were found between heart weight and total hydroxyproline in the epicardium and endocardium. In the right ventricle, a significant negative correlation was noted between heart weight and total hydroxyproline content. Though no correlations were evident between age and hydroxyproline content in females, significant correlations were observed between age and the total hydroxyproline content of the endocardium and papillary muscle in males. Furthermore, soluble collagen increased in most parts of the heart in females, but insoluble collagen increased in all parts of the heart in males. It is concluded that the hydroxyproline content of heart muscle increases in proportion to age and is in inverse proportion to heart weight. The increase occurs in the TCA-soluble and residual fractions, and extends from the endocardium to the papillary muscle. More profound changes in collagen metabolism are observed in males.

Adult↗
PubMed1977

Atrial receptors in the dog and rabbit.

1. Action potentials were recorded from slips of the cervical vagi in anaesthetized dogs and rabbits. Single functional units with atrial patterns of discharge (Paintal Type A, B and intermediate) were obtained and then attempts were made to alter (i.e. convert) their patterns of discharge. Finally the points of origin of these action potentials were located.2. Thirty unselected units were investigated in thirty dogs. Twenty-seven of these were located in the endocardium of the vein-atrial system and the ratio of the type A, type B and intermediate type receptors was 1:16:10; three units were located elsewhere in the chest. Conversion of the pattern of discharge was achieved in twenty of the twenty-seven units; conversion was achieved in the single type A unit.3. In a second series of experiments in dogs, eight Paintal Type A units were selectively studied in fifteen animals. Four of these were located in the endocardium and all were converted. The remaining four were located outside the endocardium and conversion could not be achieved in two of these. Thus in the entire investigation, the ;type A' units which could not be converted were all located at sites other than the atrial endocardium.4. In the corresponding unselected study in the rabbit, eleven units were studied in eleven animals. Nine of these units were located in the atrial endocardium and the ratio of the type A, type B and intermediate type receptors was 2:1:6. Conversion was achieved in both type A units, the sole type B unit and two of the intermediate units. One of the two units found outside the atrial endocardium was a ;type A' unit and could not be converted.5. The present investigation has shown that the atrial receptors with a Paintal Type A pattern of discharge are relatively rare in both dogs and rabbits. Conversion of the pattern of discharge is a relatively common phenomenon. Evidence for the proposition that there is one basic type of atrial receptor whose pattern of discharge is determined by its precise location in the vein-atrial system is discussed.

Action Potentials↗
PubMed2001

Transmural distribution of three-dimensional systolic strains in stunned myocardium.

BACKGROUND: Regional function in stunned myocardium is usually thought to be more depressed in the endocardium than the epicardium. This has been attributed to the greater loss of blood flow at the endocardium during ischemia. METHODS AND RESULTS: We measured transmural distributions of 3D systolic strains relative to local myofiber axes in open-chest anesthetized dogs before 15 minutes of left anterior descending coronary artery occlusion and during 2 hours of reperfusion. During ischemia, regional myocardial blood flow was reduced 84% at the endocardium and 32% at the epicardium (P<0.005, n=7), but changes in end-systolic fiber length from baseline were transmurally uniform. Relative to baseline, radial segments in stunned tissue were significantly thinner at the endocardium than the epicardium at end systole (24+/-5% versus 16+/-3%; P<0.05, n=8), consistent with previous reports. Unlike radial and cross-fiber segments, however, the increase of end-systolic fiber lengths in stunned myocardium had no significant transmural gradient (23+/-8% epicardium versus 21+/-4% endocardium). We also observed significant 3D diastolic dysfunction in the ischemic-reperfused region transmurally. CONCLUSIONS: Myocardial ischemia/reperfusion in the dog results in a significant transmural gradient of dysfunction between epicardial and endocardial layers in radial and cross-fiber segments, but not for fiber segments, despite a gradient in blood flow reduction during ischemia. Perhaps systolic fiber dysfunction rather than the degree of perfusion deficit during the preceding ischemic period may be the main determinant of myocardial dysfunction during reperfusion.

Animals↗
PubMed1993

Pinacidil-induced electrical heterogeneity and extrasystolic activity in canine ventricular tissues. Does activation of ATP-regulated potassium current promote phase 2 reentry?

BACKGROUND: Pinacidil is known to augment a time-independent outward current in cardiac tissues by activating the ATP-regulated potassium channels. Activation of this current, IK-ATP, is thought to be responsible for increased potassium permeability in ischemia. The contribution of IK-ATP activation to arrhythmogenesis and the role of activation of this current in suppression of arrhythmias are areas of great interest and debate. Because electrical depression attending myocardial ischemia is more accentuated in ventricular epicardium than in endocardium, we endeavored to contrast the effects of pinacidil-induced IK-ATP activation on the electrophysiology of canine ventricular epicardium and endocardium. METHODS AND RESULTS: Standard microelectrode techniques were used. Pinacidil (1 to 5 mumol/L) produced a marked dispersion of repolarization and refractoriness in isolated canine ventricular epicardium as well as between epicardium and endocardium. In endocardium, pinacidil abbreviated action potential duration (APD90) and refractoriness by 8.0 +/- 2.3%. In epicardium, the effects of pinacidil were nonhomogeneous. At some sites, pinacidil induced an all-or-none repolarization at the end of phase 1 of the action potential, resulting in 55.5 +/- 8.7% abbreviation of APD90 and refractoriness. Adjacent to these were sites at which the dome was maintained with only minor changes in APD and refractoriness. Extrasystolic activity displaying features of reentry was observed in isolated sheets of epicardium (63.2%) after exposure to pinacidil (1 to 5 mumol/L) but never in its absence. Dispersion of repolarization and ectopic activity was most readily induced in epicardium by a slowing of the stimulation rate in the presence of pinacidil. Electrical homogeneity was restored and arrhythmias abolished after washout of pinacidil or addition of either a transient outward current blocker, 4-aminopyridine, or a blocker of the ATP-regulated potassium channels, glybenclamide. CONCLUSIONS: Our data suggest that the activation of IK-ATP can produce a marked dispersion of repolarization and refractoriness in epicardium as well as between epicardium and endocardium, leading to the development of extrasystolic activity via a mechanism that we have called phase 2 reentry. The available data also suggest that blockade of the transient outward current and/or the ATP-regulated potassium channels may be useful antiarrhythmic interventions under ischemic or "ATP depleted" conditions.

Action Potentials↗
PubMed1994

Relation of regional cross-fiber shortening to wall thickening in the intact heart. Three-dimensional strain analysis by NMR tagging.

BACKGROUND: The mechanism by which small amounts of myofiber shortening lead to extensive wall thickening is unknown. When isolated fibers shorten, they thicken in the two orthogonal directions. In situ fibers, however, vary in their orientation through the wall, and each is tethered to near or distant neighbors, which allows shortening to occur both in the direction of the fibers and also perpendicular to them. This "cross-fiber" shortening may enable the wall to shorten in two directions and thereby thicken extensively in the third. METHODS AND RESULTS: Nuclear magnetic resonance tagging is a noninvasive method of labeling and tracking myocardium of the entire heart in three dimensions that does not interfere with myocardial motion. To investigate the presence and importance of cross-fiber shortening in the intact left ventricle, 10 closed-chest dogs were studied by nuclear magnetic resonance tagging. Five short-axis and four long-axis images were acquired to reconstruct 32 cubes of myocardium in each dog at end diastole and end systole. Pathological dissection was performed to determine the fiber direction at the epicardium, midwall, and endocardium of each cube. Strain was computed from the three-dimensional cube coordinates in the fiber and cross-fiber directions for epicardial and endocardial surfaces, and thickening of the full wall and its epicardial and endocardial halves was determined. Shear deformations were also calculated. Fiber strain at the epicardium and endocardium was -6.4 +/- 0.7% and -8.5 +/- 0.6% (mean +/- SEM), respectively (difference, P > .05). Cross-fiber strain at epicardium and endocardium was -0.6 +/- 0.5% and -25 +/- 0.6%, respectively (difference, P < .05). Thickening of the full wall reached 32.5 +/- 1.0%, composed of epicardial thickening of 25.5 +/- 0.6% and endocardial thickening of 43.3 +/- 1.0% (difference, P < .05). Fiber/cross-fiber shear strain was small (< 3%). Significant regional differences were present in all strains. A significant correlation was found between the extents of regional thickening and cross-fiber shortening. CONCLUSIONS: Cross-fiber shortening at the endocardium, therefore, far exceeds cross-fiber shortening at the epicardium and fiber shortening at both epicardium and endocardium. Since no active shortening can occur locally in the cross-fiber direction, the extensive endocardial cross-fiber shortening must result from interaction with differently aligned fibers at a distance. The correlation between regional thickening and cross-fiber shortening supports the hypothesis that this interaction is the mechanism for amplifying small amounts of fiber shortening to cause extensive endocardial thickening.

Animals↗
PubMed1981

The relationship between myocardial blood flow and contraction by myocardial layer in the canine left ventricle during ischemia.

We investigated the relationship between regional myocardial blood flow (MBF) and segmental shortening in 17 open-chest dogs. The left anterior descending coronary artery was cannulated and perfused from the left carotid while measuring perfusion pressure. Graded occlusion was produced by a screw clamp. Extent of occlusion was monitored by perfusion pressure. Percent systolic shortening (% delta L) was measured using ultrasonic crystals implanted in normal and ischemic endocardium and ischemic epicardium. MBF was measured in ischemic and normal endocardium and epicardium with tracer microspheres. Dogs underwent 1 to 4 grades of coronary stenosis. Myocardial blood flow both to endocardium and epicardium was found to be linearly related to diastolic perfusion pressure below 50 mmHg (r = 0.803 and 0.748, respectively). Normalized % delta L (N% delta L) was best related to fraction normal zone MBF in the endocardium by the sigmoidal equation, N% delta L = e9.01 MBF-4.03/1 + e9.01 MBF-4.03. % delta L was only weakly related to myocardial blood flow in the epicardium (r = 0.584), and, in four dogs, % delta L was zero in the epicardium despite normal regional blood flow. However, % delta L in the epicardium was linearly related to % delta L in the endocardium (r = 0.78). Thus, endocardial wall motion is related to MBF by a sigmoidal relationship while epicardial wall motion is tethered to endocardial wall motion.

Animals↗
PubMed1990

Differences in the electrophysiological response of canine ventricular subendocardium and subepicardium to acetylcholine and isoproterenol. A direct effect of acetylcholine in ventricular myocardium.

A prolongation of the ventricular effective refractory period in response to cholinergic agonists or vagal stimulation has been demonstrated in a number of in vivo animal models. However, exposure of isolated myocardial tissues obtained from these hearts to as much as 10(-4) M acetylcholine has been shown to produce essentially no change in action potential duration or effective refractory period. The discrepancy between the in vivo and in vitro findings generally has been explained on the basis of accentuated antagonism, whereby parasympathetic agonists exert their influence through antagonism of the effects of beta-adrenergic tone in vivo. The fact that acetylcholine exerts little if any direct effect on the electrical activity of ventricular myocardium, although well accepted, is based exclusively on studies performed using endocardial preparations. Our recent demonstration of major electrophysiological differences between canine ventricular endocardium and epicardium prompted us to examine the effects of acetylcholine and the role of accentuated antagonism in these two tissue types. Using standard microelectrode techniques, we show that acetylcholine (10(-7)-10(-5) M) has little if any effect in canine ventricular endocardium but a pronounced effect to either prolong or markedly abbreviate action potential duration and effective refractory period in epicardium. These effects of acetylcholine on epicardium are attended by an accentuation of the spike and dome morphology of the action potential, are readily reversed with atropine, fail to appear when epicardium is pretreated with the transient outward current blocker 4-aminopyridine, are accentuated in the presence of isoproterenol (10(-7) to 5 x 10(-6) M), and persist in the presence of propranolol. Isoproterenol-induced abbreviation of action potential duration and effective refractory period is also shown to be more pronounced in epicardium than in endocardium; equimolar concentrations of acetylcholine completely antagonize the effects of isoproterenol in endocardium and epicardium. We conclude that acetylcholine exerts important direct effects on the electrical response of canine ventricular myocardium, which are accentuated in the presence of beta-adrenergic agonists. Our findings suggest the differential response of epicardium and endocardium to acetylcholine is due to the presence of a transient outward current-mediated spike and dome morphology in the epicardial action potential. Finally, the data suggest that acetylcholine may exert antiarrhythmic as well as arrhythmogenic effects through its actions to alter conduction and refractoriness.

4-Aminopyridine↗
PubMed1991

A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell.

Recent studies have shown that canine ventricular epicardium and endocardium differ with respect to electrophysiological characteristics and pharmacological responsiveness and that these differences are in large part due to the presence of a prominent transient outward current Ito and a spike-and-dome morphology of the action potential in epicardium but not endocardium. In attempting to quantitate these differences and assess their gradation across the ventricular wall, we encountered a subpopulation of cells in the deep subepicardial layers with electrophysiological characteristics different from those of either epicardium or endocardium. These cells, which we have termed M cells, display a spike-and-dome morphology typical of epicardium but a maximal rate of rise of the action potential upstroke that is considerably greater than that of either epicardium or endocardium. Using the restitution of the amplitude of phase 1 of the action potential as a marker for the reactivation of Ito, we showed M cells to possess a prominent 4-aminopyridine-sensitive Ito with a reactivation time course characterized by two components with fast and slow time constants. The rate dependence of action potential duration of M cells was considerably more accentuated than that of epicardium or endocardium and more akin to that of Purkinje fibers (not observed histologically in this region). Phase 4 depolarization was never observed in M cells, not even after exposure to catecholamines and/or low [K+]o. In summary, our study presents evidence for the existence of a unique subpopulation of cells in the deep subepicardium of the canine left and right ventricles with electrophysiological features intermediate between those of conducting and myocardial cells. Although their function is unknown, M cells may facilitate conduction in epicardium and are likely to influence or mediate the manifestation of electrocardiographic J waves, T waves, U waves, and long QT intervals and contribute importantly to arrhythmogenesis.

4-Aminopyridine↗
PubMed1975

Regional differences in fatty acid oxidation by the adult rabbit myocardium.

Differences in coronary perfusion and tissue oxygenation between the epicardium and endocardium have been shown. Thus, intrinsic capacity for substrate oxidation may also exhibit regional variation. Accordingly, homogenates of left ventricular papillary muscle ("endocardium") and left ventricular free wall trimmed of endocardium ("epicardium") were compared for their capacity to oxidize palmitic acid-1-14C (PA) and octanoic acid-1-14C (OcA). Homogenates from one to three rabbits were combined for each study; 18 studies were performed using PA, and 10 using OcA. The protein content of endo- and epicardial homogenates was the same (Biuret method). At ambient PA concentrations of 0.2 mM, oxidation of PA by "endocardium" was 64 +/- 6.3% that of the "epicardium" (p less than 0.001). At ambient concentrations of 1.0 mM, oxidation of OcA by "endocardium" was not different from that of "epicardium" (118 +/- 10.5%; p greater than 0.1). Thus, the oxidative capacity for long chain FFA by the endo- and epicardial homogenates are at variance. Differences in carnitine-mediated transmitochondrial transport of long chain fatty acids may be the explanation. Such regional metabolic differences could play a role in regional alterations in myocardial function under adverse hemodynamic and metabolic circumstances.

Animals↗
PubMedDate not supplied

[Forensic-medical assessment of pathomorphological changes in the myocardium in blunt chest trauma with an isolated heart contusion].

A total of 37 autopsy cases were divided into two groups. Group 1 consisted of 17 victims who had died of closed blunt trauma of the chest with isolated heart contusion made by fists, feet in shoes. Group 2 (control) consisted of 20 cases of sudden death of ischemic heart disease because of atherosclerotic cardiosclerosis. Fragments of the heart containing endocardium were studied on the microscope JEIL-SM200 (Japan). Endocardium pathomorphology was represented by relief changes of the endocardium, structural arrangement of separate groups of muscular fibers above the endocardium surface, hemorrhages and blood clots, endotheliocyte desquamation, prelacerations, lacerations and destruction of the endocardium.

Adult↗
PubMed1979

Endocardial alterations in myocardial infarction.

Transmural infarcts of the ventrolateral wall of canine left ventricle were produced by ligation of the ventral interventricular (anterior descending) branch of the left coronary artery. Endocardium from these infarcted hearts was sampled at sites corresponding to the infarct center and periphery, and to uninfarcted (normal) area at 24 and 48 hours after ligation, and examined by correlative scanning and transmission electron microscopy and by light microscopy. Endocardial samples from sham-ligated hearts were included as a further control. Striking alterations were observed in the endocardium that lined infarcted myocardium. There was endothelial desquamation coextensive with leukocytic invasion. Leukocytes appeared to initiate sloughing by separating the endothelial cells from their basal lamina and partially from one another. The latter cells desquamated in sheets, leaving behind a denuded basal lamina. Although altered in form, the individual endothelial cells seemed to remain largely intact. Denuded subendothelial surfaces only rarely contained thrombi. In areas where the cardiac endothelium was altered, the subjacent subendocardium, myocardium, and usually the remainder of the endocardium also showed leukocytic exudate. Samples from uninfarcted regions showed an intact, leukocyte-free endocardium, as did the sham-ligated controls. The appearance of abnormal endocardium was qualitatively similar wherever found, whether in different areas of the same heart or from one heart to another, and regardless of age of infarct. In 48-hour infarcts, almost all of the central and most of the peripheral samples exhibited the changes described. The data suggested a similar pattern for hearts with 24-hour infarcts. By locating biopsy sites in frozen cardiac sections processed for histologic staining and 201-thallium autoradiography, the electron microscopy results were shown to correlate with the intramural histopathologic topography of the infarcts. The alterations described here represent the endocardial manifestation of the inflammatory stage of transmural infarcts, known to be well developed in 1- and 2-day-old lesions.

Animals↗
PubMed1990

Monophasic action potential recordings in response to rapid transient elevation of extracellular potassium and their modification by beta-adrenoceptor blockade in the anaesthetized dog.

1. Monophasic action potentials (MAPs) were recorded simultaneously from the endocardium and the epicardium in open-chested dogs (n = 16) during bolus intravenous injections of potassium chloride at 0.1 mmol/kg and 0.2 mmol/kg. MAP duration was measured at 90% repolarization. Local conduction was measured as the delay between the pacing artefact and upstroke of the MAP. 2. The animals were anaesthetized with alpha-chloralose and urethane. Heart block was created by atrioventricular nodal ablation with 0.1% (v/v) formalin. Infra-nodal pacing was established. 3. Bolus injections of potassium chloride at 0.1 mmol/kg shortened MAP duration. The effect was maximal at 15 s after the injection [epicardium: 171.5 +/- 3.0 (control) and 148.9 +/- 5.2 ms at 15 s (P less than 0.001); endocardium: 178.7 +/- 4.4 (control) and 165.6 +/- 5.3 ms (P less than 0.001)]. The shortening on the epicardium was significantly greater than on the endocardium (P less than 0.05). 4. Local conduction time showed no significant change [epicardium: 37.8 +/- 1.8 (control) and 41.2 +/- 2.4 at 15 s; endocardium: 41.1 +/- 1.6 (control) and 45.0 +/- 3.4 at 15 s]. 5. After beta-adrenoceptor blockade, MAP duration shortened, exhibiting a maximum effect at 20 s after a bolus injection of potassium chloride at 0.1 mmol/kg [epicardium: 184.7 +/- 7.1 (control) and 130.7 +/- 9.0 ms at 20 s (P less than 0.001); endocardium 192.0 +/- 7.4 (control) and 148.6 +/- 10.8 ms at 20 s (P less than 0.001)]. The greater shortening observed on the epicardial surface did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2002

Intramyocardial analysis of regional systolic and diastolic function in ischemic heart disease with Doppler tissue imaging: role of the different myocardial layers.

BACKGROUND: Preliminary experimental data have shown a nonuniform distribution of myocardial velocities (MVs) across the myocardial wall in normal conditions. However, after ischemic damage to the myocardium, a different pattern of reduction in the myocardial layers has been reported. The aim of this study is to analyze the spatial distribution of MVs and the resultant myocardial velocity gradients (MVGs) during the systolic and diastolic time periods. Doppler tissue imaging (DTI) in color M-mode was used to evaluate 3 different myocardial layers (endocardium, mesocardium, and epicardium) and their changes as a result of ischemia. METHODS: Thirty-two consecutive patients were studied with DTI color M-mode: 18 patients with a history of previous or ongoing myocardial infarction and 14 healthy subjects. Postprocessing of images was accomplished with proprietary software. MV and MVG values of all layers along both systolic and diastolic time were calculated. For temporal analysis, systole was subdivided in 3 equal periods. Early- and late-diastolic times were also identified. RESULTS: In ischemic patients, the mean MV and maximum MV throughout systole decreased significantly in the endocardium and mesocardium, whereas only slightly in the epicardium. The mean MVG was less in ischemic patients (0.66 +/- 0.11 vs 0.23 +/- 0.15, P <.03). Temporal analysis showed a decrease in the maximal MV and MVG in all layers over the 3 systolic periods. This decrease was the more consistent in mesocardium. In diastole, there was a decrease in maximal MV in all layers, being more pronounced in endocardium and mesocardium. Diastolic mean MVG was shown to be different between control and ischemic groups (-0.2 +/- 0.05 vs -0.10 +/- 0.04, P <.06). A significant decrease of the maximal MV in endocardium and mesocardium was reported in the temporal analysis during early diastole. No change was reported in the epicardium. The MVG value also showed a significant decrease (-2.69 +/- 0.29 vs -1.59 +/- 0.89, P <.02). In ischemic patients in late diastole, the maximum MV was increased in all layers of the myocardium, and this increase was observed mainly in the endocardium. An increase in the MVG (-0.78 +/- 0.18 vs -1.47 +/- 0.85, P = NS) was also reported during late diastole. CONCLUSION: There is a nonuniform distribution of velocities in the different myocardial layers under normal conditions. This distribution of velocities undergoes a significant change in patients with ischemic myocardial damage. Intramyocardial wall motion analysis could have clinical applications in both the early detection of ischemia and myocardial viability.

Adolescent↗