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PubMed1979

The role of beta-adrenoceptors in coronary blood flow distribution in normal and ischemic canine myocardium.

beta-Adrenoceptor agonists increase myocardial ischemic injury, mainly by elevating myocardial oxygen consumption. Moreover, it has been shown that isoprenaline may "steal" regional myocardial blood flow (RMBF) from ischemic to non ischemic areas and from epicardium to endocardium. The mechanisms of these two isoprenaline-induced redistributions of RMBF have been investigated by the use of radioactive microspheres in an experimental model of canine myocardial ischemia with simultaneous measurement of ST-segment elevation. Isoprenaline increased RMBF in both epi- and endocardial non ischemic areas and in epicardial ischemic areas, leading to a significant decrease in the endo/epi ratio. After atenolol, isoprenaline still increased RMBF but to a lesser extent and the endo/epi ratio was still decreased. Salbutamol, in doses inducing no significant changes in cardiac parameters or myocardial oxygen consumption, produced effects similar to those of isoprenaline. These results indicate a non-homogeneous beta2-stimulation-induced vasodilation in endo- and epicardium, which might be due either to the higher epicardial coronary vasocilatory reserve or to a heterogeneous distribution of transmural beta2-adrenoceptors. Isoprenaline also decreased the ischemic/non ischemic total blood flow ratio (I/NI) and caused further increases in ST-segment elevation. These effects were abolished by atenolol pretreatment, indicating the deleterious effects of isoprenaline-induced tachycardia in this I/NI decrease and in the ischemic injury.

Albuterol↗
PubMed1983

Regional sensitivity to verapamil in ventricular myocardium.

The effects of verapamil (0.1-4.0 micrograms/ml) on transmembrane action potential configuration was examined in various regions of the normal cat left ventricular endocardium. Surface electrograms showed that the sequence of activation of anterior papillary muscle fibers was from the base of the muscle to its apex, while overlying Purkinje fibers were activated in the opposite direction. Action potential duration in basal muscle fibers was relatively unaffected by verapamil, while cells at the tip of the papillary muscle showed increased slope in phase 2 and a more rapid rate of early repolarization. Regional sensitivity to verapamil may reflect disparate patterns of endocardial activation, and could influence the effectiveness of the drug against ventricular arrhythmias.

Action Potentials↗
PubMed1985

Vasodilating beta-adrenoceptor blocking drugs do not redistribute myocardial flow during acute coronary ligation in dogs.

The effects of two nonselective beta-adrenoceptor blocking drugs, additionally endowed with vasodilating properties with different mechanisms: labetalol which blocks alpha-adrenoceptors, and bucindolol which nonspecifically relaxes vascular smooth muscle, were investigated on regional myocardial blood flow (RMBF) distribution in ischemic and nonischemic areas and on ST-segment elevation in ischemic areas during intermittent coronary artery occlusion in dogs. Both labetalol and bucindolol reduced heart rate, arterial blood pressure and myocardial oxygen consumption. However, they did not affect coronary vascular resistance and did not induce any favorable coronary blood flow redistribution phenomenon either from the epicardium to the endocardium or from the nonischemic to the ischemic areas. These results indicate that the inability of labetalol and bucindolol to favorably redistribute RMBF was due to the fact that their vasodilating properties counteract one major determinant of RMBF redistribution. i.e. the beta-adrenoceptor blockade-induced increase in regional coronary vascular resistance. Finally, both labetalol and bucindolol dose dependently decreased ST-segment elevation in ischemic myocardial areas.

Adrenergic beta-Antagonists↗
PubMed1987

Cardiovascular effects of UD-CG 212 CL, a metabolite of pimobendan, in anaesthetized pigs.

Systemic and regional haemodynamic effects of UD-CG 212 CL (0.5-16 micrograms X kg-1 X min-1), the major metabolite of the vasodilator and cardiotonic drug pimobendan, were studied in anaesthetized pigs. The drug caused a dose-dependent decrease in left ventricular (LV) end-diastolic and arterial blood pressures while it increased systemic vascular conductance, heart rate and maxLVdP/dt. The decrease in LV end-diastolic pressure was observed at lower plasma concentrations than the increase in systemic vascular conductance. Cardiac output tended to decrease but statistical significance was achieved only with the highest concentration. These effects of UD-CG 212 CL were not altered by the blockade of beta-adrenoceptors with propranolol. The vasodilator action of UD-CG 212 CL was noticed in several organs but the effects were relatively more marked (in decreasing order of magnitude) in the adrenals, kidneys, gastrointestinal tract, brain and LV epicardium. Since both arterial pressure and cardiac output decreased, the blood flow increased significantly only in the adrenals and decreased moderately in the spleen, LV endocardium and skeletal muscles. The effects of UD-CG 212 CL on the renal and skeletal muscle haemodynamics were different from those of pimobendan, which causes vasodilatation in the skeletal muscles but not in the kidneys. The results of this study show that, like the parent compound pimobendan, UD-CG 212 CL has independent cardiotonic and vasodilator actions; the latter being more pronounced on the venous side. However, the contribution of this metabolite to the overall pharmacological activity of pimobendan appears to be limited.

Adrenergic beta-Antagonists↗
PubMed1989

Atrial and brain natriuretic peptides share binding sites in the kidney and heart.

We examined the distribution of binding sites for atrial natriuretic peptide (ANP) and the recently discovered brain natriuretic peptide (BNP) in rat kidney and heart by receptor autoradiography. In frozen kidney sections, both 125I-ANP and 125I-BNP exhibited localized binding to cortical glomeruli. The binding of each radiolabeled peptide was abolished by inclusion of either excess (1 microM) unlabeled ANP or excess unlabeled BNP, suggesting that ANP and BNP share cortical glomerular binding sites. In frozen cardiac sections, ANP and BNP binding sites were localized to the endothelium of the endomural channels and endocardium. As was the case for kidney, binding of each peptide at these sites was abolished by the presence of excess unlabeled ANP or BNP, suggesting that these natriuretic peptides share binding sites in the heart as well. To explore further the possibility that ANP and BNP utilize the same receptor(s), we performed competitive binding experiments using cultured pulmonary artery endothelial (CPAE) cells. ANP and BNP competitively displaced one another with equivalent IC50 values from CPAE cell binding sites. Furthermore, both ANP and BNP elevated the levels of cGMP, a putative second messenger for ANP, in these cells. These data are consistent with the observation that BNP, like ANP, causes a natriuresis and diuresis in rats, and suggest that BNP may possess other biological activities known for ANP.

Animals↗
PubMed1984

Cardiac morphologic alterations in acute minoxidil cardiotoxicity in miniature swine.

Minoxidil, a vasodilating antihypertensive drug, was given orally at 10 mg/kg daily for 2 days to twelve 25- to 35-kg miniature pigs. Twelve control pigs were also studied. Minoxidil-treated pigs had tachycardia and hypotension and were killed 24 hr after the second dose. Gross examination showed diffuse hemorrhage in left atrial epicardium in all pigs, and also in ventricular epicardium (2 of 12 pigs) and endocardium (3 of 12 pigs). Pale areas of necrosis were observed on incision of the left ventricular papillary muscles in 3 pigs. Light and electron microscopic studies showed acute vascular damage with hemorrhage in the left atrial epicardium. Affected arterioles had endothelial cell swelling and transmural and perivascular accumulations of leukocytes, edema fluid, fibrin clumps, and erythrocytes. The swollen endothelial cells had large, irregularly shaped nuclei with abundant euchromatin; mitotic figures were frequent. The cytoplasm contained numerous polysomes and cisterns of rough endoplasmic reticulum. Fibroblasts adjacent to damaged vessels had edematous cytoplasm and increased amounts of rough endoplasmic reticulum. In the affected left ventricular papillary muscles, necrotic myocytes showed contraction bands, mitochondrial matrical densities, lipid accumulation, initial lysis of I bands, and pyknotic nuclei. The lesions were judged to result from two mechanisms: (1) hemorrhagic lesions from drug-induced vascular injury centered on epicardial and subepicardial arterioles and (2) papillary muscle necrosis from ischemic injury from hypoperfusion during minoxidil-induced tachycardia and hypotension.

Animals↗
PubMed1989

Studies on cardiovascular fluke (Digenea: Spirorchiidae) infections in sea turtles from the Great Barrier Reef, Queensland, Australia.

Twenty-seven sea turtles (23 Chelonia mydas and four Eretmochelys imbricata) from northeast Queensland were found to be infected with cardiovascular flukes and/or their eggs. Five had originated from turtle farms in the Torres Strait, five from an oceanarium on Magnetic Island (146 degrees 56'E, 19 degrees S) and the remainder from coral reefs in the Torres Strait or near Townsville. The incidence of flukes and/or eggs in the groups was 4.8 per cent (5 of 104), 33.3 per cent (5 of 15) and 72.2 per cent (17 of 22), respectively. Affected animals ranged in size from 18 to 108 cm (curved carapace length) and weighed between 0.5 and 77 kg. The average number of flukes per host was 47. Flukes were recovered from the three chambers of the heart and major vessels (right aortic arch and brachiocephalic artery), where they were attached to the walls or free in the lumen. They were subsequently identified as Haplotrema spp. and/or Learedius spp. In 59.2 per cent (16 of 27) of turtles, flukes were not found, although their eggs were detected microscopically. Gross pathological changes associated with the presence of flukes included thickening and hardening of arterial walls (four turtles), thrombus formation (three), chronic pneumonia (two) and an excess of pericardial or peritoneal fluid (four). Microscopically, the essential changes was that of chronic inflammation, as evidenced by the proliferation of epithelial cells, reticulo-endothelial cells and fibroblasts in areas accessible to flukes and/or eggs. Multiple diffuse egg granulomas were a prominent feature of most organs, the spleen and lungs being predilection sites. Proliferative changes had occurred in the endocardium and in the endothelium of vessels supplying the spleen, stomach, intestine and pancreas (18 turtles). The walls of major arteries, lungs, liver, brain, crop and stomach were also acutely inflamed (eight turtles). Haemorrhage was recorded in the lungs and/or brain of eight turtles with heavy fluke infestations. Other vascular changes, viz. congestion, oedema and hypertrophy of arterial/arteriolar walls, resulted from the inhibition of blood flow by parasitic emboli.

Animals↗
PubMed1989

Complications of a permanent transvenous pacing catheter in a horse.

Gross and histopathological findings in a 9-year-old horse implanted with permanent transvenous pacing cardiac catheters, 18 and 34 months before its death, are described. Lesions consisting of extensive fibrino-haemorrhagic thrombi with large numbers of bacterial colonies were present along the electrode wires and on mural and valvular endocardial surfaces of the right heart. There was a locally extensive area of suppurative endocarditis around the attachment site of the atrial electrode, which was loosely attached by a thin band of membranous tissue to the endocardium. The ventricular electrode was firmly embedded in the myocardium and was surrounded by a dense area of fibrous connective tissue in which multifocal mineralized areas were seen. Histologically, there was evidence of terminal bacteraemia. The observed lesions are discussed with respect to findings in man and other animals with similar cardiac implants.

Animals↗
PubMed1991

Computer model of excitation and recovery in the anisotropic myocardium. I. Rectangular and cubic arrays of excitable elements.

A computer model of propagated excitation and recovery in anisotropic cardiac tissue is presented that consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. The model's performance was first tested in a two-dimensional configuration with uniform anisotropy; this method allowed comparison of simulated isochrones of excitation and extracellular electrograms with the results of experimental in vitro studies of cardiac tissue. Next the model was used to study propagated excitation in a three-dimensional region representing the anisotropic properties of the ventricular wall, with attention to the effects produced by variable fiber direction from "endocardium" to "epicardium."

Action Potentials↗
PubMed1993

Electrical current paths in acute pericarditis.

The electrocardiographic changes accompanying pericarditis consist of ST elevation in most of the leads of the 12-lead electrocardiogram. The source of this ST elevation is thought to be local inflammatory changes in the epicardium underlying the inflamed pericardium. The current from this area of ST elevation must return to some unaffected region of the heart and this should be associated with a region of ST depression. This current path from the external epicardial surface has been postulated to flow back into the endocardium through the great vessels and atria. To test this hypothesis, 18 patients with pericarditis were studied by body surface potential mapping and inverse epicardial potential distributions were computed. The resultant maps were compared to those of normal people and patients with acute anterior infraction. Epicardial maps from patients with pericarditis showed a region of current flow into the heart over the great vessels and atria in all 18 patients. This pattern was not seen in normal patients or infarction patients and was consistent with the mechanism resulting in ST elevation in pericarditis being one of current flowing from the epicardium out into the thorax and back into the heart through the great vessels and atria.

Acute Disease↗
PubMed1993

ECG body surface potential mapping many years after successful surgery for coarctation of the aorta.

Patients with coarctation of the aorta (CoA) who previously underwent successful surgery are often diagnosed on standard electrocardiograms as having partial right bundle branch block. After surgery 24 patients with CoA had body surface potential mapping (BSPM) with the Case Western Reserve University 180 electrode system; of these 7 had additional aortic stenosis and none had ever had intracardiac communication. The average age at the initial surgery for CoA was 4.0 +/- 3.3 years and at the time of the BSPM it was 12.7 +/- 5.9 years. For the 17 patients with CoA without aortic stenosis the average age at the initial surgery was 5.0 +/- 3.4 years and at the time of the BSPM it was 14.2 +/- 6.0 years. In 11 of the 24 patients, a cardiac catheterization was performed, and each patient demonstrated normal pulmonary artery and right ventricular systolic pressure except for one child with 40 mmHg systolic. In the others all indications were that right ventricular pressure was normal. In 11 of the 24 patients, congestive heart failure had been present in infancy. All 24 cases had evidence for epicardial right ventricular breakthrough on the BSPM, a finding believed to indicate right ventricular activation from endocardium to epicardium via the normal Purkinje system. There were no findings on the BSPM suggesting that right bundle branch block was present. Right ventricular hypertrophy with or without terminal right conduction delay was present on the BSPM in 19 of the 24 patients (9 with additional left ventricular hypertrophy--left ventricular hypertrophy alone in 5). Right ventricular hypertrophy could be considered in 6 of 19 patients in the electrocardiogram, and in 11 of 19 in the vectorcardiogram. The mechanism for the persistent electrocardiographic right ventricular hypertrophy is postulated to involve right ventricular hyperplasia in utero or in early neonatal life, which never disappears.

Adolescent↗
PubMed1991

The morphology of the developing canine conducting system: bundle branch and Purkinje cell architecture from birth to week 12 of life.

This is a qualitative and quantitative study of dog bundle branch and Purkinje cell development from day 0 to week 12 of life; we correlate the morphologic data with changes observed in the functional properties of developing dog Purkinje tissue. The bundle branch itself has a roughly cylindrical shape and is surrounded by a collagen sheath covered with endocardium. Within the bundle, Purkinje cells are packed closely together in fascicles distributed evenly around a central artery. Cross-sectional area doubles in the right bundle and increases 5-fold in the left bundle system between day 0 and week 12 of life. About one third of the bundle by volume is Purkinje tissue; the rest is extracellular space containing an increasing amount of collagen as the animal ages. Purkinje cell cross-sectional area is constant during the first week of life, but its length doubles and the cell changes from a relatively round to a more cylindrical shape. Between day 7 and week 12, cell diameter doubles; Purkinje cell surface area increases 5-fold and its volume almost 10-fold. As a consequence, the surface to volume ratio halves and approaches the value reported for adult dogs by week 12 of life. The percent of the intercalated disc occupied by nexal junctions virtually doubles by week 12, the same period over which Purkinje fiber conduction velocity increases. The disc itself becomes less dominant as the cell enlarges; the total percent of sarcolemma involved in its formation decreases by a fourth and has achieved the adult value by week 12 of life. As this happens, the percent of cell membrane facing on clefts increases almost 6-fold, so that the total percent of sarcolemma facing on small spaces (approximately 340A wide) is constant over the age period studied. The paucity of clefts in newborn tissue compared with the value reported for the adult dog may help explain the relative lack of responsiveness to extracellular potassium concentration of the resting membrane potential described for fetal Purkinje tissue. Within the Purkinje cell itself, the percent by volume occupied by mitochondria remains relatively constant over the age span studied, while sarcomeric mass increases 3-fold over the same period of time; these data are consonant with the relative resistance of this tissue to hypoxia.

Animals↗
PubMed1992

Bovine mitral valve organ culture: role of interstitial cells in repair of valvular injury.

The atrial and ventricular surfaces of the mitral valve are lined by endothelial cells termed endocardial cells, while the valve stroma contains interstitial cells. Bovine mitral valve organ cultures were immunoperoxidase-stained for Factor VIII RAg, alpha smooth muscle actin, and PCNA/cyclin in order to identify the cell types involved in mitral valve wound repair. Factor VIII RAg is a well-characterized endothelial cell marker, alpha smooth muscle actin is an indicator of smooth muscle differentiation and PCNA/cyclin is a marker for S phase. Bovine mitral valve endocardium was Factor VIII RAg positive and remained positive after culturing for 6 days (n = 7). Mitral valve interstitial cells were Factor VIII RAg negative and positive for alpha smooth muscle actin. By 6 days in culture, the lateral edges of the preparations, where the tissue was originally dissected from the mitral valve leaflet, were covered by multiple layers of cells. These cells were Factor VIII RAg negative (n = 7), and hence not endocardial, but were alpha smooth muscle actin positive like interstitial cells. Interstitial cells subjacent to the lateral edges were negative for PCNA/cyclin in uncultured preparations (n = 5), but positive in 12 out of 15 specimens cultured for 6 days. The results suggest that mitral valve interstitial cells are responsible for the repair process seen in the lateral edges of mitral valve organ cultures.

Animals↗
PubMed1985

Compliance, mass, and shape of the canine left ventricle after global ischemia analyzed with two-dimensional echocardiography.

End-diastolic pressure (EDP)-volume (EDV) curves were constructed for the left ventricle (LV) in 10 dogs on cardiopulmonary bypass before and after 45 min of normothermic ischemic arrest. LVEDV and mass were calculated from three perpendicular two-dimensional echocardiographic sections using a Simpson's rule algorithm. The echocardiographic method employed was specially developed in earlier work for physiologic studies in dogs. Postmortem pressure-volume curves were measured for comparison by direct saline infusion into sealed ventricles. LVEDV was plotted against LVEDP (0-20 mm Hg) and data were analyzed by two-way analysis of variance and also by exponential curve fitting to the relation EDP = alpha e beta EDV, where beta is the derived exponential constant reflecting slope and thereby ventricular stiffness. Postischemic EDP-EDV curves shifted to the left and the beta constant increased (beta = 0.02 +/- 0.005 (SE) vs 0.05 +/- 0.01, P less than 0.05). LV eccentricity, the ratio between long- and short-axis measurements, was unchanged (1.43 +/- 0.05 vs 1.46 +/- 0.06 postischemia, NS), but LV mass increased (105 +/- 7 vs 128 +/- 9 g postischemia, P less than 0.001). Postischemic LV mass by echo was not significantly different from measured postmortem LV mass (r = 0.87). The nonparallel alteration in the EDP-EDV curves, lack of change in LV shape (eccentricity), and increase in LV mass in the postischemic ventricle suggest that increased ventricular stiffness rather than direct encroachment by the edematous endocardium on chamber volume is responsible for postischemic changes in LV diastolic properties.

Animals↗
PubMed1987

Hypothermic cardiopulmonary bypass: a comparison between alpha and pH stat regulation in the dog.

The accepted normal pH of 7.40 may not be optimal at lower temperatures. This study evaluated the effect of maintaining pH in the accepted normal range at hypothermia (group 1, pH stat) or at normothermia (group 2, alpha stat) on organ blood flow and hemodynamics in dogs. The desired pH was achieved at all temperatures by adjusting pCO2. Hypothermia to 20 degrees C was induced by high flow bypass in both groups followed by 45 min of reduced flow before rewarming. In group 1 (n = 10), pH was 7.45 +/- 0.02 at 20 degrees C and in group 2 (n = 11) it was 7.64 +/- 0.01. A greater base excess developed by the end of the low flow period in pH stat animals (-9.4 +/- 1.1 vs -2.8 +/- 0.8, P less than .001) and resulted in continued acidosis after rewarming in the pH stat group compared to those in the alpha stat group (7.32 +/- 0.03 vs 7.38 +/- 0.01, P less than .02). Expressed as a percentage of baseline, regional blood flows after rewarming for group 1 were: brain 112 +/- 8%, renal cortex 48 +/- 8% (P less than 0.005, rewarm vs baseline), renal medulla 36 +/- 9% (P less than 0.005, rewarm vs baseline), epicardium 198 +/- 40% (P less than 0.05, rewarm vs baseline), endocardium 151 +/- 25%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Electron microscopic changes in tropical endomyocardial fibrosis.

Electron microscopic examination of cardiac tissue from seven patients with tropical endomyocardial fibrosis showed the endocardium to be replaced by maturing granulation tissue containing haphazardly arranged collagen bundles, smooth muscle cells, blood vessels and degranulated mast cells. Mature collagen was present on the luminal aspect of the granulation tissue. Myofibres showed mitochondrial swelling, lamella bodies, focal myocytoplasmic clearing and collapsed intercalated discs. Small calibre blood vessels exhibited endothelial swelling, areas of basement membrane duplication and collections of neutrophilic and eosinophilic leucocytes. Eosinophils showed alteration in granule morphology. These changes are similar to the lesions reported in endomyocardial disease with eosinophilia.

Adolescent↗
PubMed1991

Immunohistochemical localization of environmentally induced cytochrome P450IA1 in multiple organs of the marine teleost Stenotomus chrysops (Scup).

Differences in expression of cytochrome P450 forms and their functions in different organs and cell types could determine the response of those cells and organs to xenobiotics. Recently, we described the cellular localization of cytochrome P450IA1 (P450E) induced in 10 organs or organ systems of the fish, Stenotomus chrysops (scup) treated with 3,3',4,4'-tetrachlorobiphenyl or with 2,3,7,8-tetrachlorodibenzofuran. (R.M. Smolowitz, M.E. Hahn, and J.J. Stegeman, Drug Metab. Dispos. 19, 113, 1991). Here we describe the presence and localization of P450IA1 in organs of scup sampled directly from an environment contaminated by chlorinated biphenyls and bibenzofurans, the outer New Bedford Harbor of Massachusetts. Western blot analysis of microsomes from selected organs (liver, kidney, gill, and heart), using monoclonal antibody 1-12-3, revealed induced levels of P450IA1 in each. The localization of P450IA1 in these and other organs was determined in sections prepared by standard histological methods and stained with MAb 1-12-3 in an indirect peroxidase labeling method. P450IA1 was detected in multiple cell types in liver, including hepatic, pancreatic, and vascular tissue. Kidney and gut also showed prominent P450IA1 levels in epithelial structures and in vascular endothelial cells. Specific staining was detected in endothelial cells, but not other cell types, in heart, gill, spleen, testis, ovary, nose, and brain. In heart, the staining was present in the endocardium of atrium and ventricle, and endothelium of the coronary vasculature and great vessels. The results demonstrate that P450IA proteins are induced in many organs of fish exposed to environmental chemicals in the wild, with patterns of cellular localization like those seen in fish experimentally treated with known inducers. The strong staining of P450IA1 in endothelial cells in all organs examined supports experimental results indicating that endothelium is a major site of P450IA1 induction. Our results indicate further that immunohistochemistry is a useful method for detecting P450 induction as a biomarker for exposure.

Animals↗
PubMed1980

Determination of left ventricular dimensions with ultrasound.

A new ultrasonic measuring system (UM 3) is described. In addition, the construction of simple piezoelectric transducers is outlined. These can be implanted either in the epicardium or in the endocardium of the left ventricle in anesthetized or conscious dogs. The total system has a high accuracy and linearity, and zero drift is small. An automatically controlled floating window excludes most artifacts due to unwanted echoes. Together with a modified delay-time measuring circuit, better recordings of dimensions are obtained. Sources of error due to the technique of implantation or due to electrical disturbances are described. A modified technique of implantation of endocardial transducers is presented.

Animals↗