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Biomedical subjects

K Grong

Publications and source records attributed to K Grong.

68 records · Page 4Linked to original sources
PubMed1987

Local myocardial function following coronary occlusion in cats. Effect on non-ischaemic regions.

The mechanical function and perfusion in ischaemic and non-ischaemic myocardium after coronary occlusion was studied in 10 cats using pressure-length loop analysis and radiolabelled microspheres. Measurements in three regions--ischaemic, adjacent normal and remote normal myocardium--all showed different responses to coronary occlusion. In the ischaemic region loop area, segment shortening and tissue flow were markedly reduced. In the adjacent normal region, both loop area and segment shortening as well as flow increased. In the remote normal region, neither loop area, segment shortening nor flow showed consistent changes. End-diastolic segment length increased in all regions, most in the ischaemic region and least in the remote region. The increased end-diastolic segment length in all regions after coronary occlusion indicates activation of the Frank-Starling mechanism as an attempt to maintain stroke volume. However, the end-diastolic segment length did not increase uniformly for all normal myocardium: it depended on the proximity to the ischaemic region. Increased contractile function in the adjacent normal myocardium due to non-uniform distribution of the Frank-Starling effect is the most likely mechanism behind the left ventricle's ability to partially compensate for loss of contractile mass during acute regional ischaemia in anaesthetized cats.

Animals↗
PubMed1987

Anesthetic interaction in cardiovascular research models: effects of xylazine and pentobarbital in cats.

The effects of xylazine given to cats before anesthetization was induced with pentobarbital were determined. Cardiac hemodynamic variables and regional blood flow rates in the heart and other organs were measured, using radiolabeled microspheres. Two groups, each of 10 cats, were included in the study: one group (group 1) was anesthetized with pentobarbital given intraperitoneally and subsequently given xylazine; the other group (group 2) was first given 1 mg of xylazine/kg, IM, and then anesthetized with pentobarbital given IV. Anesthesia was maintained in both groups with nitrous oxide. The preanesthetic administration of xylazine decreased the amount of pentobarbital used for surgical anesthesia by approximately 50%. It also resulted in decreased heart rate, cardiac contractility, and cardiac output and increased left ventricular end-diastolic pressure, compared with those values in cats given pentobarbital (group 1). After the latter cats (anesthetized with pentobarbital) were given xylazine, heart rate, cardiac contractility, and cardiac output decreased and left ventricular end-diastolic pressure increased to values similar to those found in group 2 (given xylazine before anesthetization). Myocardial tissue blood flow rates in the left and right ventricles were lower in the cats of group 2. In group 1 cats, myocardial blood flow rates decreased when xylazine was subsequently added. Blood flow rates in the kidneys and gastrointestinal tract were generally decreased by xylazine. Xylazine profoundly changed cardiac hemodynamic function and perfusion in the heart, as well as several other organ systems, because of marked cardiodepression.

Animals↗
PubMed1986

The ultrastructure of the myocyte in different regions of experimental infarcts in the cat heart.

The ultrastructure of myocytes was studied in the left ventricular myocardium of the cat heart after 3 h of LAD ligation. The ischemic, borderline, and normally perfused myocardium was defined by in vivo injection of fluorescein and by regional myocardial blood flow measurements with 15.5 microns radio-labeled microspheres. A semiquantitation of the number of irreversible injured cells in per cent of total counted in the three different zones showed that 53%-63% were irreversibly injured in the ischemic zone, 7%-26% in the borderline area, while none were irreversibly injured in the normally perfused myocardium. The interior excitation-contraction couplings in the normally perfused myocardium comprise interior dyads, triads, reversed triads, and encircling couplings. While the couplings in general were structurally resistant to ischemia, injured interior couplings were apparent in severely damaged cells of the hypoperfused tissue. Such injuries comprise a widening of the junctional gap and a disintegration of the junctional processes.

Animals↗
PubMed1986

Cellular lipid accumulation in different regions of myocardial infarcts in cats during beta adrenergic blockade with timolol.

The effects of non-selective beta adrenergic blockade on intracellular lipid accumulation in hearts with acute ischaemia were studied by electron microscopy of myocardial biopsy specimens using quantitative stereological techniques. Pentobarbital anaesthetised cats with coronary ligation were divided into eight controls and eight cats treated with timolol intravenously just before ligation. Biopsy specimens were collected from ischaemic, borderline, and normally perfused myocardium, defined by an in vivo injection of fluorescein and verified by regional myocardial blood flow measurements with 15 microns radiolabelled microspheres. During a 3 h occlusion period timolol treated cats had a lower heart rate, left ventricular dP/dt, and plasma free fatty acid concentration. In control cats the cytosolic volume fraction of lipids was 0.71 X 10(-3) in non-ischaemic myocardium, 2.63 X 10(-3) in central ischaemic tissue, and 6.53 X 10(-3) in borderline tissue. Timolol reduced the appreciable lipid accumulation in borderline tissue by 24% (to 4.97 X 10(-3)) compared with controls, whereas accumulation in central ischaemic tissue was not affected. Thus timolol diminished lipid accumulation in borderline myocardial tissue. The mechanism is most likely related to reduced ischaemic intensity and better preserved metabolic function.

Animals↗
PubMed1986

Is reduced cardiac performance the only mechanism for myocardial infarct size reduction during beta adrenergic blockade?

Equal reductions in heart rate (44 beats X min-1) were obtained in cats by treatment with either the beta blocking agent timolol or alinidine, an agent claimed to cause bradycardia without interfering with beta adrenoceptor function. Infarct size was measured by staining with triphenyltetrazolium-chloride after 5 h of coronary occlusion and related to the area of hypoperfused myocardium as measured by autoradiography. Regional myocardial blood flow was measured by 15 micron radiolabelled microspheres. Compared with the control cats, in whom 87.4 (SEM 2.2)% of hypoperfused myocardium developed into necrosis, timolol reduced infarct size to 65.8 (SEM 2.6)% (p less than 0.001) and alinidine to 76.2 (SEM 3.1)% (p less than 0.01) of the hypoperfused area. Timolol reduced infarct size more than did alinidine (p less than 0.01). Necrosis was more extensive in the endocardium than in the epicardium in all groups. In the subendocardium timolol and alinidine reduced infarct size to the same extent, whereas timolol reduced infarct size more than alinidine in the subepicardium. Although heart rate proved to be the dominant haemodynamic predictor of infarct size, this study indicates that mechanisms other than reduced oxygen demand associated with bradycardia and cardiodepression are operating in the ischaemic myocardium during beta adrenergic blockade.

Animals↗
PubMed1985

Lipid accumulation in the myocardium during acute regional ischaemia in cats.

Accumulation of lipid material in the myocardium was studied in cat hearts with acute regional ischaemia of 3 h duration. The fractional volume of lipid droplets in cytosol was analysed by electron microscopy of myocardial biopsies using a quantitative stereologic technique. Ischaemic and normally perfused myocardium were identified by fluoresceine injection, and tissue blood flow measurements were performed with labelled microspheres. In normal myocardium only small amounts of lipid droplets were found. A marked accumulation of lipid droplets occurred in borderline tissue between the two types of myocardium, whereas lipid accumulation in ischaemic myocardium was less pronounced. The arterial concentration of nonesterified fatty acids was clearly increased during the 3 h coronary artery occlusion period. Increased triglyceride synthesis from arterial fatty acids, or redistribution of intracellular lipids, are suggested as possible explanations for lipid accumulation during acute myocardial ischaemia.

Acute Disease↗
PubMed1985

Effects of isoproterenol on adenine nucleotide catabolism in cat hearts with acute regional ischaemia.

Previous studies have demonstrated that beta-adrenergic agonists cause extension of ischaemic lesions in the myocardium. In the present study the effects of isoproterenol on adenine nucleotide metabolism were investigated in cat hearts with regional ischaemia following permanent coronary occlusion for 45 min. Adenine nucleotides and their metabolites were measured by high performance liquid chromatography and regional myocardial blood flow was measured by 15-microns radiolabelled microspheres in a total of 255 paired tissue samples. Compared with untreated control cats, ATP and the energy charge were more reduced in ischaemic myocardium of isoproterenol-treated cats. Increased amounts of the degradation products inosine and hypoxanthine/xanthine were also found in these regions. These results could be ascribed to increased cardiac performance caused by isoproterenol, which augments the imbalance between energy production and oxygen supply in ischaemic myocardium.

Adenosine Diphosphate↗
PubMed1984

Effects of timolol on adenine nucleotide catabolism in cat hearts with acute regional ischaemia.

The effects of the beta-adrenergic blocking agent timolol on cardiac function and adenine nucleotide metabolism were investigated in cats with 45 min of acute ischaemia following coronary occlusion. Regional myocardial blood flow was measured by 15 micron radiolabelled microspheres, and adenine nucleotides and their degradation products were measured by high performance liquid chromatography in 16 tissue regions in each cat. During ischaemia, cats treated with timolol exerted a reduced cardiac performance as judged from reduced heart rate and cardiac contractility; consequently preocclusion tissue blood flow was reduced compared with a control group of cats. The ATP concentration was less severely depleted in ischaemic regions of the left ventricle in cats treated with timolol. The energy charge was reduced to a lesser extent in ischaemic regions, and in intermediate flow ranges the contents of the inosine and hypoxanthine/xanthine were reduced compared with untreated cats. These results indicate that the beta-adrenergic blocking agent timolol might protect the myocardium within a 45 min ischaemic period. The mechanism for this effect is most probably related to the reduction in overall cardiac performance.

Acute Disease↗
PubMed1984

Regional myocardial tissue blood flow during beta-adrenergic blockade in cat hearts with acute ischaemia.

Selective beta 1- or beta 2-adrenergic blockade was achieved by practolol or IPS 339, respectively, in cats with acute ligation of a coronary artery. During blockade, heart rate was kept constant by atrial pacing and blood pressure reduction was prevented by aortic clamping. Regional myocardial blood flow was measured by the distribution of 15 micron labelled microspheres. Practolol slightly reduced epicardial blood flow in ischaemic myocardium, while blood flow in border and normally perfused myocardium remained unchanged. Following IPS 339, myocardial tissue flow increased in normally perfused myocardium, on average by 37% in the endocardium and 30% in the epicardium. No changes occurred in the other regions. The flow changes brought about by IPS 339 were unrelated to haemodynamic changes, and the coronary vascular resistance was reduced. These results are indicative of coronary vasodilation related to beta 2-adrenergic receptor blockade and was confined to well-oxygenated areas surrounding the acutely ischaemic zone.

Adrenergic beta-Antagonists↗
PubMed1984

Relationship between myocardial adenine nucleotide catabolism and tissue blood flow rate in experimental ischaemia.

A method was developed for tissue preservation and evaluation of the adenine nucleotide metabolism in small samples of myocardium after 45 min of ischaemia. Ischaemia was produced by coronary artery occlusion in anaesthetized cats. Adenine nucleotides and their metabolites were measured by isocratic liquid chromatographic systems which allow quantitative analysis of the nucleotides and their metabolites inosine, hypoxanthine and xanthine in biopsies of 5-20 mg tissue. Regional myocardial blood flow was measured in the tissue surrounding the biopsies by the distribution of 15 micron radiolabelled microspheres. In central ischaemic regions the ATP level was approximately 1 mumol/g wet weight, whereas in normally perfused myocardium the ATP level was approximately 5 mumol/g tissue. In tissue with intermediate flow values, intermediate ATP levels were found. Energy charge, which summarizes all adenine nucleotide concentrations, was reduced from 0.88 to 0.50, and the molar concentrations of inosine, hypoxanthine and xanthine increased in ischaemic tissue. We conclude that this method provides reliable characterization of the local cellular energy status in cat hearts with ischaemic regions.

Adenine Nucleotides↗
PubMed1983

Regional myocardial tissue blood flow during sequential beta 1- and beta 2-adrenergic blockade in cat hearts with acute ischaemia.

beta-Adrenergic blockade was imposed on cats with ischaemic regions of the left ventricle produced by coronary artery occlusion. Ten animals first received a beta 1-blocking agent (atenolol) followed by a beta 2-blocking agent (IPS 339). In ten more animals this sequence was reversed. Combined blockade, obtained after both agents were administered, showed clear reduction of tissue blood flow in all areas of the ventricle, except for the central ischaemic zone. The flow reduction could be ascribed to bradycardia and reduced coronary perfusion pressure. By analysing the sequential changes it was evident that blockade of beta 1-adrenergic receptors was responsible for the haemodynamic changes, and the coronary vascular resistance rose so as to match the quantity of blood flow to the functional state of the ventricle. Blockade of beta 2-receptors by IPS 339, however, showed no evidence of coronary vasoconstriction but rather maintained vascular resistance at an unchanged level despite a weak beta 1-adrenergic blocking effect.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of timolol on blood flow distribution in the feline myocardium with acute regional ischaemia during controlled haemodynamic conditions.

The beta-adrenergic blocking agent timolol was given to cats with acute coronary artery ligation under controlled haemodynamic conditions. Regional myocardial tissue flow was measured by the distribution of labelled microspheres. Timolol reduced cardiac contractility and left ventricular end-diastolic pressure rose, whereas heart rate and ventricular systolic pressure were kept constant by atrial pacing and aortic clamping. The systolic period increased following timolol administration under these conditions. Myocardial blood flow remained unchanged in central ischaemic and border areas, whereas flow increased both endocardially and epicardially in normally perfused area following timolol administration. Without pacing there was a significant flow reduction in the epicardium of the normally perfused area, compared with the situation where heart rate was constant. Under controlled haemodynamic conditions, therefore, timolol appears to improve coronary perfusion in normal myocardium, whereas blood flow to ischaemic myocardium remains essentially unchanged.

Animals↗
PubMed1981

Effect of timolol on blood flow distribution in the myocardium during acute regional ischaemia in cats.

The beta-adrenergic blocking agent timolol was given to cats with acute coronary artery ligation. Regional myocardial tissue flow was measured by the distribution of 15 micrometers labelled microspheres. Timolol reduced heart rate, cardiac contractility and left ventricular systolic pressure, but end-diastolic pressure rose. Ischaemic tissue blood flow remained unchanged following timolol, thus improving the marked imbalance between oxygen demands and delivery. In normal areas of the myocardial tissue flow was reduced, indicating the beta 2-adrenergic blocking effect of timolol. This was also the case for the border area between ischaemic and non-ischaemic tissue, but significantly less flow reduction was found on the endocardial side than on the epicardial side in the border area. Except for this latter observation, timolol does not appear to improve coronary perfusion. The present study, therefore, indicates that beneficial effects of timolol on ischaemic myocardium are mainly related to a reduction of myocardial oxygen demand.

Animals↗