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Biomedical subjects

H Vik-Mo

Publications and source records attributed to H Vik-Mo.

At least 73 records · Page 4Linked to original sources
PubMed1986

Limitation of myocardial infarct size by metabolic interventions that reduce accumulation of fatty acid metabolites in ischemic myocardium.

The effects on myocardial damage of metabolic interventions by nicotinic acid, oxfenicine, or a combination of the two were assessed in open-chest dogs exposed to coronary artery occlusion for 6 hours. The accumulation of metabolites of free fatty acids (FFAs) was studied in tissue samples of the left ventricle taken 60 minutes after coronary occlusion in separate animals. The percentage of the hypoperfused zone that evolved to infarction was 96 +/- 3% (mean +/- SEM) in control dogs, 74 +/- 4% in dogs treated with nicotinic acid (p less than 0.05 vs control dogs), 72 +/- 2% in dogs treated with oxfenicine (p less than 0.05 vs control dogs), and 54 +/- 5% in dogs with combined nicotinic acid and oxfenicine (p less than 0.05 vs control dogs, p less than 0.05 vs nicotinic acid and oxfenicine). Arterial FFA concentration was markedly reduced in dogs treated with nicotinic acid and those treated with combination nicotinic acid and oxfenicine. The accumulation of long-chain acyl carnitine was substantially reduced in the ischemic myocardium after nicotinic acid, oxfenicine, and a combination of the two, whereas the lowering of long-chain acyl CoA was less pronounced. Thus, nicotinic acid and oxfenicine, which depress myocardial FFA metabolism by different mechanisms, both reduce myocardial infarct size and their effects are additive.

Acetylcarnitine↗
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↗
PubMed1986

Left main or proximal left anterior descending coronary artery disease: detection by echocardiographic evaluation of interventricular septal function during exercise.

Forty patients with coronary artery disease were studied prospectively to investigate whether stenosis of the left main (LMCA) or left anterior descending coronary artery, proximal to the first septal branch (proximal LAD), could be detected by M-mode echocardiography during exertion. The interventricular septum was visualized in 30 of the patients during bicycle exercise in the semisupine position, all with simultaneous occurrence of electrocardiographic evidence of myocardial ischaemia. Fifteen of these had LMCA or proximal LAD stenosis. Systolic motion and thickening of the septum decreased significantly from rest to peak exercise in patients with LMCA or proximal LAD disease while it increased in those without. The results suggest that M-mode echocardiography during exercise in patients with coronary artery disease might identify those with LMCA or proximal LAD stenosis.

Adult↗
PubMed1986

Cerebral ischemic attacks as a complication of heart disease: the value of echocardiography.

The association of heart disease and cerebral ischemic attacks, and the usefulness of echocardiography in detecting heart disease and possible embolic source, were studied in 194 patients with transitory cerebral ischemic attack or stroke. The study revealed 95 patients with heart disease, and 63 of them had positive echocardiographic findings. All together, 35 patients had heart disease as a probable source for systemic embolism. An undetected cardiac disorder, not found by clinical examination or electrocardiography, was detected in 25 patients. The cardiac disorder found by echocardiography only, was most frequently aortic and mitral valve disease. Thus, echocardiography is an useful tool in detecting heart disease in these patients.

Atrial Fibrillation↗
PubMed1986

Does infarct size influence loss of embolised 15-micrometer microspheres from ischaemic myocardium?

The relationship between myocardial infarct size and loss of 15-micron microspheres from ischaemic tissue was investigated in anaesthetized cats. Radioactive microspheres were injected in the left atrium before and 5 h after left anterior descending coronary artery occlusion. Left ventricular hypoperfused zone (HZ) averaged 36.6% and infarct size (IS) 31.6%. Thus, 86% of HZ evolved into necrosis. Preocclusion blood flow was lower in ischaemic (1.62 ml/min per g) compared with non-ischaemic myocardium (2.09, p = 0.002), indicating 22% microsphere loss. In ischaemic subendocardium, oedema (3.7%) could account for the apparent loss. In ischaemic subepicardium, oedema was less pronounced and 18% physical sphere loss occurred. Subepicardial loss increased in proportion to IS and IS/HZ ratio (r2 = 0.71; p less than 0.005). Non-entrapment of 15-micron spheres in coronary circulation averaged 0.6%, and preocclusion spheres appeared in coronary sinus blood throughout the ischaemic period. In systemic circulation, non-entrapment during injection of preocclusion spheres was 7.8%, but only 1.8% 5 h later. Release of postocclusion spheres took place during KCl injection. Thus, myocardial ischaemia is associated with alterations in microvascular function allowing release of entrapped 15-micron spheres. Also, the magnitude of microsphere loss per gram tissue is related to infarct size.

Animals↗
PubMed1986

Left ventricular function in aortic valve endocarditis. Echocardiographic evaluation and comparison with findings in chronic aortic regurgitation.

The value of M-mode echocardiography in assessment of left ventricular (LV) function in patients with aortic regurgitation due to aortic valve endocarditis (AVE) was studied in 12 consecutive patients and compared with the findings in 30 patients with chronic aortic regurgitation (CAR). Patients with AVE had markedly increased LV end-diastolic and end-systolic diameters, whereas fractional shortening was normal. A linear correlation was found between the LV ejection fractions calculated by echocardiography and angiography, but echocardiography markedly overestimated the ejection fractions. There was a close linear correlation between the prematurity of mitral valve closure (MVC) and LV end-diastolic pressure. Patients with CAR had lower end-diastolic pressure, similarly increased LV internal diameters and none had premature MVC. Thus, M-mode echocardiography can identify patients with premature MVC and high LV filling pressure. However, echocardiographic LV function indices based on measurement of internal dimensions overestimate the LV function and these data should be interpreted with caution.

Adult↗
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

Improved haemodynamics but reduced arterial blood oxygenation, at rest and during exercise after long-term oral prazosin therapy in chronic cor pulmonale.

The effect of vasodilator therapy in chronic obstructive lung disease with pulmonary hypertension was evaluated in eight patients during oral prazosin therapy (2-10 mg day-1). After one week, prazosin reduced mean pulmonary artery pressure and pulmonary and systemic vascular resistance, and increased cardiac index both at rest and during exercise. Similarly improved haemodynamics were observed after two months of therapy. Arterial PO2 and oxygen saturation fell significantly after two months both at rest and during exercise, but were not changed after one week. Lung function tests were not altered by prazosin. Thus, although prazosin improves the haemodynamics in patients with chronic obstructive lung disease, caution is advised in long-term therapy since prazosin worsens the arterial blood oxygenation.

Administration, Oral↗
PubMed1985

Male breast cancer from pacemaker pocket.

One year following implantation of a mercury zinc pulse generator under the right breast, a 75-year-old man developed an ulcerative tumor of the nipple. Initially, the process was misinterpreted as a pacemaker pocket infection, until a diagnosis of papillary adenocarcinoma was made. The patient died from generalized metastases. To our knowledge, the association of a pacemaker implant and male breast cancer has not been previously reported; the probability of this occurring by chance seems rather low.

Adenocarcinoma, Papillary↗
PubMed1984

Comparative effects of propranolol, timolol and metoprolol on myocardial infarct size after experimental coronary artery occlusion.

The effects of equiblocking doses of three beta-adrenergic blocking agents, propranolol, timolol and metoprolol, on myocardial infarct size were evaluated in 28 dogs after acute experimental coronary artery occlusion. Heart rate, arterial pressure and arterial free fatty acid concentration were measured in an attempt to evaluate their effects on the extent of myocardial injury. The zone at risk of infarction in each dog 1 minute after left anterior coronary artery occlusion was assessed by injecting highly radioactive albumin microspheres into the left atrium, and the hypoperfused zone was determined by autoradiography. After 15 minutes, the dogs were randomized into four groups: control dogs (n = 7), propranolol-treated dogs (1.2 mg/kg intravenously, n = 7), timolol-treated dogs (0.2 mg/kg intravenously, n = 7) and metoprolol-treated dogs (1.2 mg/kg intravenously, n = 7). After 6 hours, the dogs were killed. The left ventricle was sliced and stained with triphenyl-tetrazolium chloride for measurement on infarct size. The same slices were then autoradiographed for measurement of the hypoperfused zone. The percent of hypoperfused zone that evolved to infarction (the ratio of infarct size to hypoperfused zone) was 90.4 +/- 1.9% in the control group, 72.4 +/- 2.4% in the propranolol-treated dogs (p less than 0.05 versus control group); 57.9 +/- 4.4% in the timolol-treated dogs (p less than 0.01 versus control group; p less than 0.05 versus propranolol) and 54.4 +/- 3.7% in the metoprolol-treated dogs (p less than 0.01 versus control group; p less than 0.05 versus propranolol). Thus, propranolol, timolol and metoprolol reduced myocardial infarct size in dogs by 20, 36 and 40%, respectively, after experimental coronary artery occlusion. Metoprolol and timolol protected the ischemic myocardium more effectively than did propranolol.

Animals↗
PubMed1984

Increased left ventricular emptying at maximal exercise after reduction in afterload.

Twelve healthy men were studied by M mode echocardiography during exercise to investigate the effect of afterload reduction on left ventricular function at maximal exertion. They performed two maximal exercise bicycle tests 4 hr apart while in the semisupine position and were given 20 mg nifedipine sublingually 30 min before the second test. During the first test end-systolic dimension decreased (p less than .01) and fractional shortening increased from rest to peak exercise (p less than .01), while end-diastolic dimension did not change significantly. At maximal exercise systolic blood pressure was lower after nifedipine than in the preceding control test (202 +/- 10 [mean +/- SD] vs 212 +/- 14 mm Hg; p less than .01), while heart rate was not significantly changed (168 +/- 15 vs 162 +/- 13 beats/min). End-systolic dimension was lower (25.6 +/- 3.3 vs 28.8 +/- 4.2 mm; p less than .01) and fractional shortening higher (50.7 +/- 6.0% vs 45.3 +/- 7.0%; p less than .01) while end-diastolic dimension was unchanged (52.3 +/- 1.9 vs 52.4 +/- 2.6 mm). Our data indicate increased left ventricular emptying at maximal exercise after nifedipine, most probably due to reduction in afterload.

Adult↗
PubMed1984

Effects of spontaneous respiration on left ventricular function assessed by echocardiography.

The effects of quiet respiration on assessment of left ventricular function by two-dimensional echocardiography were investigated in 12 healthy men. End-diastolic area in the parasternal short-axis view decreased with inspiration (from 17.3 +/- 2.1 [mean +/- SD] to 16.0 +/- 2.1 cm2, p less than .01), while end-systolic area did not change (from 7.6 +/- 1.4 to 7.7 +/- 1.5 cm2; NS). A fixed cursor that was located through the center of the left ventricular area at end-expiration made a tangential cut of the area at end-inspiration were smaller along the cursor than through the center of the short-axis area both at end-diastole (1.9 +/- 1.7 mm; p less than .01) and end-systole (3.8 +/- 4.0 mm; p less than .01). Our results suggest a need for standardization with regard to respiratory phases in assessment of left ventricular function by two-dimensional echocardiography and indicate the occurrence of inspiratory reduction of left ventricular stroke volume associated with decreased diastolic filling. Motion of the heart relative to the echo beam may play a part in the respiratory variations in left ventricular dimensions assessed by M mode echocardiography.

Adult↗
PubMed1983

Progression of myocardial damage following coronary microembolization in dogs.

The aim of the present study was to determine whether induction of ischaemic heart failure by micro-embolization leads to only a single episode of myocardial injury or whether it sets up a vicious cycle of progressive myocardial damage. Acute left ventricular (LV) failure was produced in 15 closed-chest anaesthetized dogs by injection of 50 microns plastic microspheres into the left main coronary artery. The dogs showed signs of severely depressed LV function; there was a marked increase in LV end-diastolic pressure and a marked decrease in stroke volume. Myocardial lactate uptake decreased or reversed to production. Six dogs with very high LV end-diastolic pressure died during the subsequent 3 days and autopsy revealed pulmonary edema. The LV function was re-examined in four dogs at 2 and 4 weeks after embolization. Except for a modest elevation of LV end-diastolic pressure there were no haemodynamic or metabolic signs of myocardial dysfunction. Gross and light microscopic examination of the heart in dogs 8 hours to 6 weeks following microsphere injections revealed numerous small infarcts or focal areas of granulation or scar tissue throughout the entire left ventricle. At 1 to 6 weeks close to the infarcts there were scattered myocytes with strong eosinophilia and pyknosis or loss of nuclei, interpreted as myocytolysis. In two dogs killed at six weeks after the embolization there were areas of granulation tissue, similar to a recent infarction about 1 week old. Thus, in spite of apparent functional restoration there were morphological signs of repeated and progressive myocardial injury several weeks after coronary embolization.

Animals↗
PubMed1982

Electrophysiologic effects of flecainide acetate in patients with sinus nodal dysfunction.

Flecainide acetate (R818) is a new antiarrhythmic agent for oral and intravenous use; it has predominantly class I properties and a long plasma half-life. Electrophysiologic effects were evaluated in 11 patients with sinus nodal dysfunction before administration of flecainide acetate and 15 to 60 minutes after intravenous administration of 1.5 mg/kg body weight of flecainide acetate given over 15 minutes. In 8 of 11 patients with maximal sinus nodal recovery time increased after flecainide acetate. However, the mean maximal sinus nodal recovery time was not statistically significantly increased from 1,929 +/- 184 (mean +/- standard error of the mean [SEM]) to 2,770 +/- 500 ms (p less than 0.10). The corrected sinus nodal recovery time increased from 875 +/- 181 before to 1,727 +/- 507 ms after administration of flecainide acetate (p less than 0.05). The sinus cycle length and sinoatrial conduction time were not significantly changed. Flecainide acetate induced a marked prolongation of the H-V interval (from 41 +/- 3 to 52 +/- 4 mg [p less than 0.01]) as well as a significant increase in the A-H interval, QRS duration, and QT100 interval. The effective and functional refractory periods of the atria increased by 12% (p less than 0.01) and 11% (p less than 0.01), respectively. The atrioventricular (AV) nodal functional refractory period increased significantly by 7% (p less than 0.01), whereas the 9% prolongation of the effective refractory period was not statistically significant. No side effects were observed. It is concluded that flecainide acetate prolongs atrial and ventricular conduction and refractoriness, and thus appears to be a potent antiarrhythmic agent. However, the sinus nodal function is depressed, and thus caution is advised in the use of flecainide acetate in patients with sinus nodal dysfunction.

Adult↗