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Biomedical subjects

B Ostádal

Publications and source records attributed to B Ostádal.

At least 73 records · Page 4Linked to original sources
PubMed1985

Thyroxine-induced cardiomegaly in rats of different age.

In the present study the effect of thyroxine treatment on the development of cardiomegaly was compared in young (10-day-old) and adult (12-week-old) rats. L-thyroxine was administered subcutaneously in a dose of 1 mg per kg b.w. for 5 days. In young thyroxine-treated rats the heart weight increased by 79% in comparison with the control rats. The number of blood capillaries and muscle fibres per mm2 remained unchanged. The concentration of hydroxyproline was even lower than in control animals. The number of 3H-thymidine-labelled muscle cell nuclei was significantly higher both in the left and right ventricles of thyroxine treated rats. The density of capillaries and muscle fibres was significantly lower in adult rats than in the group of young animals. In adult thyroxine-treated animals the heart weight was higher by 36%, the number of capillaries and muscle fibres as well as the concentration of hydroxyproline was unchanged. Thyroxine induced significant increase in the number of DNA synthesizing nuclei of muscle cells in the left ventricle while the change in the right ventricular myocardium was not statistically significant. The present data indicate that a hyperplastic response of cardiac muscle cells to thyroxine occurs in both ventricles of young rats and also in the left ventricle of adult animals.

Aging↗
PubMed1985

A cytophotometric and karyometric study of the cardiac muscle cells of young rats exposed to intermittent high altitude hypoxia.

Thirty-day-old rats were exposed to intermittent high altitude in barochamber (7000 m, 4 h per day, 4 exposures) and number of mono- and binucleated myocytes as well as DNA content per nucleus were determined in the right ventricular myocardium. The data indicate enhancement of mitotic division of mono- and binuclear diploid cells in hypoxic animals. Simultaneously, an increase in mononuclear and binuclear tetraploid cells occurred; the latter is probably due to DNA synthesis not followed by mitosis of some binuclear diploid cells.

Altitude↗
PubMed1985

Response of the rat cardiovascular system to a moderate altitude in connection with endurance training.

The authors investigated whether an altitude of 1,350 m would affect the rat cardiovascular system in the same way as genuine altitude hypoxia and the way it would take effect when combined with endurance training in the form of swimming It was found that 8 weeks spent at this altitude led to an increase in absolute and relative heart weight, to right ventricular hypertrophy, and to increased resistance of the myocardium to acute anoxia. Physical training at a moderate altitude resulted in an increase in the relative weight of the musculature of both the right and the left ventricle and of the septum. Unlike low altitude training, however, growth of the two compartments of the heart was proportional. The resistance of the myocardium of trained animals against anoxia was the same, irrespective of whether they trained at a low or a high altitude. The results show that even a moderate altitude is not a matter of indifference for the rat organism, but that it leads to characteristic manifestations of altitude hypoxia in the cardiovascular system.

Altitude↗
PubMed1984

Comparison of cardiopulmonary responses of male and female rats to intermittent high altitude hypoxia.

Intermittent high altitude hypoxia (8 hours a day, 5 days a week, stepwise up to the altitude of 7000 m, total number of exposures 24) induced in male and female rats, chronic pulmonary hypertension and right ventricular hypertrophy. No significant sex differences were found in both these parameters. A significant sex difference was demonstrated in the resistance of the cardiac muscle to acute anoxia in vitro: the myocardium of control female rats proved to be significantly more resistant to oxygen deficiency. Intermittent altitude hypoxia resulted in significantly enhanced resistance in both sexes, yet the sex difference was maintained. Sex differences were further observed in the growth response of experimental animals to the acclimatization process. Whereas the body weight of male rats exposed to intermittent altitude hypoxia was significantly lower, hypoxic females had body weights comparable to those of control animals.

Altitude↗
PubMed1984

Isoproterenol--induced damage to the liver of chick embryos.

Isoproterenol has been shown to cause severe liver damage in chick embryos. Most severe lesions were observed in embryos 10 to 12 days old, which showed extensive parenchymal necrosis. In older embryos, the lesions were mostly represented by areas of fatty degeneration. In 6 to 9-day-old embryos, the changes were indistinct (slight). The necrotic foci underwent slow resorption with disperse dystrophic calcification. Surviving hepatocytes around the damaged areas revealed some regenerative phenomena. The possible cause of marked hepatotoxicity of isoproterenol for chick embryos is discussed.

Animals↗
PubMed1983

Intermittent high altitude hypoxia - induced structural changes in the pulmonary myocardium in young mice.

Seven-day-old mice, strain H, were exposed to intermittent high altitude hypoxia (IHA) in a barochamber (7,000 m, 4 h/day, 5 days a week); a total number of exposures was 10. It has been shown that the layer of cardiac musculature in the adventitia of the pulmonary veins, the so-called pulmonary myocardium, reacts to IHA hypoxia by enlargement even sooner than the right ventricular myocardium. The average thickness of the layer of pulmonary myocardium was significantly greater in animals exposed to IHA hypoxia as compared with the controls. Furthermore, IHA hypoxia induces the extension of the pulmonary myocardium to the periphery of the pulmonary venous bed. Ultrastructural investigation of the pulmonary myocardium in hypoxic animals revealed the presence of unoriented myofilaments in the peripheral myofibril-free sarcoplasma, increase in the number of ribosomes and appearance of profiles of granular endoplasmic reticulum. Our data provide quantitative support for the hypothesis that it is not only the contraction of pulmonary arteries, but also venoconstriction which contribute to the hypoxic pressure response in mice.

Altitude↗
PubMed1983

Effect of beta adrenergic blocking agents on erythropoiesis in rats.

The purpose of the present study was to analyze the effect of two different beta blocking agents, metipranolol (Trimepranol) and dl-propranolol (Inderal), upon erythropoietin production, erythropoietin responsive cell compartment and erythrocyte production. The effect on erythropoietin production: in rats metipranolol or dl-propranolol was injected daily in a single dose of 10 mg/kg b.wt. On the 5th day, the rats were exposed to an atmospheric pressure of 353.7 torr (47.1 kPa, 6000 m) to stimulate erythropoietin production. The onset of hypoxic exposure was started 1, 4, 12 or 24 hr after the last injection of beta blocking drugs. After the termination of hypoxia, erythropoietin plasma levels were determined in polycythemic mice. The rats treated with metipranolol 1 and 4 hr before hypoxia produced significantly less erythropoietin in response to hypoxia than saline-treated control animals. The effect on erythropoietin responsive cell compartment: polycythemic mice were treated with metipranolol or dl-propranolol in doses of 10 to 40 mg/kg b.wt. and with an erythropoietin standard. Radioiron incorporation into red blood cells in control mice and in mice pretreated with beta blocking agents was not significantly different. The effect on erythrocyte production: in rats treated daily with metipranolol in a single dose of 10 mg/kg b.wt., for a period of 10 days, the rate of erythropoiesis measured by the incorporation of 59Fe into red blood cells was decreased, dl-propranolol (10 mg/kg b.wt.) did not reduce the rate of erythropoiesis. Our results demonstrate that the changes in erythropoiesis after administration of metipranolol may be caused by reduction of erythropoietin production with a consequent reduction of the erythrocyte production rate.

Adrenergic beta-Antagonists↗
PubMed1981

Effect of verapamil on pulmonary hypertension and right ventricular hypertrophy induced in rats by intermittent high altitude hypoxia.

Adult male Wistar rats were used for studying the effect of Ca2+ antagonist verapamil on pulmonary hypertension, right ventricular hypertrophy and the medial thickness of pulmonary arterioles, induced by intermittent high altitude (IHA) hypoxia. This was simulated in a hypobaric chamber (7,000, 8 h daily, 5 days a week, 24 exposures). Verapamil was injected subcutaneously in a single dose of 8 mg/kg before each IHA exposure. Administration of verapamil to IHA-exposed animals significantly reduced right ventricular systolic pressure, right ventricular hypertrophy and pulmonary arteriolar medial thickness. Our results support the hypothesis that the transmembrane influx of extracellular calcium is an important component of the mechanisms of hypoxic pulmonary vasoconstriction.

Altitude Sickness↗
PubMed1981

Changes of the right and left ventricles in rats exposed to intermittent high altitude hypoxia.

Significant structural, functional and metabolic differences between the right and left ventricles are present already in control animals. Intermittent high altitude (IHA) hypoxia (4 hr daily, 5 days a week, stepwise up to an altitude of 7000 m in a hypobaric chamber) induced in adult rats pulmonary hypertension and right ventricular hypertrophy; prolonged hypoxia also increased the relative left ventricular mass. Both chambers show proportionate increase in concentration of myofibrilar and collagenous proteins; the right-left difference, characteristic of animals living in normoxic environment, remains unaffected. The relative right and left ventricular bloodflow in hypoxic animals increases and so doses also the activity of glycolytic enzymes in both ventricles. Necrotic lesions, localized predominantly in the right ventricle, develop only at the beginning of adaptation to IHA. Parallel changes in the structure and enzyme activity of the myosine molecule in both ventricles can be observed. Administration of beta-blocking agent (Trimepranol, Spofa) significantly decreased pulmonary hypertension and right ventricular hypertrophy; the relative left ventricular mass normalized. Furthermore, Trimepranol significantly reduced necrotic changes in the right ventricle after a dose of 10 mg/kg, in the left ventricle - after 1 mg/kg. These results support the hypothesis of a possible impairment of left ventricular function in the presence of a primary right ventricular disturbance.

Altitude Sickness↗
PubMed1980

The in vivo uptake of [3H]isoprenaline by the chick embryonic heart and liver.

Seven-day-old embryos received 3.7 x 10(5) Bq (10 muCi) of [3H]isoprenaline (IPRO) hydrochloride intraamnially. The capacity of myocardial and liver tissue for taking up administered catecholamine increased rapidly during the first 10 min after administration. The peak concentration (disintegrations per minute per milligram) in the heart, however, was significantly lower as compared with the liver. Thereafter the uptake in both organs markedly decreased and reached its lowest values between 15 and 30 min. From then on, the concentration of the tritium-labelled compound increased again and 6 h after administration it attained the second peak in both organs. This value was more than five times higher in the liver as compared with the myocardium. Radiometric evaluation of chromatograms from myocardial and liver extracts has revealed that IPRO is rapidly metabolized to 3-O-methyl IPRO. The proportion of this fraction in both organs represents approximately 40% of total radioactivity as early as 5 min after administration. The time course of IPRO uptake indicates that the following factors may participate in the development of cardiac and hepatic lesions: (a) IPRO immediately after administration, and (b) subsequently its toxic metabolites.

Animals↗
PubMed1980

Intermittent high altitude hypoxia.

The effect of intermittent high altitude (IHA) hypoxia on the myocardium and lesser circulation was investigated in adult male Wistar rats. IHA can induce intermittent pulmonary hypertension and right ventricular hypertrophy in a relatively short time. Even marked pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular changes can be normalized when rats are removed from the hypoxic atmosphere. At the beginning of the exposure to IHA acute myocardial necrotic changes were found; prolongation of IHA did not lead to further acute lesions. Experimentally induced CO polycythemia leads to mild pulmonary hypertension; IHA-induced pulmonary hypertension may, thus, be partly due to polycythemia. Beta blocking agents are able to decrease chronic hypoxic pulmonary hypertension, hypertensive changes in the pulmonary circulation, the degree of right ventricular hypertrophy, and necrotic myocardial changes.

Altitude Sickness↗
PubMed1980

Effect of intermittent high altitude hypoxia on the structure and enzymatic activity of cardiac myosin.

The time course of structural and enzymatic changes in cardiac myosin was studied in the right and left ventricle of rats exposed to intermittent high altitude (IHA) hypoxia. In the controls, ATPase activity and myosin structure in both ventricles was the same. After the third exposure to simulated high altitude (2 600 m), myosin enzymatic activity rose significantly in the left ventricle and a significant right-left difference appeared. In the next phase of adaptation (11 exposures, 6 000 m), myosin ATPase activity fell in both ventricles and the right-left difference disappeared. After the 16th exposure (7 000 m), enzymatic activity increased again in both ventricles and attained control values. IHA also produced significant structural changes in cardiac myosin, particularly in the rigaht ventricle. The changes were characterized by the formation of myosin aggregates with significantly lower ATPase activity that the myosin monomer. The time course and localization of structural and enzymatic changes in cardiac myosin corresponded to the morphological damage to the heart fibres.

Adaptation, Physiological↗