PubMed Health⌕ Search

Biomedical subjects

V Pelouch

Publications and source records attributed to V Pelouch.

At least 73 records · Page 4Linked to original sources
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

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↗
PubMed1978

Effect of intermittent high altitude hypoxia on the synthesis of collagenous and non-collagenous proteins of the right and left ventricular myocardium.

The incorporation of 14C-proline into collagenous and non-collagenous proteins of the right and left ventricular myocardium was investigated in rats exposed to intermittent high altitude hypoxia. Experimental results have shown that even in control animals significant differences exist in the concentration and synthesis of individual protein fractions between the right and left ventricular myocardium. Long-term exposure to intermittent high altitude hypoxia induced a significantly increased concentration of collagenous and non-collagenous proteins in both ventricles. The incorporation of 14C-proline was not affected at this period (ie period of stabilised hypertrophy) in either of the fractions studied.

Altitude Sickness↗
PubMed1977

Relative organ blood flow in rats exposed to intermittent high altitude hypoxia.

Circulating blood volume, cardiac output and relative organ perfusion changes were studied, using the Sapirstein method of 86RB tissue uptake, in male 75-day-old rats exposed to intermittent high altitude hypoxia (gradually up to 7000 m, 4 h daily, 5 days a week; the total number of exposures was 24). Intermittent hypobaric exposure caused a significant rise of the erythrocyte volume, whereas the plasma volume remained unchanged. The relative perfusion of the left and particularly of the right ventricular myocardium, as well as of the spleen, liver, lung, small intestine and skeletal muscle, was significantly higher. The cardiac output determined in other experimental animals similarly treated was significantly higher after 24 exposures to the intermittent high altitude hypoxia. We suggest that these changes are triggered by tissue hypoxia and a greater blood flow demand.

Adaptation, Physiological↗
PubMed1977

The development of myocardial changes during intermittent high altitude hypoxia in rats.

The initial phase and the development of myocardial focal necroses were studied in 50 rats adapted successively to intermittent high altitude. The altitude hypoxia was produced in a low pressure chamber (7000 m, five days a week, four hours daily). First-minute myocardial changes detected by histochemical methods were found after 4 exposures at a level of 3000 m and distinct ones after 8 exposures at a level of 4500 m. Histologically, acute focal necroses were found after 11 exposures at a level of 6000 m. Hypoxia and stress are suggested to account for these myocardial focal changes. During further adaptation no further acute focal necroses were observed.

Acid Phosphatase↗
PubMed1976

Structural and enzymatic properties of cardiac myosin in ischaemic and non-ischaemic regions of the rat myocardium.

In rats with ligation of the left coronary artery changes in ATPase activity and structure of cardiac myosin in both ischaemic and non-ischaemic zones of the myocardium were followed. In control animals, ATPase activity and the structure of the myosin molecule in right and left ventricles did not differ. Non-specific factors, such as anaesthesia and thoracotomy, can result in a decrease or an increase in ATPase activity respectively. One hour after ligation of the left coronary artery ATPase activity increased in the right, non-ischaemic myocardium and there was a significant right-to-left difference. Four hours after ligation, ATPase activity in both ventricles significantly decreased and the right-left difference disappeared. Within 48 h, normal values were found only in the non-ischaemic right ventricle. Ligation of the left coronary artery results after 48 h in the formation of structural alterations in cardiac myosin, primarily in the left, ischaemic myocardium. These changes are characterised by the formation of myosin aggregates, which have a significantly lower ATPase activity in comparison with monomeric myosin.

Adenosine Triphosphatases↗