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Biomedical subjects

J Ressl

Publications and source records attributed to J Ressl.

At least 19 recordsLinked to original sources
PubMed1982

Echocardiographic assessment of the left ventricle in juvenile hypertension.

We studied with M-mode echocardiography the morphology and function of the left ventricle in a group of 36 juvenile hypertensives with borderline hypertension, whose cuff arm pressure exceeded 150/90 mmHg in at least three separate sessions. The results were compared with those of 23 age-matched normotensives with no evidence of any cardiovascular disease. Left ventricular hypertrophy (i.e. septum and/or posterior wall thicknesses in diastole greater than or equal to 12 mm) was present in 13 subjects of the hypertensive group (36%). Significant increase of interventricular septal thickness together with higher septum/posterior wall ratio and a higher incidence of asymmetric septal hypertrophy were the most characteristic findings in juvenile hypertensives. Of the functional parameters the only observed difference between the two groups was an elevated peak velocity of left ventricular contraction in hypertensives which tended to correlate inversely with the values of septum/posterior wall ratio. Additional comparison of electrocardiographic and echocardiographic detection of left ventricular hypertrophy in young hypertensives revealed a lower sensitivity but a satisfactory specificity of electrocardiography (31 and 87% respectively). The results indicate that besides an elevated systemic arterial pressure, other factors such as increased sympathetic or humoral activity may play a role in the incipient stage of essential hypertension and that isolated septal hypertrophy seems to be an early sign of cardiac involvement.

Adolescent↗
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↗
PubMed1981

Character of mitral valve flow in left atrial tumor.

The pulsed Doppler echocardiography (PDE) was used to evaluate the character of mitral valve flow in a large atrial tumor. The tumor obstructed the mitral orifice during diastole. PDE findings, however, showed normal triphasic diastolic flow within the actual mitral orifice and no changes typical for mitral stenosis. The same turbulence pattern as in mitral stenosis was detected in the left ventricle. In addition, PDE revealed the presence of mild mitral regurgitation in agreement with angiography.

Aged↗
PubMed1980

Pulmonary gas exchange after propranolol in patients with ischaemic heart disease.

Pulmonary gas exchange was evaluated after 10 mg i.v. propranolol in 12 patients 3-6 months after acute myocardial infarction undergoing haemodynamic examination in our outpatient department. None of them exhibited clinical signs of heart failure or obstructive airways disease. Routine spirometric examination was normal in all patients. Propranolol led to a distinct deterioration of LV function and to a fall in left ventricular filling pressure both at rest and during exercise. At rest, the administration of propranolol resulted only in a significant decrease of total ventilation. During exercise, its administration was followed by a significant decrease of the tidal volume, alveolar ventilation and VA/VE index. Arterial CO2 tension and physiological dead space ventilation increased significantly. Arterial oxygen tension decreased after propranolol insignificantly both at rest and during exercise. No patient reported dyspnoea after propranolol; 8 patients reported a decrease or disappearance of effort dyspnoea. None exhibited clinical signs of bronchospasm.

Adult↗
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↗