Subject(s)
Heart Failure/diagnosis , Adolescent , Adult , Female , Heart/physiopathology , Heart Failure/physiopathology , Hemodynamics , Humans , Male , Middle AgedSubject(s)
Cardiomyopathies/physiopathology , Hemodynamics , Adolescent , Adult , Cardiomyopathies/diagnosis , Female , Humans , Male , Middle AgedSubject(s)
Cardiomyopathies/diagnosis , Electrocardiography , Adolescent , Adult , Female , Humans , Male , Middle AgedSubject(s)
Heart Failure/pathology , Muscles/ultrastructure , Adult , Aged , Female , Humans , Male , Microscopy, Electron , Middle AgedSubject(s)
Heart Failure/pathology , Muscles/ultrastructure , Adult , Female , Humans , Male , Microscopy, Electron , Middle Aged , Myofibrils/ultrastructure , Shoulder/ultrastructureSubject(s)
Indomethacin/pharmacology , Prostaglandins E/pharmacology , Pulmonary Circulation/drug effects , Adult , Female , Humans , Male , Middle AgedABSTRACT
The effects of prostaglandin E1 on pulmonary circulation and left ventricular performance have been studied in 20 patients with mitral valve disease and pulmonary hypertension. Prostaglandin E1 was administered intravenously over a period of 30 minutes. The dose used was 0.01 microgram/kg per min during the first 15 minutes and 0.02 microgram/kg per min subsequently. The first dose led only to an insignificant fall in left ventricular end-diastolic pressure. Infusion of prostaglandin E1 in a dose of 0.02 microgram/kg per min resulted in a significant fall in the pulmonary arterial pressure (P less than 0.001), total pulmonary resistance (P less than 0.001), left ventricular end-diastolic pressure (P less than 0.001), and aortic pressure (P less than 0.01), and an increase in the pulmonary blood volume (P less than 0.01), cardiac index (P less than 0.01), and heart rate (P less than 0.05). No significant differences were noted in stroke volume index or left ventricular dP/dt at 50 mmHg after prostaglandin E1. These results indicate that exogenously administered prostaglandin E1 causes active vasodilatation of the pulmonary vascular bed and has no inotropic action on the cardiac muscle.
Subject(s)
Hypertension, Pulmonary/drug therapy , Prostaglandins E/therapeutic use , Adult , Female , Heart Ventricles/drug effects , Humans , Male , Middle Aged , Mitral Valve Insufficiency/complications , Mitral Valve Stenosis/complications , Prostaglandins E/administration & dosage , Prostaglandins E/pharmacology , Pulmonary Circulation/drug effectsSubject(s)
Cardiomegaly/etiology , Cardiomyopathies/physiopathology , Heart Ventricles/physiopathology , Adolescent , Adult , Cardiac Volume , Female , Hemodynamics , Humans , Male , Middle AgedSubject(s)
Heart Septum , Myocardial Infarction/complications , Follow-Up Studies , Humans , Male , Middle Aged , Myocardial Infarction/mortality , Rupture , Time FactorsSubject(s)
Cardiomyopathies/pathology , Liver/pathology , Adolescent , Adult , Female , Heart Failure/pathology , Hepatitis/pathology , Humans , Male , Middle AgedSubject(s)
Glucagon/pharmacology , Hypertension, Pulmonary/physiopathology , Pulmonary Circulation/drug effects , Adolescent , Adult , Chronic Disease , Female , Humans , Male , Middle AgedABSTRACT
Investigations of the hemodynamics of pulmonary circulation, right and left heart venticle and ventilatory function of the lungs were carried out in a group of 12 patients with primary pulmonary hypertension. The results were discussed in the light of data obtained in a group of 16 patients with chronic cor pulmonale syndrome and 16 healthy subjects. It was found that patients with primary pulmonary hypertension show a markedly raised pressure in the pulmonary artery mean pressure x = 60.3 +/- 24.2 mm Hg, in the right ventricle (systolic pressure x = 90.6 +/- 27.9 mm Hg, end-diastolic pressure x = 11.7 +/- 4.3 mm Hg), very high total pulmonary vascular resistance (x = 1571 +/- dynes. sec. cm-5) and increased work of right ventricle (x = 2.3 +/- 1.5 kgm/min/m2). In patients with chronic cor pulmonale syndrome the load on the right ventricle was much lower. The indices determining left ventricle function as a pump indicated that this function was impaired, with lower cardiac index (x = 2.1 +/- 0.8 1/min/m2), stroke volume (x = 41.7 +/- 17.2 ml) and left ventricular work (x = 2.7 +/- 1.1 kgm/min/m2). These changes might, however, be due also to impaired blood flow into the left ventricle. In contrast to patients with chronic cor pulmonale syndrome, the indices of ventilatory function of the lungs were normal or only slightly decreased. No significant correlations were observed between hemodynamic indices of pulmonary circulation and right ventricle and the parameters of the ventilatory function of the lungs.
