ABSTRACT
Application of contrast cineventriculography and probe of the left ventricle indicated that there was a relationship between the status of myocardial contractility, its function, some hemodynamic parameters, the severity of regional left ventricular wall contractility impairments and the nature of a hemodynamic response to Valsalva's test. Normal left ventricular contractility determined sinusoidal responses. Decompensated impairments of myocardial contractility gave rise to a square wave. A response represented as a nil ++super-elevation was caused by a moderate impairment of left ventricular contractility and, probably, by the absence of adequate vasoconstriction in the fourth phase of Valsalva's test.
Subject(s)
Cardiomyopathy, Dilated/physiopathology , Coronary Disease/physiopathology , Hemodynamics/physiology , Myocardial Contraction/physiology , Ventricular Function, Left/physiology , Adult , Cardiomyopathy, Dilated/diagnosis , Cardiomyopathy, Dilated/etiology , Coronary Disease/complications , Female , Humans , Male , Middle Aged , Severity of Illness Index , Valsalva ManeuverABSTRACT
Changes in hemodynamics associated with Valsalva's test are responsible for a reduction in myocardial oxygen consumption and a decrease in diastolic coronary perfusion pressure in ischemic patients and subjects free of coronary heart disease. Due to stenosis and occlusion of coronary arteries lowering of perfusion coronary pressure in relevant patients becomes more profound and may induce ischemia in spite of diminished oxygen consumption. The main cause underlying onset of myocardial ischemia in patients with marked lesions of coronary arteries is initially low perfusion pressure and limited coronary reserve.
Subject(s)
Coronary Disease/etiology , Valsalva Maneuver/physiology , Adult , Blood Pressure/physiology , Coronary Circulation/physiology , Coronary Disease/diagnosis , Coronary Disease/physiopathology , Humans , Male , Middle AgedABSTRACT
The binding of propranolol with plasma proteins and erythrocytes after oral administration of 80 mg of anapriline was studied in 12 patients with hypertensive disease. The content of propranolol fraction bound to plasma proteins was on the average 0.84 +/- 0.4. It was shown that propranolol to a considerable degree is captured by erythrocytes. The ratios of the erythrocyte content of propranolol free form to the plasma content were on the average 3.72 +/- 0.92 and 2.70 +/- 1.20, respectively, 2 and 4 hours after anapriline intake. During the assessment of the pharmacological parameters it is recommended to determine the contents of the total and free forms of propranolol in the whole blood rather than in plasma.
Subject(s)
Blood Proteins/drug effects , Erythrocytes/drug effects , Propranolol/blood , Adult , Blood Proteins/chemistry , Blood Proteins/metabolism , Chromatography, High Pressure Liquid , Erythrocytes/chemistry , Erythrocytes/metabolism , Humans , Hypertension/blood , Hypertension/drug therapy , Middle Aged , Propranolol/therapeutic use , Protein Binding/drug effects , Time FactorsABSTRACT
Right ventricular (RV) function was investigated using rheopulmonography at Valsalva's manoeuvre and echocardiography in 36 patients with rheumatic heart disease which were divided into three groups: with RV normal-size chamber and normal thickness of the wall (I), with normal-size RV chamber and myocardial hypertrophy (II), with RV dilatation and hypertrophy. In patients of group I there appeared mitral stenosis of degree I (Gorlin) and insignificant elevation of pressure in the pulmonary artery. Mitral defect was compensated through the mechanism "stress-mobilization" underlying homeometric autoregulation of the heart. As a result, muscular thickness grows without hypertrophy and becomes stronger. In more pronounced narrowing of mitral opening (group II) the second stage of the compensation comes: in latent pulmonary hypertension hypertrophy develops as a prolonged adaptation to greater load. Hypertrophic myocardium is the most resistant to overloading with external pressure. In group III patients with mitral narrowing degree 2 and more distinct pulmonary hypertension one can observe an addition of Frank--Starling mechanism--heterometric type of autoregulation. In spite of its triggering compensation of the defect remains insufficient (circulation deficiency becomes clear-cut in patients of group III).
