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Biomedical subjects

J Brod

Publications and source records attributed to J Brod.

At least 37 records · Page 2Linked to original sources
PubMed1980

[The effect of combined alpha and beta blockade with labetalol on the haemodynamics of stress reaction in hypertensives (author's transl)].

The haemodynamic reaction to an acute emotional stress was tested in nine patients with essential and eleven with renal hypertension after an intravenous bolus of labetalol (0.6--1.6 mg/kg body-weight). Labetalol reduced the arteriolar tone at rest. The emotional blood pressure rise was maintained, but started from a lower level due to labetalol and under stress only rose to the pre-labetalol level. The diastolic pressure rose significantly less compared with control values, while systolic and mean blood pressure responses were not uniform. The usual emotional rise in heart rate and cardiac output was clearly diminished by labetalol. Total peripheral vascular resistance, which had been significantly reduced by labetalol, remained unchanged under acute emotional stress. In contrast to untreated hypertensives, venous distensibility and regional blood volume in the lower arm rose significantly on stress while on labetalol medication. Lower arm vascular resistance, which had also been reduced by labetalol, remained uninfluenced by stress: as a result, emotional hyperaemia was much less.

Adult↗
PubMed1980

[Pathogenesis of renal hypertension (author's transl)].

99 patients with a chronic renal disease (glomerulonephritis, pyelonephritis, polycystic kidneys) with a GFR reduced to 2/3 normal and without anaemia were subjected to detailed haemodynamic investigation. The earliest haemodynamic abnormality was found even before the blood pressure became elevated. This consisted in a rise of the cardiac output. Ist most likely cause was an increase in the circulating blood volume. As the arteriolar and capacitance vessels adjusted to it, the blood pressure remained unchanged and the central venous pressure slightly decreased. Blood pressure rises, when this vascular adjustment subsides. At this moment the raised blood volume will drop to normal. These changes do not correlate with the minor fluctuations of the PRA which obviously are not responsible for the subsidance of the vascular adjustment and for the rise of blood pressure.

Blood Pressure↗
PubMed1980

Effect of the angiotensin antagonist saralasin on hemodynamics in hypertensive non-uraemic chronic renal disease.

The effect of an intravenous infusion of saralasin in a rising dosage on blood pressure, central haemodynamics, forearm blood flow and venous distensibility was tested in 11 subjects with chronic non-uraemic renal disease. Only 1 subject had an elevated resting plasma renin activity, and in him saralasin produced a drop in systolic and diastolic blood pressures due to a decrease of the total peripheral vascular resistance whereas the plasma renin activity markedly rose. Among the remaining 10 subjects, whose plasma renin activity was within the normotensive range, blood pressure rose transiently in 3, with the lowest dose of aralasin, due to an increase in the total peripheral vascular resistance. Both these parameters returned to the control level when continuing the infusion and increasing its dosage. Excluding this initial period from the analysis, no relevant change, even with a more than tenfold increase in the saralasin dosage and a duration of the infusion of 1 h, was found in the following: blood pressure, cardiac and stroke index, heart rate, total peripheral vascular resistance, central and peripheral venous pressures, forearm blood flow and vascular resistance, forearm blood volume and venous distensibility. The haemodynamic response to the Valsalva manoeuvre remained unaffected by saralasin. It is concluded that angiotensin plays an active role in changing the haemodynamics and in elevating the blood pressure in subjects with chronic non-uraemic renal disease only in those cases where plasma renin activity is raised.

Adult↗
PubMed1979

Effect of an alpha- and beta-adrenoceptor-blocking agent (labetalol) on haemodynamics in hypertension.

1 The effect of an intravenous bolus of labetalol (0.6--1.6 mg/kg body weight) on central and peripheral haemodynamics was studied in nine subjects with essential hypertension and in eleven subjects with chronic renal disease and hypertension. 2 The BP reduction amounting to 20/13 mmHg was entirely due to the lowering of the total peripheral vascular resistance. This also included the vascular resistance in the muscles. 3 This peripheral vasodilatation was not counteracted by a reflex increase of the cardiac output. 4 The reflex tachycardia and overshoot of BP in Valsalva's manoeuvre were largely abolished. 5 Central and peripheral venous BPs, vascular volume of the forearm and venous distensibility did not show any significant change after treatment with labetalol. 6 In spite of the lowering of the vascular resistance of the forearm by labetalol, forearm blood flow was not significantly affected due to the parallel decrease in the perfusion pressure. 7 Plasma renin activity fell after labetalol in all instances.

Adult↗
PubMed1978

Effect of diazoxide on capacitance vessels.

Haemodynamic changes after an i.v. bolus of diazoxide 300 mg were studied in 11 hypertensive subjects. A hypotensive effect due to a fall in total peripheral vascular resistance was found in all of them, but changes in the peripheral circulation were less regular. A uniform change in forearm blood volume, blood flow, vascular resistance and venous distensibility was not found after diazoxide. This is interpreted as being due to a reflex increase in sympathetic activity, which counteracts the direct vasodilator action of the drug.

Adult↗