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Biomedical subjects

J Bahlmann

Publications and source records attributed to J Bahlmann.

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↗
PubMed1977

Central and peripheral haemodynamic effects of angiotensin.

In 10 normotensive subjects intravenous infusion of angiotensin was followed by a significant increase in the arterial pressure, total peripheral resistance, central venous pressure and by a marked reduction of the intravascular forearm volume and venous distensibility. Forearm circulation time was shortened. The cardiac index, heart rate, forearm vascular resistance and the forearm blood flow did not change significantly.

Adolescent↗
PubMed1976

[Studies on the pituitary-testicular axis in male patients with chronic renal failure with different glomerular filtration rate (author's transl)].

In 32 male patients with chronic renal failure (age 22-60 yrs), of which 17 showed a creatinine clearance below 20 ml/min (group I) and 15 above 20 ml/min (group II), plasma levels of total testosterone (T) and total oestradiol-17beta (E2) were measured before and after stimulation with HCG i.m. LH and FSH were evaluated before and after stimulation with LH-RH i.v. Additionally, testosterone binding capacity (TeBG), free testosterone fraction (%FT) and "absolute" free testosterone (AFT) were determined. In comparison with normal persons T was clearly reduced before and after HCG in group I, whereas in group II it was reduced only after HCG. E2 showed normal basal values in both groups, but in group I it was decreased after HCG. Except for LH values after stimulation in group II, both groups showed increased LH and FSH levels before and after LH-RH in comparison with controls. TeBG and %FT did not show any changes in either group, whereas AFT was reduced in both of them. Comparing the results of group II and I we found in the latter decreased values for T before and after HCG and for E2 after HCG as well as decreased values for AFT, whereas LH and FSH before and after LH-RH were increased. There existed no significant correlation between any of the parameters T, AFT and E2 on the one hand and LH and FSH on the other hand. Significant correlations are found between creatinine clearance and T, AFT, LH and FSH. The results indicate a primary defect of the testis which gradually depends on the degree of renal insufficiency, but with well working feed-back mechanism. The possibility of an additional central regulation defect in the sense of a relative autonomy of the hypophyseal gonadotropin secretion is discussed.

Adult↗
PubMed1976

The effect of intravenous angiotensin II on the peripheral circulation with particular reference to its bearing on general haemodynamics.

1. Central and peripheral haemodynamic effects of intravenous infusion of angiotensin II have been investigated in ten normotensive subjects. Angiotensin II was given at the rate of 0-12-5-0 microng/min. 2. The pressor response to angiotensin II was accompanied by a significant increase in the total peripheral resistance, central venous pressure and by a marked reduction of the intravascular forearm volume and venous distensibility. Forearm circulation time was shortened. 3. Cardiac index, heart rate, forearm vascular resistance and the forearm blood flow did not change significantly in the whole group but in the individual subjects some of the variables changed markedly in either direction. 4. Direct action of angiotensin II on the vessels and its central and peripheral sympathomimetic aciton as well as the role of the baroreflex as responsible causes for haemodynamic changes after angiotensin II are discussed.

Adolescent↗
PubMed1976

Clinical and haemodynamic study of a new vasodilator drug L6150 (3-[bis-(2-hydroxyethyl)amino]-6-hydrazinopyridazine) in man.

1. L6150 is a highly effective vasodilator which produces an acute reduction of blood pressure when administered intravenously. 2. This is due entirely to a decrease in total peripheral vascular resistance. 3. On oral administration it can effectively lower blood pressure in mild hypertension and is effective in combination with other hypotensive agents with different mechanisms of action.

Administration, Oral↗
PubMed1976

[Rapidly progressive glomerulonephritis in a child. Clinical and histological observation over 3 1/2 years (author's transl)].

At the age of 5 years and 10 months a boy suffered from rapidly progressive glomerulonephritis. After 14 days of treatment with peritoneal dialysis and chlorambucil the acute renal failure was overcome and the kidneys started to function again. 3 1/2 years later 2/3 of normal values for glomerular filtration had been regained, though proteinuria is still 2,8 g/day. Histologically mainly extracapillary proliferations and a partially necrotizing glomerulonephritis were seen in the beginning. 1 1/4 years later sklerosed glomerula predominated (80%) over almost normal glomerula with only minor proliferations. The prognosis remains doubtful in spite of the benign course in the beginning.

Acute Disease↗
PubMed1975

[Obliterative intimofibrosis of the renal arteries under the influence of hemodialysis in patients with chronic renal insufficiency (author's transl)].

Histologic and morphologic methods were employed to study the influence of chronic hemodialysis on kidney vessels in chronic renal insufficiency. Arteries of contracted kidneys from patients with and without hemodialysis treatment were investigated. The dialysis group was made up of 33 patients, 28 having undergone bilateral nephrectomy and 5 having died. The control group consisted of 21 patients with chronic renal insufficiency, who died in uremic coma without prior hemodialysis. A statistical evaluation was done by comparing measurements from corresponding arteries in the dialysis- and control groups. The correlation pattern from a BMD 03D-program, in which each group was separately assessed for the possible influence of various clinical findings, was determined. Clinical influences taken into account included the course of the kidney disease, grade of renal insufficiency, duration and degree of hypertension as affecting the renal arteries. The statistical results showed that hemodialysis treatment, even taking clinical data into consideration, influenced the development of intimal fibrosis in the arteries of contracted kidneys in an increasing positive manner. Decreased perfusion of the kidneys during hemodialysis suggested as a possible cause. The examination of early lesions in renal arteries following short-term dialysis treatment lends support to this possibility. Here edema and proliferation of the intimal cells in the arteries, similar to that in vessels having a reduced blood flow, is observed.

Adolescent↗
PubMed1975

[Forearm and digital blood flow after arteriovenous anastomosis (author's transl)].

Forearm and digital blood flow were measured by venous occlusion plethysmography in 7 patients with terminal renal failure before and 8 days after surgically created arterio-venous end-to-end fistula similar to the method of Brescia and Cimino. The forearm blood flow rose significantly from 3.30 +/- 1.75 to 6.98 +/- 4.74 ml/min - 100 ml. Total forearm blood flow increased from 32.9 +/- 16.8 ml/min to 69.8 +/- 45.8 ml/min. Digital blood flow was not significantly altered. The relatively low fistula flow was due to the early postoperative measurement since it increased later.

Adult↗