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Biomedical subjects

M D Lifschitz

Publications and source records attributed to M D Lifschitz.

At least 55 records · Page 3Linked to original sources
PubMed1978

Effect of saralasin in hypertensive patients on chronic hemodialysis.

Hypertension in patients on chronic hemodialysis is thought to be largely of two types--volume dependent or renin dependent. If renin-dependent hypertension is mediated by angiotensin II, then angiotensin II antagonism should lower blood pressure. To test this hypothesis, the angiotensin II antagonist saralasin was given to 15 hypertensive patients on chronic hemodialysis. Patients were separated into two groups by their blood pressure response. In responders blood pressure was 191/112 mm Hg and fell to 147/85 during saralasin administration (P less than 0.01). In contrast, nonresponders had blood pressures of 190/111 mm Hg before and 188/110 during saralasin administration. Five responders subsequently ahd nephrectomies with normalization of their blood pressures. Plasma renin activity averaged 70 ng/ml . 3 h of angiotensin I in responders and increased to 110 after saralasin (P less than 0.05), while nonresponders had values of 21 before and after saralasin. These results offer strong support for the hypothesis that renin-dependent hypertension is an important mechanism in certain patients on chronic hemodialysis and that such patients will respond to angiotensin II antagonism.

Adolescent↗
PubMed1978

Renal failure with posttransplant renin-angiotensin mediated hypertension.

Ten days after receiving a kidney transplant, severe hypertension and renal failure developed in a patient with a previously functioning graft. Although moderate blood pressure control was achieved with dialysis and antihypertensive medications, the graft did not function well. A trial of sar-ala-angiotensin II (an angiotensin II antagonist) was associated with a dramatic fall in blood pressure. Subsequently, the patient's own two kidneys were removed, the blood pressure fell to normal on the operating table, and within days graft function improved. The possible explanation for the changes in graft function, including angiotensin II-mediated changes of glomerular filtration rate, are discussed.

Adult↗
PubMed1977

Spontaneous remission of accelerated (malignant) hypertension in renal infarction.

Malignant hypertension occurred in a young man who also was found to have a left renal infarct and higher renal vein renin levels on the left side. His hypertension was controlled with drugs and subsequently treatment with these medications was gradually discontinued over a period of nine months. He remained normotensive when no longer receiving medication, and another intravenous pyelogram demonstrated a persistent cortical defect in the left kidney.

Adult↗
PubMed1976

Plasma renin activity during exercise in the dog.

Previous workers have suggested that a rise in plasma renin activity (PRA) may mediate some of the hemodynamic changes associated with exercise. To test this hypothesis in nine dogs chronically instrumented for measurement of aortic pressure (catheter) or cardiac output (ascending aorta electromagnetic flow probe) PRA was measured by radioimmunoassay in blood samples drawn before and during running on a level treadmill at 4-8 miles per hour. Exercise caused increases in heart rate from 96 +/- 5 (SE) to 186 +/- 7 beats/min, cardiac output from 2.8 +/- 0.3 to 6.2 +/- 0.6 liters/min, and mean aortic pressure from 115 +/- 5 to 132 +/- 5 mm Hg (P less than 0.01). Mean PRA was 6.6 +/- 0.7 (SE) ng of angiotensin 1/ml per 3 hours before and 7.6 +/- 1.2 ng Ang I during exercise, values that are not different statistically. Propranolol reduced PRA at rest from 8.6 +/- 1.1 to 5.9 +/- 1.1 ng Ang 1 (P less than 0.05), but there was no significant difference between resting and exercise levels, although the increments in heart rate, cardiac output, and mean aortic pressure were reduced. Standing on hindlimbs for 5 minutes did not cause a change in mean aortic pressure or PRA. However, administration of pentolinium reduced mean aortic pressure, and PRA rose from 6.0 +/- 1.1 to 9.8 +/- 1.5 ng Ang I. Exercise, with or without beta-adrenergic blockade, does not cause increased PRA in conscious dogs in which the renin-angiotensin system is normally responsive.

Animals↗
PubMed1976

The natriuretic effect of the organic acid para-aminohippurate.

Infusion of para-aminohippurate (PAH) during renal clearance experiments has been shown to increase urinary sodium excretion (UNAV). In addition, it has recently been suggested that accumulation of PAH and/or related compounds may be responsible for the increased UNAV per nephron in chronic renal failure. Therefore, studies were designed to determine the mechanism for the natriuretic effect of PAH. PAH administration at (0.19 mM per minute) into the dog renal artery led to an average increase in UNAV of 56+/-11 muEq per minute. Mannitol given at this rate (0.19 mM per minute) led to an increase in UNAV of 26+/-10 muEq per minute, which was less than the increase in UNAV with PAH. NA2SO4 given at this (0.19 mEq per minute) or a higher rate (0.60 mEq. per minute) was associated with an increase in UNAV of 53+/-18 and 228+/-38 muEq per minute, respectively. In the PAH and SO4 studies the increase in UPAHV or USO4V was not different from the increase in UNAV. These results suggest that the natriuretic effect of PAH is mainly due to its effect as a nonreabsorbable anion and offer no support for an osmotic effect or a direct effect on active sodium transport.

Aminohippuric Acids↗