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Biomedical subjects

L Speroff

Publications and source records attributed to L Speroff.

At least 91 records · Page 5Linked to original sources
PubMed1976

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Cardiac prostaglandin release was studied in closed-chest dogs during acute coronary occlusion. Aortic and coronary sinus blood was obtained before, and at intervals after, balloon occlusion of the left anterior descending artery in seven dogs. Samples were assayed for prostaglandins F, E, and A by randioimmunoassay. All dogs demonstrated prostaglandin F release, Mean +/- SE postocclusion aortic levels were 0.26 +/- 0.01 ng/ml; coronary sinus levels were 0.67 +/- 0.01 ng/ml (P less than 0.001). In six dogs, prostaglandin E also was released. Mean postocclusion aortic levels were 0.24 +/- 0.01 ng/ml; coronary sinus, 0.44 +/- 0.01 ng/ml (P less than 0.001). There was no release of prostaglandin A. To examine the site of prostaglandin release, simultaneous samples from the aorta, the coronary sinus, and the great cardiac vein were obtained before and after left circumflex artery occlusion in six additional studies. The great cardiac vein drained effluent from nonischemic myocardium, whereas the coronary sinus drainage included blood from both ischemic and nonischemic zones. All six dogs demonstrated prostaglandin F release from the ischemic region. Mean postocclusion aortic prostaglandin F was 0.32 +/- 0.01 ng/ml. Coronary sinus prostaglandin F was 1.69 +/- 0.03 ng/ml (P less than 0.001), whereas the great cardiac vein level remained at 0.34 +/- 0.01 ng/ml (P greater than 0.05). Prostaglandin E was released from both ischemic and nonischemic regions. Mean aortic prostaglandin E was 0.21 +/- 0.01 ng/ml; great cardiac vein, 0.55 +/- 0.02 ng/ml (P less than 0.001); and coronary sinus, 1.07 +/- 0.04 ng/ml (P less than 0.001). These results have led us to conclude that the different local availability of prostaglandins E and F may influence the cardiac response to ischemia.

Animals↗
PubMed1976

The effect of aspirin and indomethacin on the TRH response in man.

A double-blind study of the effect of two inhibitors of prostaglandin synthesis on the TRH stimulation of serum TSH and prolactin was carried out in 35 normal males. The subjects were evaluated before and after the administration of indomethacin or aspirin for one week. Both indomethacin and aspirin lowered plasma prostaglandin E and F levels significantly. Indomethacin treatment had no effect on the serum TSH or prolactin response to 100 mug TRH or the serum T3 and T4 levels. In contrast, aspirin treatment significantly decreased the serum TSH response to TRH and significantly lowered mean total serum T3 (RIA) and T4 (D). There was no effect on the prolactin response to TRH. These findings suggest that aspirin blocks TRH responsiveness by a mechanism other than the inhibition of prostaglandin synthesis, probably by its previously demonstrated effect on increasing the fraction of unbound thyroid hormone.

Adolescent↗
PubMed1976

Uterine artery blood flow studies in the pregnant monkey.

Studies were performed in anesthetized monkeys in the third trimester of pregnancy, with continuous monitoring of maternal blood pressure and uterine artery blood flow by electromagnetic flow probe and with measurement of prostaglandin levels in uterine vein samples. Acute elevation of the systemic blood pressure by intravenous infusion of angiotensin II was associated with increased uterine artery blood flow and an increase in the levels of prostaglandin E measured in the uterine vein. An increase in PGE levels was also observed following the discontinuation of the angiotensin II infusion, when blood pressure and uterine artery blood flow returned to baseline levels. Intravenous administration of indomethacin was associated with a slight rise in maternal blood pressure. The changes in uterine artery blood flow following indomethacin treatment were variable, perhaps reflecting the stresses of surgery and anesthesia. In single experiments, intravenous diazoxide produced a profound hypotension, and intravenous furosemide induced a prompt and marked diuresis, associated with a very marked fall in uterine artery blood flow.

Angiotensin II↗
PubMed1975

An autoregulatory role for prostaglandins in placental hemodynamics: their possible influence on blood pressure in pregnancy.

This review asserts that prostaglandins of the E family play a vital regulatory role in uteroplacental blood flow. This role appears to be similar to activity within other organs, especially the kidney, in a process referred to as autoregulation of blood flow. This mechanism may serve as a system for ehmodynamic homeostasis in pregnancy. Moreover, hypertension in pregnancy (toxemia) may be due to a specific or generalized abnormality in this system.

Angiotensin II↗
PubMed1973

The effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations in normal humans.

It has been suggested that prostaglandins may be involved in the control of sodium homeostasis. Prostaglandin A and prostaglandin E have been shown to increase renal blood flow and urinary sodium excretion and prostaglandin A has been shown to stimulate aldosterone release. The purpose of this study was to determine the effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations. SEVEN NORMAL HUMAN VOLUNTEERS WERE PLACED ON THREE SODIUM INTAKE DIETS: (a) ad lib. sodium intake, (b) high sodium intake, and (c) low sodium intake. Plasma prostaglandin A, E, and F concentrations were measured by radioimmunoassay. Mean prostaglandin A levels on the ad lib. diet were 1.60 ng/ml. Prostaglandin A levels decreased 49% to 0.82 ng/ml on the high sodium intake and increased 34% to 2.14 ng/ml on the low sodium intake. Prostaglandin A levels increased 161% on the low sodium diet in comparison with levels on the high sodium diet. Plasma prostaglandin E and F concentrations did not change significantly during variation in sodium intake. These results show that dietary sodium content markedly effects plasma prostaglandin A levels and that prostaglandins may play a role in the physiologic mechanism of sodium homeostasis.

Adult↗