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Biomedical subjects

H S Cheung

Publications and source records attributed to H S Cheung.

121 records · Page 7Linked to original sources
PubMed1976

Effect of substrate concentration on inhibition of prostaglandin synthetase of bull seminal vesicles by anti-inflammatory drugs and fenamic acid analogs.

Although microsomes of bull seminal vesicle synthesize prostaglandins F2alpha, E2 and D2 from arachidonic acid under suitable assay conditions, prostaglandin E2 is the only significant product at either low concentration of arachidonic acid or high concentration of microsomes. Studies of inhibition of prostaglandin synthesis in vitro by anti-inflammatory drugs at both high (1 mM) and low (1 muM) concentrations of arachidonic acid, suggest three distinct mechanisms of inhibition. Benzydamine and flazalone are non-competitive or weakly competitive with arachidonic acid and, at high concentrations of arachidonic acid, they augment sythesis of prostaglandin E2 while inhibiting production of prostaglandins F2alpha and D2. Niflumic acid and the arylacetic acids naproxen and ibuprofen are competitive inhibiting all products equally, but with 100-500-fold greater potency at the low substrate concentration. The fenamic acids, indomethacin, aspirin, and phenylbutazone also inhibit equally all prostaglandin products, but are only 20--50 times more potent at the low substrate concentration. Studies with analogs of the fenamic acids indicate that the diphenylamine protion of their structure is essential for inhibition of prostaglandin synthesis, whereas the o-carboxyl and m-alkul substitutents greatly enhance inhibitory potency.

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PubMedDate not supplied

Vasodilator actions of interleukin-1 in the canine coronary circulation.

The effects of intracoronary ultrapure human Interleukin-1 on the regional distribution of coronary blood flow (radioactive microspheres), contractile function (subendocardial ultrasonic length gauges) and systemic hemodynamics were studied in open-chest, anesthetized dogs (n = 7). Bolus doses of Interleukin-1 (10, 20, and 30 u) administered directly into the left anterior descending coronary artery increased coronary blood flow from 43 to 71, 80 and 87 ml/min, respectively. The increase in blood flow produced by Interleukin-1 was distributed uniformly to the subendocardium, midmyocardium, and subepicardium of the left ventricular free wall without effect on regional function or systemic hemodynamics. Indomethacin (1 mg/kg i.v.) attenuated the increase in blood flow, especially to the subepicardium. Due to the selective diminution of the Interleukin-1-mediated increase in subepicardial blood flow by indomethacin, the subendocardial to subepicardial perfusion ratio was increased by Interleukin-1 in the presence of indomethacin. The present results demonstrate that Interleukin-1 has direct coronary vasodilator actions, a portion of which is mediated by a product of cyclooxygenase metabolism.

Animals↗