1. Reperfusion inhibits elevated splanchnic prostanoid production after hemorrhagic shock.
- Author
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Myers SI, Taylor BJ, and Stanislawska M
- Subjects
- 6-Ketoprostaglandin F1 alpha antagonists & inhibitors, Animals, Dinoprost antagonists & inhibitors, Dinoprostone antagonists & inhibitors, Indomethacin pharmacology, Intestine, Small blood supply, Male, Mesenteric Arteries metabolism, Rats, Rats, Inbred Strains, Shock, Hemorrhagic therapy, Thromboxane B2 antagonists & inhibitors, Time Factors, 6-Ketoprostaglandin F1 alpha biosynthesis, Dinoprost biosynthesis, Dinoprostone biosynthesis, Reperfusion, Shock, Hemorrhagic metabolism, Spleen metabolism, Thromboxane B2 biosynthesis
- Abstract
The effect of reperfusion following hemorrhagic shock on splanchnic prostanoid release was studied. Anesthetized male rats were bled to a mean arterial blood pressure of 30 mmHg for 30 minutes and either killed or treated with shed blood for 60 minutes and then killed. The superior mesenteric arterial bed was cannulated and perfused in vitro with oxygenated Krebs. Collected venous effluent (up to 180 minutes) was analyzed for 6-keto-PGF1 alpha (PGI2 metabolite), PGE2, PGF2 alpha, and thromboxane B2 by radioimmunoassay in shock, shock plus reperfusion, and sham groups. The major prostanoid released was 6-keto-PGF1 alpha and was three times higher in the shock group compared to the sham group (p less than 0.05). Reperfusion of shed blood abolished the increase in 6-keto-PGF1 alpha found in the shock group (p less than 0.05). These data show that the attempt of the rat splanchnic bed to compensate for hemorrhagic shock by increasing release of PGI2 (potent vasodilator) was abolished during reperfusion of blood.
- Published
- 1990
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