Reperfusion Inhibits Elevated Splanchnic Prostanoid Production After Hemorrhagic Shock

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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 < 0.05). Reperfusion of shed blood abolished the increased in 6-keto-PGF1.alpha. found in the shock group (p < 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.