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Reperfusion Inhibits Elevated Splanchnic Prostanoid Production After Hemorrhagic Shock

The effect of reperfusloa following hemorrtagic shock on splanchnk 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,. (PGI2 metabolite), PGE2, PGF2ay and thromboxane B2 by radiolmmunoassay in shock, shock plus reperfusion, and sham groups. The major prostanoid released was 6-keto-PGF1. and was three times higher In the shock group compared to the sham group (p < 0.05). Reperfusloa of shed blood abolished the Increase in 6-keto-PGF1a found In the shock group (p < 0.05). These data show that the attempt of the rat splanchnk bed to compensate for hemorrhagic shock by increasing release of PGI2 (potent vasodilator) was abolished during reperfusion of blood.