SPLANCHNIC PGI(2) RELEASE AND NO-REFLOW FOLLOWING INTESTINAL REPERFUSION

This study examines the hypothesis that reduced splanchnic blood flow during intestinal reperfusion (IR) is associated with impaired release of the vasodilatory prostanoid PGI(2). Sprague-Dawley rats underwent occlusion of the superior mesenteric artery (SMA) for 120 min and repe rfusion for up to 60 min. SMA blood flow was measured by transonic flo w probe and radiolabeled microspheres (Ce-141 and (103)RU). Sham-opera ted animals served as controls (SHAM). Splanchnic eicosanoid release w as quantitated by measuring thromboxane B-2 (TxB(2), stable metabolite of TxA(2)), 6-keto-PGE(1a) (6-keto, stable metabolite of PGI(2)), and PGE(2) within the portal vein (PV) and inferior vena cava (IVC) of an imals sustaining IR and SHAM. SMA flow in IR animals was <10% of basel ine and 27% of SHAM when measured by transonic flow probe (8 +/- 2% an d 29 +/- 3%, IR and SHAM, respectively, P < 0.05). Similar results wer e obtained when intestinal blood flow was measured with microspheres ( 0.33 +/- 0.12 vs 1.34 +/- 0.13 ml/min/g, IR vs SHAM, P < 0.05). The gr eatest change in IR-induced splanchnic eicosanoid release occurred wit h 6-keto. Following ischemia, 6-keto levels in the PV were twice those of SHAM (P < 0.05). Five minutes after reperfusion, PV 6-keto levels were 22 times those of controls (P < 0.05) and 4 times greater than th ose of the IVC (P < 0.05). By 60 min of reperfusion, levels of 6-keto were reduced to those in the IVC. These data support the hypothesis th at splanchnic blood flow is critically reduced by severe IR. Furthermo re, although splanchnic PGI(2) release is increased, its release is ne ither sustained nor adequate to compensate for the reduced blood flow associated with this injury model. (C) 1995 Academic Press, Inc.