Rh. Turnage et al., SPLANCHNIC PGI(2) RELEASE AND NO-REFLOW FOLLOWING INTESTINAL REPERFUSION, The Journal of surgical research, 58(6), 1995, pp. 558-564
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.