Oxygen free radical regulation of rat splanchnic blood flow.

Abstract

The role of oxygen-derived free radicals on splanchnic prostaglandin (PGI2) synthesis and superior mesenteric artery (SMA) blood flow was examined during acute hemorrhage. Sprague-Dawley rats were hemorrhaged to 30 mm Hg for 5, 30, or 45 minutes without (SK5, SK30, and SK45) or with (SK5 + R, SK30 + R, and SK45 + R) blood reperfusion. The SK30 + R and SK45 + R groups were treated with or without superoxide dismutase (10,000 units/kg intravenously). In vivo SMA blood flow was measured continuously for 100 minutes by a transonic flow probe, or in other groups the in vitro-perfused SMA and its end-organ intestine (SV+SI) were assayed for release of PGI2 by radioimmunoassay after 15 and 30 minutes of perfusion. Acute hemorrhage at all time periods increased SV+SI PGI2 release twofold to threefold compared with sham animals (p less than 0.01), which was abolished after blood reperfusion. SMA blood flow was decreased by 79.6% +/- 3.3% and 88.2% +/- 1.4% in the SK30 + R and SK45 + R groups compared with the sham animals (p less than 0.01). Superoxide dismutase treatment restored both SV+SI release of PGI2 after SK and SMA blood flow to control levels. Oxygen-derived free radicals locally produced during SK30 + R and SK45 + R inhibited splanchnic PGI2 synthesis, which contributed to decreased splanchnic blood flow.