Prostacyclin regulates splanchnic blood flow during early hemorrhage/reperfusion injury.
The effect of oxygen radicals on superior mesenteric artery (SMA) blood flow and splanchnic prostaglandin release was examined during early hemorrhage/reperfusion injury. Sprague-Dawley rats were hemorrhaged to 30 mm Hg for 5, 10, or 15 min without (SK5, SK10, and SK15) or with (SK10+R, and SK15+R) blood reperfusion. The SK15+R group were treated with or without superoxide dismutase (SOD 10 000 units/kg intravenously). In vivo SMA blood flow was measured continuously for 100 min by a transonic flow probe. The in vitro-perfused superior mesenteric artery and end organ intestine (SV+SI) were assayed for release of 6-keto-PGF1 alpha, thromboxane B2 (TXB2) and PGE2 by radioimmunoassay. Acute hemorrhage for 10 and 15 minutes increased SV+SI 6-keto-PGF1 alpha release 2-fold and 10-fold respectively compared to the sham (p < 0.01), which was abolished by blood reperfusion. SMA blood flow was decreased by 4% and 60% in the SK10+R and SK15+R groups respectively compared with the sham (p < 0.01). SOD treatment restored both SV+SI release of 6-keto-PGF1 alpha and SMA blood flow to control levels in the SK10+R and SK15+R groups. Oxygen-derived free radicals produced within 15 min of acute hemorrhage/reperfusion injury inhibited splanchnic PGI2 synthesis, which contributed to decreased splanchnic blood flow.
Hernandez
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R
Department of Surgery, University of Texas Southwestern Medical School, Dallas.
Myers
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I
D000818:Animals; D011464:Epoprostenol / Q000378:metabolism*; D005609:Free Radicals; D006470:Hemorrhage / Q000378:metabolism*; D066298:In Vitro Techniques; D017538:Mesenteric Artery, Superior; D010100:Oxygen; D011453:Prostaglandins / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism*; D013152:Splanchnic Circulation / Q000502:physiology*
D005609:Free Radicals; D011453:Prostaglandins; D011464:Epoprostenol; D010100:Oxygen