title: Effects of intestinal ischemia-reperfusion on major conduit arteries.
abstract: Intestinal ischemia-reperfusion (I-R) is a common and serious clinical condition associated with simultaneous remote organ dysfunction. The purpose of this study was to investigate the effects of intestinal I-R on the vasomotor functions of major conduit arteries. Anesthetized rabbits were randomly assigned to one of three groups: sham-operated controls (Group I), and one-hour intestinal ischemia with two-hour reperfusion (Group II) or four-hour reperfusion (Group III). The following mechanisms of vasomotor functions were studied in abdominal aorta, superior mesenteric, renal, pulmonary, and carotid arterial rings: (1) endothelial-dependent vasodilation response to acetylcholine, (2) endothelial-independent vasodilation response to nitroprusside, (3) beta-adrenergic vasodilation response to isoproterenol, and (4) phenylephrine-induced vasoconstriction. Intestinal injury was quantified using malondialdehyde (MDA) concentration and wet-to-dry intestine weight ratio. Intestinal I-R did not affect the maximal responsiveness or the sensitivity to acetylcholine, nitroprusside, and isoproterenol in all the vessels studied. The maximal contractile response to phenylephrine increased significantly in mesenteric artery in Group II, (227.1+/-15.1% vs. 152.8+/-11.7% in controls) (p<0.05). Intestinal MDA concentration, a marker of oxidant injury, increased from 39.87+/-9.41 nmol/g to 67.8+/-8.8 nmol/g in group II (p<0.01), and to 94.8+/-7.56 nmol/g in Group III (p<0.001). Wet-to-dry intestine weight ratio increased from 3.62+/-0.12 to 4.28+/-0.17 in Group II (p<0.01), to 4.62+/-0.14 in Group III (p<0.001). These data indicate that although the intestines of the animals subjected to intestinal I-R are seriously injured, the smooth muscle relaxation of major conduit arteries was not affected.
authors.affiliation: Department of Surgery, Ankara University Medical School, Turkey. ckoksoy@hotmail.com
authors.forename: C
authors.initials: C
authors.lastname: Koksoy
authors.forename: B S
authors.initials: BS
authors.lastname: Uydes-Dogan
authors.forename: M A
authors.initials: MA
authors.lastname: Kuzu
authors.forename: A
authors.initials: A
authors.lastname: Aydemir-Koksoy
authors.forename: E
authors.initials: E
authors.lastname: Demirpence
authors.forename: M
authors.initials: M
authors.lastname: Kesenci
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001012:Aorta, Abdominal / Q000502:physiology / Q000503:physiopathology; D001158:Arteries / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D002339:Carotid Arteries / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology; D066298:In Vitro Techniques; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000503:physiopathology*; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D017538:Mesenteric Artery, Superior / Q000502:physiology / Q000503:physiopathology; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011651:Pulmonary Artery / Q000502:physiology / Q000503:physiopathology; D011817:Rabbits; D012077:Renal Artery / Q000502:physiology / Q000503:physiopathology; D015424:Reperfusion; D015427:Reperfusion Injury / Q000503:physiopathology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D009599:Nitroprusside; D010656:Phenylephrine; D019335:Nitroarginine; D007545:Isoproterenol; D000109:Acetylcholine