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Titolo:
Platelet-activating factor contributes to postischemic vasospasm
Autore:
Wang, WZ; Guo, SZ; Tsai, TM; Anderson, GL; Miller, FN;
Indirizzi:
Univ Louisville, Ctr Appl Microcirculatory Res, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 ory Res, Louisville, KY 40292 USA Univ Louisville, Dept Surg, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 pt Surg, Louisville, KY 40292 USA Univ Louisville, Div Hand Surg, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 nd Surg, Louisville, KY 40292 USA Univ Louisville, Dept Physiol & Biophys, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 Biophys, Louisville, KY 40292 USA
Titolo Testata:
JOURNAL OF SURGICAL RESEARCH
fascicolo: 2, volume: 89, anno: 2000,
pagine: 139 - 146
SICI:
0022-4804(200004)89:2<139:PFCTPV>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; SKELETAL-MUSCLE; NITRIC-OXIDE; NO-REFLOW; MYOCARDIAL-ISCHEMIA; ENDOTHELIAL-CELLS; HEPATIC ISCHEMIA; ISCHEMIA/REPERFUSION; RELEASE; VASODILATION;
Keywords:
platelet-activating factor; vasospasm; ischemia/reperfusion injury; microcirculation; skeletal muscle;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, WZ Univ Louisville, Ctr Appl Microcirculatory Res, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 Louisville, KY 40292 USA
Citazione:
W.Z. Wang et al., "Platelet-activating factor contributes to postischemic vasospasm", J SURG RES, 89(2), 2000, pp. 139-146

Abstract

Background. The purpose of the present study was to determine if platelet-activating factor is an important mediator that produces vasospasm during reperfusion after ischemia in skeletal muscle. Materials and Methods. A vascular isolated cremaster muscle in male Sprague-Dawley rats was coupled with local intraarterial drug infusion as a modelto study microcirculation responses to ischemia/ reperfusion injury. Arteriole diameters and capillary perfusion were measured using intravital microscopy. Group 1: platelet-activating factor dose response. Group 2: Effects of a cyclooxygenase inhibitor; indomethacin, and a thromboxane synthetase inhibitor, imidazole, on the response to platelet-activating factor. Group 3: Effects of nitric oxide synthesis inhibitor; N omega-nitro-L-arginine methyl ester, on the response to platelet-activating factor. Group 4: Effects of a platelet-activating factor receptor antagonist, CV-3988, indomethacin, and imidazole after 4 h of warm ischemia and reperfusion. Results. Intraarterial infusion of platelet-activating factor produced a dose-related but mild vasoconstriction. Pretreatment with indomethacin or imidazole resulted in significant vasodilation actually emanating from platelet-activating factor infusion. Nitric oxide inhibition (with N omega-nitro-L-arginine methyl ester) enhanced the vasoconstriction produced by platelet-activating factor. Pretreatment with CV-3988, indomethacin, or imidazole significantly attenuated ischemia/reperfusion-induced vasospasm and capillary no-reflow in the cremaster muscles. Conclusions. Ischemia/reperfusion-induced vasoconstriction is at least in part mediated by platelet-activating factor and thromboxane A(2). (C) 2000 Academic Press.

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Documento generato il 04/04/20 alle ore 11:58:23