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Titolo:
LACK OF NITRIC-OXIDE CONTRIBUTES TO VASOSPASM DURING ISCHEMIA REPERFUSION INJURY/
Autore:
WANG WZ; ANDERSON G; FLEMING JT; PETER FW; FRANKEN RJPM; ACLAND RD; BARKER J;
Indirizzi:
UNIV LOUISVILLE,SCH MED,CTR APPL MICROCIRCULAT RES,HSC,BLDG A,ROOM 1115 LOUISVILLE KY 40292 UNIV LOUISVILLE,CTR APPL MICROCIRCULATORY RES LOUISVILLE KY 40292 UNIV LOUISVILLE,DIV PLAST & RECONSTRUCT SURG LOUISVILLE KY 40292 UNIV LOUISVILLE,DEPT SURG LOUISVILLE KY 40292 UNIV LOUISVILLE,DEPT PHYSIOL & BIOPHYS LOUISVILLE KY 40292
Titolo Testata:
Plastic and reconstructive surgery
fascicolo: 4, volume: 99, anno: 1997,
pagine: 1099 - 1108
SICI:
0032-1052(1997)99:4<1099:LONCTV>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; VASCULAR ENDOTHELIUM; PLASMA ENDOTHELIN-1; ISCHEMIA; REPERFUSION; RELEASE; NITROGLYCERIN; DYSFUNCTION; HEARTS; MUSCLE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
W.Z. Wang et al., "LACK OF NITRIC-OXIDE CONTRIBUTES TO VASOSPASM DURING ISCHEMIA REPERFUSION INJURY/", Plastic and reconstructive surgery, 99(4), 1997, pp. 1099-1108

Abstract

Vasospasm can be a complication after free tissue transfer and replant operations. Recent studies suggest that vasospasm may be due to endothelium dysfunction, resulting in impairment of nitric oxide production. The present experiment was designed to investigate acute responses of the microcirculation of skeletal muscle to local interarterial infusion of sodium nitroprusside (a direct donor of nitric oxide and thus an endothelium-independent vasodilator) or acetylcholine chloride (which stimulates endothelium release of endogenous nitric oxide) during reperfusion after 4 hours of warm ischemia. Male Sprague-Dawley rats, each weighing 100 to 120 gm, were anesthetized with sodium pentobarbitone and were surgically prepared with vascular isolated and denervated cremaster muscles that were subjected to 4 hours warm ischemia and 2 hours of reperfusion. Sodium nitroprusside (10(-3) M), acetylcholine chloride (10(-4) M), or normal saline (eight rats for each group) were administered by local infusion (0.1 ml/hour) through the femoral arteryinto the natural blood flow of the cremaster. The arterial tree in the cremaster was observed and arteriole diameters (A1-A4) were measuredusing intravital microscopy. The number of arteriole branches having temporary stoppage of flow were counted in each cremaster. The resultsfrom this study show that local infusion of sodium nitroprusside, butnot acetylcholine chloride, prevents ischemia/reperfusion vasoconstriction in A3 and A4 arterioles and thus improves microvascular blood flow. Generalized vasoconstriction caused by topically applied norepinephrine (10(-6) M) to sham ischemia cremasters could be completely reversed by the local infusion of 10(-4) M acetylcholine chloride. These results indicate that vasospasm after ischemia/reperfusion may be related to temporary endothelial cell dysfunction, resulting in the inability to produce sufficient nitric oxide during early reperfusion. Vascular smooth muscle, however, is responsive to locally administered sodiumnitroprusside infusion (which is thought to provide exogenous nitric oxide).

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Documento generato il 14/07/20 alle ore 07:03:03