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Titolo:
Nitric oxide release from coronary vasculature before, during, and following cardioplegic arrest
Autore:
Gohra, H; Fujimura, Y; Hamano, K; Noda, H; Katoh, T; Zempo, N; Esato, K; Ueda, T; Sadamitsu, D; Maekawa, T;
Indirizzi:
Yamaguchi Univ, Sch Med, Dept Surg 1, Ube, Yamaguchi 755, Japan Yamaguchi Univ Ube Yamaguchi Japan 755 Surg 1, Ube, Yamaguchi 755, Japan Yamaguchi Univ, Sch Med, Dept Crit Care & Emergency Med, Ube, Yamaguchi 755, Japan Yamaguchi Univ Ube Yamaguchi Japan 755 ncy Med, Ube, Yamaguchi 755, Japan
Titolo Testata:
WORLD JOURNAL OF SURGERY
fascicolo: 12, volume: 23, anno: 1999,
pagine: 1249 - 1253
SICI:
0364-2313(199912)23:12<1249:NORFCV>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL-ISCHEMIA; ENDOTHELIAL DYSFUNCTION; RELAXING FACTOR; CARDIOPULMONARY BYPASS; REPERFUSION INJURY; TIME COURSE; L-ARGININE; BLOOD; CELLS; PATHOGENESIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Gohra, H Yamaguchi Univ, Sch Med, Dept Surg 1, 1144 Kogushi, Ube, Yamaguchi 755, Japan Yamaguchi Univ 1144 Kogushi Ube Yamaguchi Japan 755 hi 755, Japan
Citazione:
H. Gohra et al., "Nitric oxide release from coronary vasculature before, during, and following cardioplegic arrest", WORLD J SUR, 23(12), 1999, pp. 1249-1253

Abstract

Nitric oxide (NO) is known as a vasodilatory molecule synthesized by vascular endothelium. The NO-dependent vasodilatory response of coronary artery is impaired after ischemia and reperfusion. In the present study, the release of NO from coronary vasculature was evaluated before and during cardioplegic arrest and after reperfusion. Nine patients undergoing heart surgery were studied. Multidose crystalloid cardioplegics were used for myocardial protection. The coronary affluent and effluent were obtained simultaneously before cardioplegic arrest, at each cardioplegic administration, and after reperfusion; and the levels of nitrite and nitrate, the stable end-productsof NO, were measured. The NO release from the coronary vasculature was determined as the difference in the levels of nitrite and nitrate between the coronary effluent and affluent. The level of nitrite/nitrate release from coronary vasculature was 6.8 +/- 3.7 mu M before cardioplegic arrest. Duringcardioplegic arrest the nitrite/nitrate release decreased, reaching 1.3 +/- 1.3 mu M (p < 0.05, vs. before cardioplegic arrest) at the fourth administration of the cardioplegic. At 3 to 5 minutes after reperfusion, nitrite/nitrate release further decreased to 0.36 +/- 0.34 mu M (p < 0.05, vs. before cardioplegic arrest). During cardioplegic arrest the NO release decreasedand reached significance at approximately 70 minutes of cardioplegic arrest compared to that before cardioplegic arrest. After reperfusion, NO release was further reduced, with statistical significance compared to that before cardioplegic arrest. Our data may indicate that cardioplegic arrest and reperfusion cause endothelial dysfunction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:31:38