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Titolo:
Nitric oxide system in needle-induced transmyocardial revascularization
Autore:
Saito, T; Pelletier, MP; Shennib, H; Giaid, A;
Indirizzi:
McGill Univ, Montreal Gen Hosp, Dept Pathol, Montreal, PQ H3G 1A4, Canada McGill Univ Montreal PQ Canada H3G 1A4 thol, Montreal, PQ H3G 1A4, Canada Montreal Gen Hosp, Dept Surg, Montreal, PQ H3G 1A4, Canada Montreal Gen Hosp Montreal PQ Canada H3G 1A4 Montreal, PQ H3G 1A4, Canada McGill Univ, Montreal, PQ H3A 2T5, Canada McGill Univ Montreal PQ Canada H3A 2T5 Univ, Montreal, PQ H3A 2T5, Canada
Titolo Testata:
ANNALS OF THORACIC SURGERY
fascicolo: 1, volume: 72, anno: 2001,
pagine: 129 - 136
SICI:
0003-4975(200107)72:1<129:NOSINT>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
REFRACTORY ANGINA-PECTORIS; VEGF RECEPTOR-2 KDR; GROWTH-FACTOR-BETA; LASER REVASCULARIZATION; MYOCARDIAL-INFARCTION; ENDOTHELIAL-CELLS; CARDIAC MYOCYTES; ANGIOGENESIS; SYNTHASE; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Giaid, A McGill Univ, Montreal Gen Hosp, Dept Pathol, 1650 Cedar Ave,Suite13-314, Montreal, PQ H3G 1A4, Canada McGill Univ 1650 Cedar Ave,Suite 13-314 Montreal PQ Canada H3G 1A4
Citazione:
T. Saito et al., "Nitric oxide system in needle-induced transmyocardial revascularization", ANN THORAC, 72(1), 2001, pp. 129-136

Abstract

Background. Nitric oxide (NO) promotes endothelial proliferation and migration, essential for angiogenesis. The purpose of this study was to determine the cellular expression of inducible and endothelial nitric oxide synthases (iNOS and eNOS) in an ischemic cardiomyopathy animal model of needle-induced transmyocardial revascularization (TMR). Methods. Myocardial infarction was created in rats by ligating the left coronary artery, and animals were divided into two groups: no-TMR group (served as control) and TMR group (underwent concomitant TMR by the creation of six transmural channels with a 25-gauge needle in the ischemic area). Rats were sacrificed at intervals of 1, 2, 4, and 8 weeks. Immunohistochemistry using specific antisera was performed for iNOS, eNOS, and endothelial cell marker factor VIII. Vascular density and positive staining area with eitheriNOS or eNOS were assessed in the infarcted myocardium. Results. Vascular density in the infarcted myocardium was significantly increased in the TMR group (p < 0.001). The positive staining area for iNOS and the intensity of iNOS immunoreactivity in cardiomyocytes, vascular endothelium, and macrophages were significantly greater in the TMR group (p < 0.05). However, these differences were seen only in the first 2 weeks after TMR. There was no significant difference in the expression of eNOS between groups. Conclusions. A mechanical injury using needle puncture in an ischemic myocardium increased vascular density and is associated with increased expression of myocardial iNOS. Increased production of NO derived from iNOS may contribute to the angiogenic response of TMR. (C) 2001 by The Society of Thoracic Surgeons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 08:03:34