Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Role of cellular acidosis in production of nitric oxide in canine ischemicmyocardium
Autore:
Kitakaze, M; Node, K; Takashima, S; Asanuma, H; Asakura, M; Sanada, S; Shinozaki, Y; Mori, H; Sato, H; Kuzuya, T; Hori, M;
Indirizzi:
Osaka Univ, Grad Sch Med, Dept Internal Med & Therapeut, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 erapeut, Suita, Osaka 5650871, Japan Tokai Univ, Sch Med, Dept Physiol, Isehara, Kanagawa 25911, Japan Tokai Univ Isehara Kanagawa Japan 25911 l, Isehara, Kanagawa 25911, Japan
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 9, volume: 33, anno: 2001,
pagine: 1727 - 1737
SICI:
0022-2828(200109)33:9<1727:ROCAIP>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; CORONARY BLOOD-FLOW; GUINEA-PIG HEART; REACTIVE HYPEREMIA; RELAXING FACTOR; CYCLIC-GMP; ENDOTHELIUM; ADENOSINE; CELLS; DOGS;
Keywords:
NO synthase; fractional shortening; acidosis; Na+/H+ exchange;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Kitakaze, M Osaka Univ, Grad Sch Med, Dept Internal Med & Therapeut, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan Osaka Univ 2-2 Yamadaoka Suita Osaka Japan 5650871 0871, Japan
Citazione:
M. Kitakaze et al., "Role of cellular acidosis in production of nitric oxide in canine ischemicmyocardium", J MOL CEL C, 33(9), 2001, pp. 1727-1737

Abstract

We tested the hypothesis that cellular acidosis modulates the production of nitric oxide (NO) in ischemic hearts. In canine hearts, wc decreased coronary blood flow (CBF) to one third of the control by reduction of coronary perfusion pressure (105 +/- 3 to 41 +/- 5 mmHg), and thereafter we maintained CBF constant (89.8 +/- 1.6 to 30.0 +/- 0.5ml/100g/min) with an intracoronary administration of either saline, atropine, rauwolscine, HOE140. 8-sulfophenyltheophylline (8SPT), NaHCO3 or HOE642 (the inhibitor of Na+/H+ exchange). The cardiac NO levels defined as the differences of the nitrate and nitrite levels between coronary venous and arterial blood increased in the saline administration (2.9 +/-0.2 to 12.7 +/-1.7 mu mol/l), and the extents of increases were identical in the condition of either saline, atropine, rauwolscine, HOE140 or 8SPT administration. In the condition with either NaHCO3 or HOE642, the increases in the cardiac NO lck,cls were blunted (4.5 +/-0.7 and 4.8 +/-0.4 mu mol/l, respectively). Cyclic GMP content of epicardial coronary artery in the ischemic area increased, which was also attenuatedby either NaHCO3 or HOE642. We confirmed the acidosis-induced NO production in a more severe ischemic myocardium, and also showed that cellular acidosis produced by infusion of HCl increased NO production in non-ischemic myocardium. We conclude that cellular acidosis and subsequent activation of Na/H+ exchanges modulate production Of endogenous NO in canine ischemic myocardium. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/01/20 alle ore 12:24:30