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Titolo:
CARDIOPROTECTIVE EFFECTS OF NIP-121, A NOVEL ATP-SENSITIVE POTASSIUM CHANNEL OPENER, DURING ISCHEMIA AND REPERFUSION IN CORONARY PERFUSED GUINEA-PIG MYOCARDIUM
Autore:
TANAKA H; OKAZAKI K; SHIGENOBU K;
Indirizzi:
TOHO UNIV,SCH PHARMACEUT SCI,DEPT PHARMACOL,MIYAMA 2-2-1 CHIBA 274 JAPAN
Titolo Testata:
Journal of cardiovascular pharmacology
fascicolo: 5, volume: 27, anno: 1996,
pagine: 695 - 701
SICI:
0160-2446(1996)27:5<695:CEONAN>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRACELLULAR SODIUM ACTIVITY; ACTION-POTENTIAL DURATION; RAT VENTRICULAR MYOCYTES; REGULATED K+ CHANNELS; CONTRACTILE FAILURE; HEART-CELLS; CROMAKALIM; DEPLETION; HYPOXIA; MUSCLE;
Keywords:
ISCHEMIA; REPERFUSION; K+ CHANNEL OPENER; NIP-121; GLIBENCLAMIDE; MYOCARDIAL INJURY; GUINEA PIGS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
H. Tanaka et al., "CARDIOPROTECTIVE EFFECTS OF NIP-121, A NOVEL ATP-SENSITIVE POTASSIUM CHANNEL OPENER, DURING ISCHEMIA AND REPERFUSION IN CORONARY PERFUSED GUINEA-PIG MYOCARDIUM", Journal of cardiovascular pharmacology, 27(5), 1996, pp. 695-701

Abstract

We investigated the effect of NIP-121, a novel ATP-sensitive K+ channel opener, on myocardial damage during ischemia/reperfusion. The action potential and contractile force of coronary-perfused guinea pig right ventricular walls were recorded. The preparations were subjected to 30-min no-flow ischemia with or without NIP-121 or glibenclamide, followed by 60-min reperfusion. In untreated tissues, decreases in action potential duration (APD) and contractile force and an increase in resting tension were observed during the no-flow period. On reperfusion, transient arrhythmias were observed and resting or contractile force returned to <50% of preischemic values. NIP-121, at 0.3 mu M, a concentration showing only a slight negative inotropic effect, caused a fasterdecrease in APD and contractile force but abolished the increase in resting tension (RT) during the no-flow period. On reperfusion, no arrhythmia was observed in NIP-121-treated preparations, and contractile force recovered to similar to 80% of the preischemic value. Glibenclamide 1 mu M attenuated the decrease in APD but affected neither the decrease in contractile force nor the increase in RT during the :no-flow period. On reperfusion, the incidence of arrhythmia was increased in glibenclamide-treated preparations, lions, and the recovery of basal tension and contractile force was inhibited: Contractile force recovered to only similar to 15% of the preischemic value. NIP-121 was also shown to attenuate the decrease in tissue ATP during ischemia and reperfusion. We demonstrated that NIP-121 may have protective effects against myocardial injury during ischemia and reperfusion. Activation of ATP-sensitive K+ current may be an adaptive mechanism for cardioprotection under compromised blood flow.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:16:16