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Titolo:
ATP-SENSITIVE K- AN ENDOGENOUS MECHANISM FOR PROTECTION OF THE HEART(CHANNELS IN CARDIAC ISCHEMIA )
Autore:
COLE WC;
Indirizzi:
ST BONIFACE RES CTR,DEPT PHYSIOL,DIV CARDIOVASC SCI,351 TACHE AVE WINNIPEG R2H 2A6 MB CANADA UNIV MANITOBA,DEPT PHYSIOL,DIV CARDIOVASC SCI WINNIPEG R3T 2N2 MANITOBA CANADA
Titolo Testata:
Cardiovascular drugs and therapy
, volume: 7, anno: 1993, supplemento:, 3
pagine: 527 - 537
SICI:
0920-3206(1993)7:<527:AKAEMF>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
PIG VENTRICULAR MYOCYTES; EXTRACELLULAR POTASSIUM; MYOCARDIAL-ISCHEMIA; METABOLIC INHIBITION; CONTRACTILE FAILURE; INTRACELLULAR ATP; MEMBRANE CURRENTS; RAT HEARTS; ACTIVATION; CELLS;
Keywords:
ISCHEMIA; CARDIOPROTECTION; ACTION POTENTIAL; ATP-SENSITIVE K+ CHANNELS; GLIBENCLAMIDE; PINACIDIL; WHOLE-CELL VOLTAGE CLAMP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
44
Recensione:
Indirizzi per estratti:
Citazione:
W.C. Cole, "ATP-SENSITIVE K- AN ENDOGENOUS MECHANISM FOR PROTECTION OF THE HEART(CHANNELS IN CARDIAC ISCHEMIA )", Cardiovascular drugs and therapy, 7, 1993, pp. 527-537

Abstract

The Role of ATP-sensitive K+ channels (K(ATP)) in action potential shortening and protection of myocardium in ischemia were explored using isolated ventricular myocytes and arterially perfused right ventricular walls of guinea pigs. Conditions ''simulating'' some aspects of ischemia-(10.8 mM K0+, 6.9 pH0, 20 mM lactate, no glucose; 10 mM 2-deoxy-D-glucose; and either 1 mM cyanide or no O2 (bubbled with 95/5% N2/CO2)-caused a decline in action potential duration (APD) and the elaboration of time- and voltage-independent, steady-state outward conductance due to K(ATP), which could be inhibited with glibenclamide (50 muM) inmyocytes studied via the perforated patch (nystatin) whole-cell technique. Right ventricular walls subjected to no-flow ischemia +/- glibenclamide (10 muM) to block, or +/- pinacidil (1 and 10 muM) to activate, K(ATP), respectively, exhibited varied ischemic injury. Glibenclamide caused a greater fall in resting membrane potential, inhibited the decline in APD, caused an early rise in resting tension, and inhibited recovery of contractile function upon reflow. Pinacidil caused a greater decline in APD, inhibited changes in resting tension, and improved recovery during reperfusion. These results indicate that K(ATP) contributes to action potential shortening in isolated myocytes in simulatedischemia and intact myocardium in no-flow ischemia. Activation of this membrane current may be an important adaptive mechanism for protecting the myocardium when blood flow to the tissue is compromised.

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Documento generato il 30/11/20 alle ore 16:09:15