Shortening of monophasic action potential duration during hyperkalemia and myocardial ischemia in anesthetized dogs

Japanese Journal of Pharmacology

Volumn 76, Issue 2, 1998, Pages 149-154

  Hamada, Kaori ^a,b   Yamazaki, Jun ^a   Nagao, Taku ^a  

^a UNIVERSITY OF TOKYO   (Japan)

^b ASTELLAS PHARMA INC   (Japan)

Author keywords

ATP sensitive potassium channel; Extracellular potassium; Ischemia; Monophasic action potential duration

Indexed keywords

ADENOSINE TRIPHOSPHATE; GLIBENCLAMIDE; POTASSIUM; POTASSIUM CHANNEL;

ACTION POTENTIAL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BLOOD PH; CONTROLLED STUDY; CORONARY ARTERY BLOOD FLOW; DOG; FEMALE; HEART LEFT VENTRICLE PRESSURE; HEART MUSCLE ISCHEMIA; HEART RATE; HEMODYNAMICS; HYPERKALEMIA; MALE; MEAN ARTERIAL PRESSURE; MUSCLE ACTION POTENTIAL; NONHUMAN; PH; POTASSIUM BLOOD LEVEL;

EID: 0031936316     PISSN: 00215198     EISSN: None     Source Type: Journal    
DOI: 10.1254/jjp.76.149     Document Type: Article

References (19)

1. Weiss J and Shine KI: Extracellular potassium accumulation during myocardial ischemia: implications for arrhythmogenesis. J Mol Cell Cardiol 13, 699-704 (1981)
2. Cherbakoff A, Toyama S and Hamilton WF: Relation between coronary sinus plasma potassium and cardiac arrhythmia. Circ Res 5, 517-521 (1957)
3. Kagiyama Y, Hill JL and Gettes LS: Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle. Circ Res 51, 614-623 (1982)
4. Coronel R: Heterogeneity in extracellular potassium concentration during early myocardial ischaemia and reperfusion: implications for arrhythmogenesis. Cardiovasc Res 28, 770-777 (1994)
5. + loss, reduction in repolarization time, and tissue ATP levels during myocardial hypoxia and ischemia. Circ Res 72, 560-570 (1993)
6. Conte G, Canton AD, Imperatore P, Nicola LD, Gigliotti G, Pisanti N, Memoli B, Fuiano G, Esposito C and Andreucci VE: Acute increase in plasma osmorality as a cause of hyperkalemia in patients with renal failure. Kidney Int 38, 301-307 (1990)
7. Gonick HC, Kleeman CR, Rubin ME and Maxwell MH: Functional impairment in chronic renal disease. III. Studies of potassium excretion. Am J Med Sci 261, 281-290 (1971)
8. Wilde AAM and Aksnes G: Myocardial potassium loss and cell depolarisation in ischaemia and hypoxia. Cardiovasc Res 29, 1-15 (1995)
9. Ferrero JM Jr, Sáiz J, Ferrero JM and Thakor NV: Stimulation of action potentials from metabolically impaired cardiac myocytes. Cric Res 79, 208-221 (1996)
10. Kurachi Y: Voltage-dependent activation of the inward-rectifier potassium channel in the ventricular cell membrane of guinea-pig heart. J Physiol (Lond) 366, 365-385 (1985)
11. +. Am J Physiol 235, H455-H459 (1978)
12. Reid JJ and Duker G: Recording of monophasic action potentials in the horizontally perfused guinea pig heart. J Pharmacol Methods 18, 205-217 (1987)
13. Kakei M, Noma A and Shibasaki T: Properties of adenosine-triphoshate-regulated potassium channels in guinea-pig ventricular cells. J Physiol (Lond) 363, 441-462 (1985)
14. Noma A and Shibasaki T: Membrane current through adenosine-triphosphate-regulated potassium channels in guinea-pig ventricular cells. J Phyisol (Lond) 363, 463-480 (1985)
15. + channels in cardiac muscle. Nature 305, 147-148 (1983)
16. Trube G and Hescheler J: Inward-rectifying channels in isolated patches of the heart cell membrane: ATP-dependence and comparison with cell-attached patches. Pflugers Arch 401, 178-184 (1984)
17. Kakei M, Noma A and Shibasaki T: Properties of adenosine-triphosphate-regulated potassium channels in guinea-pig ventricular cells. J Physiol (Lond) 363, 441-462 (1985)
18. Dennis SC, Gevers W and Opie LH: Protons in ischemia: where do they come from; where do they go to? J Mol Cell Cardiol 23, 1077-1086 (1991)
19. Shieh RC, Tohn SA, Lee JK and Weiss JN: Inward rectification of the IRK1 channel expressed in xenopus oocytes: effect of intracellular pH reveal an intrinsic gating mechanism. J Physiol (Lond) 494, 363-376 (1996)