EFFECTS OF HYPOTHERMIA, POTASSIUM, AND VERAPAMIL ON THE ACTION-POTENTIAL CHARACTERISTICS OF CANINE CARDIAC PURKINJE-FIBERS

Citation
J. Sprung et al., EFFECTS OF HYPOTHERMIA, POTASSIUM, AND VERAPAMIL ON THE ACTION-POTENTIAL CHARACTERISTICS OF CANINE CARDIAC PURKINJE-FIBERS, Anesthesiology, 82(3), 1995, pp. 713-722
Citations number
55
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
82
Issue
3
Year of publication
1995
Pages
713 - 722
Database
ISI
SICI code
0003-3022(1995)82:3<713:EOHPAV>2.0.ZU;2-Y
Abstract
Background: Hypothermia may induce hypokalemia and increase intracellu lar Ca2+ by affecting serum K+ and Ca2+ fluxes across the cell membran e. These ionic alterations may significantly change the electrophysiol ogic characteristics of the cardiac action potential and may induce ca rdiac arrhythmias. The current study was undertaken to determine wheth er electrophysiologic changes in Purkinje fibers induced by hypothermi a could be reversed by manipulating the extracellular K+ and transmemb rane Ca2+ fluxes by Ca2+ channel blockade with verapamil. Methods: A c onventional microelectrode method was used to determine the effects of hypothermia (32 +/- 0.5 degrees C and 28 +/- 0.5 degrees C) various e xternal K+ concentrations ([K+](o)) (2.3, 3.8, and 6.8 mM) on maximum diastolic potential, maximum rate of phase 0 depolarization (V-max), a nd action potential duration (APD) at 50% (APD(50)) and at 95% (APD(95 )) repolarization in isolated canine cardiac Purkinje fibers. To evalu ate the contributional of the slow inward Ca2+ current to action poten tial changes in hypothermia, the experiments were repeated in the pres ence of the Ca2+-channel antagonist verapamil (1 mu M). Results: Varia tions of [K+](o) induced the expected shifts in maximum diastolic pote ntial, and hypothermia (28 degrees C) induced moderate depolarization, but only when [K+](o) was greater than or equal to 3.9 mM (P < 0.05). Hypothermia decreased V-max at all [K+](o) studied (P < 0.05). Regard less of the temperature, V-max was not affected by verapamil when [K+] (o) was less than or equal to 3.9 mM, but at 6.8 mM [K+](o) in hypothe rmia V-max was significantly lower in the presence of verapamil. Hypot hermia increased both the APD(50) and the APD(95). The effects of vera pamil on APD were temperature and [K+](o) dependent; between 37 degree s C and 28 degrees C with 2.3 mM [K+](o) in the superfusate, verapamil did not affect APD. At 28 degrees C in the presence of verapamil, the APD(50) and APD(95) decreased only if the [K+](o) was greater than or equal to 3.3 mM. Conclusions: Verapamil and K+ supplementation in hyp othermia may exert an antiarrhythmic effect, primarily by reducing the dispersion of prolonged APD.