Halothane protects the heart against the reperfusion injury observed after
an ischemia. In ischemic or anoxic conditions, a large ATP-sensitive K+ (K-
ATP) conductance is supposed to provide an endogenous protection to the myo
cardium. In this study, we tested the possibility that halothane acted by m
odulating this conductance. Isolated guinea-pig cardiomyocytes were success
ively studied in current clamp and in voltage-clamp conditions. Action pote
ntials regulation by halothane was tested in control conditions and in situ
ations where the K-ATP channels were activated. In control conditions, halo
thane decreased action potential duration of myocytes but did not significa
ntly alter the inward rectifying K+ current. Conversely, halothane lengthen
ed action potential of cells in which the K-ATP conductance was activated,
by inhibiting the K-ATP current. In ischemic conditions, simultaneous short
ening of long action potentials and lengthening of shortened ones would be
expected to homogenize the absolute refractory period at the border between
normoxic and anoxic zones. This effect, together with a decrease in calciu
m load, could protect the myocardium against re-entrant arrhythmias. (C) 20
00 Elsevier Science B.V. All rights reserved.