N. Kanaya et al., EFFECT OF ISOFLURANE ON EPINEPHRINE-INDUCED ARRHYTHMIAS IN ISCHEMIC-REPERFUSED DOG HEARTS, Research communications in molecular pathology and pharmacology, 100(2), 1998, pp. 181-186
Although isoflurane protects the myocardium and facilitates functional
recovery after ischemia and reperfusion, its mechanism of action is s
till unclear. We hypothesized that isoflurane maintains intracellular
Ca2+ homeostasis, thus attenuating epinephrine-induced arrhythmogenici
ty in in vivo models of myocardial ischemia and reperfusion. Adult mon
grel dogs, anesthetized with urethane and chloralose, underwent 15 min
utes of left anterior descending coronary artery occlusion followed by
reperfusion. In addition to a sham group (without occlusion, n = 5) a
nd a control group (with occlusion, n = 7), a third group (n = 5) rece
ived 1.5% isoflurane before ischemia was induced; a fourth (n = 7), is
oflurane after reperfusion; and a fifth (n = 5), isoflurane and verapa
mil (100 mu g/kg) after reperfusion. Isoflurane administered before is
chemia increased the arrhythmogenic dose of epinephrine (ADE), but had
no effect on ADE when administered after reperfusion. The addition of
verapamil further increased the ADE. These results indicate that isof
lurane has a cardioprotective effect during ischemia and reperfusion b
y, at least in part, the reduction of Ca2+ influx.