Background: Experimental evidence suggests that ATP-sensitive potassiu
m channels are involved in myocardial ischemic preconditioning, Becaus
e some pharmacologic effects of isoflurane are mediated by K-ATP chann
els, the authors tested the hypothesis: Isoflurane administration, bef
ore myocardial ischemia, can induce or mimic myocardial preconditionin
g. Methods: Myocardial infarct size was measured in three groups of pr
opofol-anesthetized rabbits, each subjected to 30 min of anterolateral
coronary occlusion followed by 3 h of reperfusion. Groups differed iu
their pretreatment: Group I (control, N = 13) no pretreatment, Group
2 (ischemic preconditioning, N = 8), 5 min of coronary occlusion and 1
5 min of reperfusion; Group 3 (isoflurane pretreatment; N = If), If mi
n of isoflurane (1.1% end-tidal) and 15 min of washout. Hemodynamics w
ere monitored serially. Myocardial infarct size and the area at risk w
ere defined using triphenyltetrazolium chloride staining and fluoresce
nt microspheres, respectively, and both were measured using computeriz
ed planimetry. Results: Infarct size ex-pressed as a percentage of are
a at risk was 23.4 +/- 8.5% (mean +/- SD in the isoflurane group compa
red with 33.1 +/- 13.3% in controls, and 8.7 +/- 6.2% in the ischemia-
preconditioned group. Analysis for coincidental regressions, followed
by tests for equality of slope and elevation, showed that the linear r
elationship between infarct size and area at risk was significantly CP
< 0.05) different in all three groups because of differences in line
elevation, Minor differences in hemodynamic variables were found betwe
en groups, which were unlikely to account for the significant differen
ces in infarct size, Conclusion: Preadministration of isoflurane, befo
re myocardial ischemia, reduces myocardial infarct size, and mimics my
ocardial preconditioning. (Rev words: Heart: ischemic preconditioning;
myocardial infarction; myocardial ischemia. Anesthetics, volatile: is
oflurane. Potassium channel: ATP-sensitive.)