Glyburide prevents isoflurane's reducing effects on hydroxyl radical formation in the postischemic reperfused rat heart.
BACKGROUND
The role of K(ATP) channels in isoflurane's reducing effects on oxygen free radical formation are not well known.


OBJECTIVE
To investigate whether glyburide, an ATP-regulated potassium (K(ATP)) channel blocker, abolishes isoflurane-induced cardioprotective effects and whether it affects hydroxyl radical formation in the postischemic reperfused heart.


METHODS
Thirty-nine male Wistar rats were divided into four groups: group C (control, n=10), group I (isoflurane, n=9), group G (glyburide, n=10) and group GI (glyburide and isoflurane, n=10). The hearts were perfused as a Neely's working heart model. Afterwards, global heart ischemia was induced for 15 min followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent and heart was measured with high performance liquid chromatography.


RESULTS
Isoflurane alone and glyburide alone produced significant decreases in the duration of ventricular fibrillation during reperfusion (group C 452+/-345, group I 247+/-60, group G 261+/-135 s; P<0.05). In the presence of glyburide, isoflurane did not further decrease the duration of arrhythmia (group GI 230+/-48 s). Isoflurane reduced hydroxyl radical formation significantly in the coronary effluent during ischemia and reperfusion, but this was prevented by glyburide.


CONCLUSIONS
The results suggest that isoflurane reduces hydroxyl radical formation, at least in part, through activation of K(ATP) channels.
Yamaguchi
Toshiaki
T
Department of Anesthesiology, Yamanashi Medical University, Yamanashi, Japan.
Kashimoto
Satoshi
S
Oguchi
Takeshi
T
Kumazawa
Teruo
T