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Am J Physiol Heart Circ Physiol 283: H1005-H1011, 2002. First published May 16, 2002; doi:10.1152/ajpheart.00054.2002
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Vol. 283, Issue 3, H1005-H1011, September 2002

MitoKATP opener, diazoxide, reduces neuronal damage after middle cerebral artery occlusion in the rat

Katsuyoshi Shimizu1, Zsombor Lacza1,2, Nishadi Rajapakse1, Takashi Horiguchi1, James Snipes1, and David W. Busija1

1 Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1083; and 2 Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary 1082

We investigated effects of diazoxide, a selective opener of mitochondrial ATP-sensitive K+ (mitoKATP) channels, against brain damage after middle cerebral artery occlusion (MCAO) in male Wistar rats. Diazoxide (0.4 or 2 mM in 30 µl saline) or saline (sham) was infused into the right lateral ventricle 15 min before MCAO. Neurological score was improved 24 h later in the animals treated with 2 mM diazoxide (13.8 ± 0.7, n = 13) compared with sham treatment (9.5 ± 0.2, n = 6, P < 0.01). The total percent infarct volume (MCAO vs. contralateral side) of sham treatment animals was 43.6 ± 3.6% (n = 12). Treatment with 2 mM diazoxide reduced the infarct volume to 20.9 ± 4.8% (n = 13, P < 0.05). Effects of diazoxide were prominent in the cerebral cortex. The protective effect of diazoxide was completely prevented by the pretreatment with 5-hydroxydecanoate (100 mM in 10 µl saline), a selective blocker of mitoKATP channels (n = 6). These results indicate that selective opening of the mitoKATP channel has neuroprotective effects against ischemia-reperfusion injury in the rat brain.

ischemia; stroke; cerebral circulation; mitochondrial adenosine 5'-triphosphate-sensitive potassium channels


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