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Am J Physiol Heart Circ Physiol (May 16, 2002). doi:10.1152/ajpheart.00054.2002
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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00054.2002
Submitted on January 22, 2002
Accepted on May 7, 2002

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

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

1 Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA

* To whom correspondence should be addressed. E-mail: KATSUYOSHIS{at}aol.com.

We investigated effects of diazoxide, a selective opener of mitoKATP, against brain damage after middle cerebral artery occlusion (MCAO) in male Wistar rats. Diazoxide (0.4 mM or 2 mM in 30 µL saline) or saline (sham) was infused into the right lateral ventricle 15 minutes before MCAO. Neurological score was improved 24 hours later in the animals treated with 2 mM diazoxide (13.8 ± 0.7, n = 13) compared to sham treatment (9.5 ± 0.2, n = 6) (p < 0.01). The total % infarct volume (MCAO versus 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 10µL saline), a selective blocker of mitoKATP (n = 6). These results indicate that selective opening of mitoKATP has neuroprotective effects against ischemia-reperfusion injury in the rat brain.




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