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Diazoxide, but not cyclosporin A or hypothermia, preserves N-methyl-D-aspartate -induced cerebral dilation after ischemia in piglets


, : Diazoxide, but not cyclosporin A or hypothermia, preserves N-methyl-D-aspartate -induced cerebral dilation after ischemia in piglets. Society for Neuroscience Abstracts 27(1): 887

We have previously shown that diazoxide, a specific activator of mitochondrial ATP-sensitive potassium channels (mKATP), preserves vascular dilator responses to application of NMDA after ischemia (Stroke 30:2713-2718, 1999). We also have shown that diazoxide administration limits infarct volume in neonatal and adult rats following cerebral ischemia. In addition, other interventions that affect mitochrondial function, such as cyclosporin A (CsA) administration and brain cooling, also reduce infarct size after ischemia. Thus, we assessed whether CsA and hypothermia were as effective as diazoxide in protecting neuronal function against ischemia. We examined effects of NMDA in anesthetized piglets on pial arteriolar diameter before ischemia and 1 hour after 10 min of global ischemia in three groups: diazoxide pretreated (10-5M; n=5), CsA pretreated (10-4M; n=6), and local brain cooling (34degreeC; n=11). Total brain ischemia was induced by increasing intracranial pressure. In the diazoxide group, arterioles (baseline diameterapprx100 microns) dilated by 15+-9% versus 14+-5% at 5X10-5M NMDA (ns) and by 41+-13% versus 39+-8% at 10-4M NMDA (ns), before and after ischemia, respectively. In the CsA group, arteriolar dilation was reduced (p<.05) by ischemia to 6+-4% at 5X10-5M NMDA and 13+-8% at 10-4M NMDA. In the hypothermia group, dilation was reduced to 8+-5% at 5X10-5M NMDA and 20+-5% at 10-4M NMDA after ischemia (p<.05). We conclude that diazoxide has specific neuroprotective effects via KATP on neuronal function in the early post-ischemic period.

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