[Treatment of experimental ischemic cerebral lactic acidosis in rats with dichloroacetate].
In the cerebral ischemic pathophysiologic mechanism, lactic acidosis is a important factor to exacerbate cerebral damage. Our research showed that the lactic level of cerebral cortex in rats increased rapidly after the focal cerebral ischemia or during blood reperfusion after cerebral ischemia, 26.99 +/- 5.89 and 28.63 +/- 5.08 mumol/g brain wight respectively, it exacerbated significantly brain edema and pathological damage. The lactic level decreased rapidly to treat with dichloroacetate (50 mg/kg body weight) after cerebral ischemia or during blood reperfusion, 14.11 +/- 2.06 and 13.23 +/- 1.71 mumol/g brain wight respectively, brain edema and pathology improved significantly. It suggested that dichloroacetate might across blood-brain barrier into the cerebral ischemic region and lowered lactic level, improved brain internal environment, relieved cerebral damage after focal cerebral ischemia or during blood reperfusion. It may improve the prognosis of patient with ischemic cerebral vascular disease to be treated with dichloroacetate early.
Hu
C L
CL
Department of Neurology, First Affiliated Hospital Chongqing University of Medical Sciences.
D000140:Acidosis, Lactic / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy*; D003999:Dichloroacetic Acid / Q000627:therapeutic use*; D007773:Lactates / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy
D007773:Lactates; D003999:Dichloroacetic Acid