Biros M H, Dimlich R V, Barsan W G
Ann Emerg Med. 1986 Apr;15(4):397-404. doi: 10.1016/s0196-0644(86)80174-3.
Cerebral ischemic insult is one of the most clinically significant conditions leading to irreversible brain cell damage and death. Animal studies have suggested that lowered intracellular pH due to the severe brain lactic acidosis following ischemia interferes with normal cell structure and function and leads to brain cell necrosis. Therefore, efforts directed to decreasing brain lactate may be beneficial in preventing brain cell damage and death. The goal of our study was to evaluate the effectiveness of postinsult treatment with dichloroacetate (DCA) in controlling increases in brain lactate following partial global ischemia (PGI) in rats. PGI was induced by bilateral carotid artery occlusion and induced hypotension. Animals that received DCA immediately after a 30-minute ischemic insult (n = 5) or 15 minutes after the end of an ischemic insult (n = 5) had cortical lactate levels that were significantly lower (P less than .005) than lactate levels in untreated insulted animals and that were not significantly different than those previously obtained with preinsult DCA treatment in rats subjected to 30 minutes of PGI. Treatment of rats with DCA following PGI may be effective in reducing cortical lactate levels and hence may limit irreversible damage to brain cells following cerebral ischemia.
