Ethanol reduces metabolic uncoupling following experimental head injury

Previous investigations have shown that ethanol is neuroprotective followin g experimental traumatic brain injury (TBI). This study sought to determine if the neuroprotective effects of ethanol in a controlled cortical impact (CCI) injury model are related to its effects on cerebral glucose metabolis m and blood flow. Adult rats were given ethanol (1.0 g/kg) or saline by int raperitoneal injection followed 40 min later by injury. Regional cerebral b lood flow (CBF) and cerebral metabolic rates of glucose (CMRglc) were deter mined immediately, and at 3, 6, 12, 24, and 72 h postinjury using quantitat ive autoradiography. Immediately after injury, CMRglc in the contusion core and penumbra was reduced in the ethanol group compared to the saline group : (core CMRglc: 52.2 +/- 16.0 versus 94.2 +/- 14.1 mu mol/100 g/min, respec tively, p < 0.001; penumbral CMRglc: 58.2 +/- 12.8 versus 82.8 +/- 19.7 mu mol/100 g/min, respectively; p < 0.05) However, at 24 and 72 h postinjury, penumbral CMRglc in the ethanol group was increased compared to the saline group (p < 0.05 and p < 0.001, respectively). Regarding CBF, contusion core values in the ethanol group were elevated compared to the saline group imm ediately postinjury, (70.4 +/- 17.1 versus 31.5 +/- 27.8 mL/100 g/min, resp ectively (p < .05), and at 6, 12, and 24 h postinjury (p < 0.05). Penumbral CBF was also higher at 6 and 72 h in the ethanol group compared to the sal ine group (p < 0.05). These results indicate that low-dose ethanol is assoc iated with a marked attenuation of immediate postinjury hyperglycolysis and with more normal glucose metabolism in the injury penumbra over the ensuin g 3 days. Simultaneously, the reduction in CBF typically seen within the co ntusion core and penumbra after CCI is less severe when ethanol is present. The net effect of these changes is a decreased degree of uncoupling betwee n glucose metabolism and CBF that otherwise occurs in the absence of ethano l. These changes may likely explain the neuroprotective effect of ethanol.