Zink B J, Schultz C H, Wang X, Mertz M, Stern S A, Betz A L
University of Michigan, Section of Emergency Medicine and the Emergency Medicine Research Laboratory, Ann Arbor, MI 48109-0303, USA.
Brain Res. 1999 Aug 7;837(1-2):1-7. doi: 10.1016/s0006-8993(99)01646-7.
Previous studies of traumatic brain injury (TBI) and hemorrhagic shock (HS) models, have shown cardiorespiratory depression in ethanol-treated animals. This study investigated the effects of ethanol (ET) on brain lactate concentrations and acidosis in a TBI/HS model.
Anesthetized swine were instrumented and subjected to injury (INJ) consisting of fluid percussion TBI of 3 atm with concurrent 30 ml/kg graded hemorrhage over 30 min. Three groups were studied: Sham, INJ and INJ/ET. ET was given preinjury as a 2-g/kg i.v. bolus over 30 min, and an infusion of 0.4 g kg(-1) h(-1). Cardiorespiratory and cerebral physiologic data were monitored continuously for 150 min postinjury. Cerebral and renal blood flow was measured with colored microspheres. Brains were frozen in situ with liquid nitrogen. Lactate was measured with an enzymatic method.
ET levels at injury were 219+/-24 mg/dl. The INJ/ET group had increased mortality, impaired ventilation, and reduced renal blood flow. Brain (cortical) lactate levels were significantly higher and cerebral venous lactate concentrations were increased in the INJ/ET group during the postinjury period. Cerebral venous glucose was significantly higher in the INJ/ET group, and cerebral venous pH was significantly lower.
In this TBI/HS model, ethanol-induced increases in lactate concentrations in brain tissue and cerebral venous blood are associated with respiratory depression and reduced organ blood flow.
