Fluid percussion injury transiently increases then decreases brain oxygen consumption in the rat

The oxygen consumption (VO2 mu L/h/mg) of sham and of traumatized rat brain s within 30 min and 6 h after a lateral fluid percussion injury (FPI) was m easured with the Cartesian microrespirometer. Brain slices were cut at the plain of injury and site-specific 20-60-mu g cores of tissue were transferr ed to the microrespirometer. In sham brains, the cortical VO2 (CVO2) was 13 .78 +/- 0.64 and the hippocampal VO2 (HPVO2) was 11.20 +/- 0.58 mu L/h/mg ( p < 0.05). Within 30 min of the injury, the respective values of 16.89 +/- 0.55 and 14.91 +/- 0.05 were significantly increased (p < 0.05). The combin ed VO2 (CVO2, HPVO2) of 12.49 +/- 0.06 mu L/h/mg in shams was significantly less than the combined VO2 of 15.90 +/- 0.59 mu L/h/mg at 30 min post FPI (p < 0.001). The maximal CVO2 of 19.49 +/- 1.10 mu L/h/mg and the maximal H PVO2 of 15.98 +/- 0.99 mu L/h/mg were both obtained from the ipsilateral si de of the injury. Whereas the contralateral cortical value for injured brai ns was not significantly different from that of the shams, both ipsilateral and contralateral hippocampal values were significantly greater than that of the shams in response to injury (p < 0.05). By 6 h postinjury, the combi ned VO2 had dropped to 10.01 +/- 0.84 mu L/h/mg but was not significantly l ower than the sham values. The data indicate that normal CVO2 is greater th an normal HPVO2. The FPI produces significant increases in both CVO2 and HP VO2. Also, while the immediate increase in CVO2 appears to be injury-site d ependent, that is, regional, the increase in HPVO2 appears to be global.