Changes in cerebral energy metabolites induced by impact-acceleration brain trauma and hypoxic-hypotensive injury in rats

Abstract

The aim of this study was to describe, in rats, brain energy metabolites changes after different levels of head trauma (T) complicated by hypoxia-hypotension (HH). Male Sprague Dawley rats (n = 7 per groups) were subjected to T by impact-acceleration with 450-g weight drop from 1.50 or 1.80 m (T 1.50 or T 1.80), or to a 15-min period of HH (controlled hemorrhage to mean arterial pressure [MAP] of 40 mm Hg, and mechanical ventilation with N(2) 90%/O(2) 10%), or to their association (T followed by HH). Invasive MAP, intraparenchymental intracranial pressure (ICP), and cerebral blood flow (CBF using Laser Doppler flowmetry) were recorded during the 5 post-traumatic hours. Cerebral microdialysis was used to measure each hour interstitial brain glucose, lactate, pyruvate, and glutamate. For the entire period, the levels of cerebral glucose, pyruvate, and glutamate were not statistically different between groups. In addition, there were no differences associated with the lactate-glucose ratio. Lactate was significantly higher overtime only in T 1.80 + HH group (p < 0.001 vs. every other groups). The lactate-pyruvate ratio increased with trauma level, and was significantly different vs. sham for the entire study period in T 1.50 + HH, in T 1.80, and in T 1.80 + HH. There was no correlation between CBF variations and the lactate-pyruvate ratio (r(2) = 0.00001). The cerebral perfusion pressure was greater than 70 mm Hg in all groups. The prolonged post-traumatic impairment in brain energy metabolism may be related to traumatic brain injury (TBI) severity. It became worse when T was complicated by HH, but was not related to changes in CBF.