• Eric A Bedell, Douglas S DeWitt, Tatsuo Uchida, and Donald S Prough.
• Department of Anesthesiology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA.
• J. Neurotrauma. 2004 Sep 1;21(9):1212-22.

AbstractIn head-injured patients and experimental traumatic brain injury (TBI), important cerebrovascular abnormalities include decreases in cerebral blood flow (CBF) and impairment of cerebral pressure autoregulation. We evaluated CBF and pressure autoregulation after fluid percussion injury (FPI) and hypothermia in rats with the hypothesis that hypothermia would ameliorate changes in posttraumatic CBF. Male Sprague-Dawley rats, intubated and mechanically ventilated, were prepared for parasagittal FPI (1.8 atm) and laser Doppler CBF flow (LDF) measurement. The abdominal aorta was cannulated for rapid removal and reinfusion of blood. Baseline autoregulatory testing in all groups consisted of LDF measurements at normothermia and a mean arterial pressure (MAP) of 100 mm Hg, followed by randomly ordered changes of MAP to 80, 60, and 40 mm Hg. Animals were then randomized to one of five groups: normothermic control without FPI; normothermia with FPI; hypothermic control (32 degrees C) without FPI; hypothermia initiated before FPI; and hypothermia initiated immediately after FPI injury. For each group, a complete, randomly ordered autoregulatory sequence was performed at 30 and 60 min after FPI or sham TBI. In a second study, rats were prepared identically, maintained at normothermic temperatures and autoregulation was tested before and after TBI using a set of randomly ordered levels of hypotension or using progressive reductions in MAP (i.e., 80, 60, 40 mm Hg) with the hypothesis that the technical manner and timing of decreasing of the blood pressure would effect CBF after TBI. Due to high acute mortality, the group in which hypothermia was induced before FPI was excluded from the analysis. At baseline, autoregulation was similar in all groups. There was no change in CBF or autoregulation in the normothermic control group at 30 and 60 min. In the other groups at 30 and 60 min, there was a similar, statistically significant decrease in absolute CBF (i.e., a decrease of 27-57% of baseline values), but pressure autoregulation was intact except at the lowest blood pressure tested at 60 min, where there was a slight improvement in the hypothermic group. Thus, in these experiments, absolute CBF decreased with hypothermia and FPI, while neither hypothermia nor FPI significantly altered autoregulation. In the second study, autoregulatory function was not different before TBI when comparing random and sequential blood pressure changes, but, when comparing the groups after TBI at the 60 mm Hg blood pressure level, CBF was significantly lower in the sequential group than in the random order group. This suggests that the mechanism of creating hypotension, whether random or sequential, significantly affects the measurement of CBF and autoregulation after TBI in rats.

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