Fentanyl infusion preserves cerebral blood flow during decreased arterial blood pressure after traumatic brain injury in cats.

Hypotension after traumatic brain injury (TBI) has been associated with significant reductions in cerebral blood flow (CBF) in experimental animals. In humans, posttraumatic hypotension is associated with significantly worsened outcome, possibly because of cerebral hypoperfusion. The existence of opioid receptor-mediated cerebrovascular dilatory effects in humans has been theorized. We studied the systemic and cerebral vascular effects of fentanyl after fluid-percussion injury (FPI) TBI in isoflurane-anesthetized cats. In an approved protocol, 17 fasted cats were anesthetized, mechanically ventilated with 1-1.5% isoflurane in 70% N2O/30% O2, and prepared for FPI. Electroencephalogram (EEG) and intracranial pressure (ICP) were monitored. Cerebral blood flow and cardiac output were measured with radiolabelled microspheres. Animals received moderate FPI (2.2 atm) followed by 15 min of stabilization. Cats were then randomized to control (isoflurane anesthesia plus saline placebo) or fentanyl (isoflurane anesthesia plus fentanyl 50 microg x kg(-1) h(-1)) groups. CBF, EEG, and ICP were recorded at baseline (Baseline), 15 min post-FPI (post-FPI), and at 15, 75, and 135 min after beginning fentanyl or saline placebo infusions (INF 15, INF 75, INF 135). EEG, ICP, PaCO2, PaO2, pH, and temperature were similar between groups. Mean arterial pressure was significantly lower than in the control group after fentanyl administration, while total CBF was not significantly different from control values. In a previous study, decreasing MAP to 80 mm Hg after TBI in isoflurane-anesthetized cats resulted in a 30% decrease in CBF. In this study, fentanyl after TBI significantly decreased MAP but not CBF. Fentanyl administration was associated with preservation of CBF despite hypotension. Further research is necessary to evaluate the effects of fentanyl on cerebral autoregulation after TBI.