The effects of traumatic brain injury on regional cerebral blood flow in rats

Alterations in cerebral blood flow (CBF) are among the most important secondary pathophysiologic consequences of traumatic brain injury. The present study compared CBF in control rats (n = 20) and in rats that received a calibrated experimental traumatic brain injury (n = 17). The traumatized rats were anesthetized with ketamine (25 mg/kg) and xylazine (10 mg/kg), and prepared for fluid percussion injury (FPI). Twenty-four hours later, the rats were anesthetized with 1% halothane in nitrous oxide-oxygen (70:30) and the left atrium was catheterized via a thoroacotomy. The atrial cannula was used to inject 15 microns radiolabeled microspheres to measure CBF. Following surgery, the concentration of halothane was reduced to 0.5% and the rats were paralyzed with pancuronium bromide (0.1 mg/kg). Thirty minutes later, baseline microsphere determinations were made, and the rats were injured (2.47 +/- 0.08 atm). Each rat received additional injections of microspheres at two of the following four times (T): 5, 15, 30, and 60 min after the brain injury. The procedures for the control group rats were the same as described above except that the rats were not subjected to the craniotomy and the FPI. The traumatized group exhibited heterogeneous decreases in CBF following trauma. Global CBF in this group was 78% (p less than 0.01), 64% (p less than 0.05), 52% (p less than 0.001) of those in the control group at T5, 15, 30, and 60, respectively. In rats, the most prominent cerebral circulatory changes following fluid percussion injury were early reductions of CBF and an increasingly heterogeneous CBF pattern. Hemorrhage, edema, and elevated prostagandin levels are mechanisms that may contribute to these changes.