Regional cerebral blood flow after cortical impact injury complicated by a secondary insult in rats.

Abstract

Traumatic injury makes the brain susceptible to secondary insults. An uncomplicated mild lateral cortical impact injury (3 m/s, 2.5-mm deformation) that causes little or no permanent sequelae results in a large contusion at the impact site when the traumatic injury is complicated by a secondary insult, such as 40 minutes of bilateral carotid occlusion. To determine whether the increased sensitivity to secondary insults in this model is caused by a vascular mechanism, cerebral blood flow (CBF) was measured with (14)C-isopropyliodoamphetamine quantitative autoradiography, and brain tissue PO(2) (PbtO(2)) was measured at the impact site and in the contralateral parietal cortex. In animals that underwent bilateral carotid occlusion 1 hour after the impact injury, CBF and PbtO(2) were lower at the impact site than they were in animals that had either the impact injury or the carotid occlusion alone. In the immediate area of the impact, CBF was 14+/-6 mL. 100 g(-1). min(-1) in the animals with the impact injury followed by carotid occlusion compared with 53+/-24 mL. 100 g(-1). min(-1) in the animals with the impact injury alone and 74+/-14 mL. 100 g(-1). min(-1) in the animals with the carotid occlusion alone (P<0.001). At the time of this very low CBF value in the animals with the carotid occlusion after the impact injury, PbtO(2) at the impact site averaged 1.3+/-1.6 mm Hg and was <3 mm Hg in 5 of the 6 animals. In contrast, PbtO(2) in the animals with the impact injury alone averaged 9.3+/-2.9 mm Hg, and none of the animals had a PbtO(2) of <3 mm Hg (P=0.008). The CBF and PbtO(2) findings in this model suggest that the reduced CBF after traumatic injury predisposes the brain to secondary insults and results in ischemia when confronted with a reduction in cerebral perfusion pressure.