WIDESPREAD HEMODYNAMIC DEPRESSION AND FOCAL PLATELET ACCUMULATION AFTER FLUID PERCUSSION BRAIN INJURY - A DOUBLE-LABEL AUTORADIOGRAPHIC STUDY IN RATS

Cerebrovascular damage leading to subsequent reductions in local cereb ral blood flow (ICBF) may represent an important secondary injury mech anism following traumatic brain injury (TBI). We determined whether pa tterns of (111)indium-labeled platelet accumulation were spatially rel ated to alterations in ICBF determined autoradiographically 30 min aft er TBI. Sprague-Dawley rats (n = 8), anesthetized with halothane and m aintained on a 70:30 (vol/vol) mixture of nitrous oxide/oxygen and 0.5 % halothane, underwent parasagittal fluid percussion brain injury (1.7 -2.2 atm). (111)Indium-tropolone-labeled platelets were injected 30 mi n prior to TBI while [C-14]-iodoantipyrine was infused 30 min after tr auma. Sham-operated animals (n = 7) underwent similar surgical procedu res but were not injured, In autoradiographic images of the indium-lab eled platelets, focal sites of platelet accumulation within the trauma tized hemisphere were restricted to the pial surface (five of eight ra ts), the external capsule underlying the lateral parietal cortex (five of eight rats), and within cerebrospinal fluid (CSF) compartments (si x of eight rats). In contrast, mild-to-moderate reductions in lCBF, no t restricted to sites of platelet accumulation, were seen throughout t he traumatized hemisphere. Flow reductions were most severe in coronal sections underlying the impact site, For example, within the lateral parietal cortex and hippocampus, 1CBF was significantly reduced [p < 0 .01; analysis of variance (ANOVA)] from 1.71 +/- 0.34 (mean +/- SD) an d 0.78 +/- 0.12 ml/g/min, respectively, versus 0.72 +/- 0.17 and 0.41 +/- 0.06 ml/g/min within the traumatized hemisphere. Significant flow reductions were also seen in remote cortical and subcortical areas, in cluding the right frontal cortex and striatum. These results indicate that focal platelet accumulation and widespread hemodynamic depression are both early consequences of TBI, Therapeutic strategies directed a t these early microvascular consequences of TBI may be neuroprotective by attenuating secondary ischemic processes.