Assessment of Posttraumatic Polymorphonuclear Leukocyte Accumulation in Rat Brain Using Tissue Myeloperoxidase Assay and Vinblastine Treatment

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Abstract
Polymorphonuclear leukocytes (PMN) are implicated in the pathogenesis of traumatic brain injury. We tested the following hypotheses: (1) leukocyte accumulation is present in brain tissue 24 h posttrauma, (2) leukocyte accumulation represents PMN, and (3) prior systemic PMN depletion attenuates brain tissue PMN accumulation. Trauma was induced in exposed right parietal cortex by weightdrop in anesthetized Wistar rats (n = 24). Of the traumatized rats, 12 were PMN-depleted with vinblastine sulfate i.v. Controls were 12 normal rats and 5 sham-operated rats (craniotomy). Sections of traumatized and contralateral hemispheres were analyzed for myeloperoxidase (MPO) activity. Brain MPO activity was increased fivefold at 24 h posttrauma, but only in the traumatized hemisphere (0.448 ± 0.133 U/g vs 0.090 ± 0.022 U/g in trauma vs normal, respectively, p < 0.05, mean ± SEM). PMN depletion attenuated this increase in MPO activity and decreased circulating PMN counts (0.07 ± 0.032 × 109/L vs 0.894 ± 0.294 × 109/L PMN-depleted–trauma vs trauma rats, respectively, p < 0.05). Leukocyte accumulation in the brain posttrauma was confirmed by MPO assay. Inhibition of MPO activity in the PMN-depleted group and the specificity of vinblastine treatment for depletion of circulating PMN suggest that leukocyte accumulation in the brain at 24 h posttrauma is largely due to PMN.