ANTINEUTROPHIL ANTISERUM REDUCES INFARCT VOLUME AFTER MOUSE PERMANENTMIDDLE CEREBRAL-ARTERY OCCLUSION WITHOUT PRODUCING NEUTROPENIA

Accumulation of neutrophils during ischemia has been suggested to play a role in the pathogenesis of ischemic brain injury. It has been repo rted that an anti-rat antiserum that depletes peripheral neutrophils r educes neuronal damage after reversible occlusion of the rat middle ce rebral artery (MCA). We have investigated the effects of this same ant iserum in mouse following permanent occlusion of the middle cerebral a rtery. Administration of the anti-neutrophil antiserum (0.2 ml, ip) ju st after occlusion of the MCA resulted in a significant reduction in l esion volume 24 hrs after the occlusion. The lesion was reduced from 2 8.0 +/- 1.1 mm3 in normal serum treated mice to 16.7 +/- 2.4 mm3. Inje ction of normal serum did not affect the size of the lesion relative t o an injection of saline (26.0 +/- 3.0 mm3). The magnitude of this pro tection was similar to that reported in the rat. However, in distincti on to rats, the antiserum did not substantially reduce the number of p eripheral neutrophils. This suggests that some other property of this antiserum is responsible for its neuroprotective effect.