Application of rhIL-1 beta augmented the increase of brain water content, and application of anti-IL-1 beta depressed the increase of water content. These results tended to correlate with the neutrophilic infiltration into the parenchyma. It thus appears that IL-1 beta may play an important role in ischemic brain damage after reperfusion.
Background and Purpose Neutrophils have been implicated in the pathogenesis of ischemia-reperfusion injury. The aim of the present study was to evaluate the correlation between neutrophil infiltration into ischemic tissues and brain injury after transient focal ischemia.Methods We evaluated the effects of depletion of circulating neutrophils by administration of an antineutroph.il monoclonal antibody (RP3) on brain edema formation, infarct size, and neutrophil infiltration (myeloperoxidase [MPO]-quantified) in rats with 1 hour of middle cerebral artery (MCA) occlusion.Results In the cerebral cortex perfused by the anterior cerebral artery (ACA area), there was a significant increase in MPO activity only 24 hours (P<.05) after reperfusion. In the cerebral cortex perfused by the middle cerebral artery (MCA area) and caudate putamen, MPO activity was significantly increased at 12 (MCA area, P<.01; caudate putamen, P<.05),
We describe a new focal ischemia model consisting of unilateral middle cerebral artery occlusion with a silicone rubber cylinder attached to a nylon surgical thread inserted through the internal carotid artery in rats. Recirculation was accomplished by pulling the thread out of the artery. We evaluated the reliability of this model and studied the influence of reperfusion of the brain by measuring regional cerebral blood flow in 30 rats and by using conventional neuropathologic methods after different periods of occlusion in 48 rats. The anterior neocortex and the lateral part of the caudate putamen, which were supplied by the occluded middle cerebral artery, were the regions most frequently damaged. After 1 hour of occlusion in five rats, in the cortex supplied by the occluded artery mean±SD blood flow was 0.19±0.08 ml/g/min (approximately 15% of that in the corresponding region of five sham-operated control rats), and mild scattered ischemic cell change was observed. Three (n=5) or six («=5) hours of occlusion reduced blood flow more severely and caused severe ischemic cell changes in the cortex supplied by the occluded artery in proportion to the duration of ischemia. Characteristically, in five rats subjected to 3 hours of occlusion followed by 3 hours of recirculation, blood flow was restored and spongy edematous change was observed in the cortex supplied by the recirculated artery. This change resulted in hypoperfusion of the neighboring cortical region surrounding the recirculated area. Our model should be useful in various investigations of the influence of reperfusion on focal ischemic brain injury. {Stroke 1989;20:1037-1043) R ecirculation affects cerebral ischemia and modifies postischemic events in various ways. Recirculation occurs frequently after spontaneous thrombolysis and break-up of cerebral emboli in a common clinical event. Focal ischemic models induced by occlusion of an intracranial artery, usually the proximal middle cerebral artery (MCA), have been widely studied in various animals such as cats, 1 dogs, 2 squirrel monkeys, 3 and rats. 4 It is difficult to produce reliable recirculation models using the above models because after recirculation cerebral blood flow (CBF) often varies regionally due to spasm or direct mechanical damage to the occluded vascular wail from dipping or ligation and because hemodynamic patterns are also variable due to changes in intracranial pressure caused by craniotomy. On the other hand, after an From the Department of Neurology, Tohoku University, School of Medicine, Sendai, Japan.Supported by a grant-in-aid (for special project Research of Selected Intractable Neurological Disorders) from the Ministry of Education, Science and Culture.Address for correspondence: Dr. Haruo Nagasawa, Department of Neurology, Institute of Brain Diseases, Tohoku University, 1-1 Seiryo-machi, Sendai, 980 Japan.Received August 24, 1987; accepted February 27, 1989. extracranial artery has been occluded without craniotomy, the development of ischemic brain damage can usually be p...
Regional changes in the amount of free fatty acids, polyphosphoinositides, and water content in the cerebral cortex were examined using a middle cerebral artery occlusion model of rats. The amount of various free fatty acids increased as polyphosphoinositides decreased during 3 and 6 hours of ischemia in the occluded middle cerebral artery territory. After 3 hours of reperfusion following 3 hours of ischemia, free fatty acids partially recovered while polyphosphoinositides did not. Water content increased significantly after 3 and 6 hours of ischemia, and a further increase was found after 3 hours of reperfusion following 3 hours of ischemia. The change of polyenoic fatty acids in this occluded middle cerebral artery territory was much smaller than that in the case of decapitation ischemia, although the amounts of polyphosphoinositides and monoenoic and saturated fatty acids showed almost identical changes in both cases, probably because polyenoic fatty acids may be washed out and/or peroxidatively consumed in the middle cerebral artery occlusion model due to its residual blood flow. Changes in the area surrounding the occluded middle cerebral artery territory were similar to the above results, although less dramatic However, there was no change in free fatty acids, polyphosphoinositides, and water content in the contralateral cortex. A novel free radical scavenger (MCI-186), which prevents both nonenzymatic peroxidation and lipoxygenase activity in vitro, markedly attenuated the ischemic and postischemk brain swelling. These results suggest that free radical mechanisms may be involved in ischemk and postischemic brain edema. A peroxidative mechanism has been implicated as one of the detrimental factors in ischemic and postischemic brain cell damage. 1 "4 Since Demopoulos 5 indicated the possibility of free radical damage in ischemic brain, various approaches have been tried in an effort to detect some species of oxygen radicals in the ischemic or postischemic brain. However, all attempts have failed to detect oxygen radicals in vivo and in situ because of their short half-lives and/or because of methodologic difficulties involved in trapping and extracting such radicals.*"" Due to the above reasons, only indirect evidence has been obtained indicating the generation of free radicals during and after ischemia. Such evidence includes decreases in ascorbate (reduced form) and ot-tocopherol and an increase in conjugated dienes. 112 -13 Thus, although no radical species have yet been directly detected, it seems to be widely accepted that a certain species of free radicals may exist and may play a role in ischemic and/or postischemic brain damage. 1 ' 5 There are two pathways generating peroxidative reactions in damaged brain as well as in any tissue. One is an auto-oxidation (nonenzymatic peroxidation) and the other is enzyme-processing peroxidation. Nonenzymatic peroxidations have been artificially generated in vitro using brain slices, and they were shown to induce brain swelling. 14 " 17 Cell damage induced by t...
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