| Cerebral ischemic and reperfusion injury result form a number of reasons including shock, trauma, cerebral blood clot or cardiac arrest. It results from an inadequate blood supply to the brain which can be further exacerbated during the reperfusion period when blood flow resumes. It is important to understand the mechanisms involved during this process so that therapeutic interventions be directed at reducing the resulting injury.; White blood cells (leukocytes) are competent scavengers of tissue debris and are a vital component of the proinflammatory response generated during ischemia and reperfusion. Their role in this injury process has also been shown to be deleterious as well as beneficial in the heart, skeletal muscle and intestine. Leukocytes may contribute to this increased injury by either physically plugging the vasculature or by the release of chemical mediators which result in increased damage. It was the purpose of this study to determine if white blood cells contribute to the injury which results from ischemia and reperfusion in the brain.; Control and vinblastine-induced leukopenic rats were compared using a model of global forebrain ischemia with reperfusion in the rat. Somatosensory evoked potentials (SSEP), EEG activity, and TTC defined cerebral infarcts were compared as indices of functional cortical damage. In addition, pentoxifylline, a drug shown to increase leukocyte deformability and function was tested along with controls on influencing SSEP and EEG activity following cerebral ischemia and reperfusion.; Results indicate that white blood cells contribute to the injury that results from cerebral ischemia and reperfusion. This was indicated by a preservation of the SSEP and EEG activity as well as a reduction in the cerebral infarct size in the leukopenic rats. The preservation of cortical functional damage also indicated a therapeutic potential for Pentoxifylline along with implicating a white blood cell mechanism for its effect. |
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