To obtain direct evidence of oxygen radical activity in the course of cerebral ischemia under different intraischemic temperatures, we used a method based on the chemical trapping of hydroxyl radical in the form of the stable adducts 2,3-and 2,5-dihydroxybenzoic acid (DHBA) following salicylate administration . Wistar rats were subjected to 20 min of global forebrain ischemia by two-vessel occlusion plus systemic hypotension (50 mm Hg) . Intraischemic striatal temperature was maintained as normothermic (37°C), hypothermic (30°C), or hyperthermic (39°C) but was held at 37°C before and following ischemia. Salicylate was administered either systemically (200 mg/kg, i .p .) or by continuous infusion (5 mM) through a microdialysis probe implanted in the striatum . Striatal extracellular fluid was sampled at regular intervals before, during, and after ischemia, and levels of 2,3-and 2,5-DHBA were assayed by HPLC with electrochemical detection . Following systemic administration of salicylate, stable baseline levels of 2,3-and 2,5-DHBA were observed before ischemia . During 20 min of normothermic ischemia, a 50% reduction in mean levels of both DHBAs was documented, suggesting a baseline level of hydroxyl radical that was diminished during ischemia, presumably owing to oxygen restriction to tissue at that time . During recirculation, 2,3-and 2,5-DHBA levels increased by 2 .5and 2 .8-fold, respectively . Levels of 2,3-DHBA remained elevated during 1 h of reperfusion, whereas the increase in 2,5-DHBA levels persisted for 2 h . The increases in 2,3-and 2,5-DHBA levels observed following hyperthermic ischemia were significantly higher (3.8-and fivefold, respectively) . In contrast, no significant changes in DHBA levels were observed following hypothermic ischemia . The postischemic changes in DHBA content observed following local administration of salicylate were comparable to the results obtained with systemic administration, thus confirming that the hydroxyl radicals arose within brain parenchyma itself . These results provide evidence that hydroxyl radical levels are increased during postischemic recirculation, and this process is modulated by intraischemic brain temperature . Hence, these data suggest a possible mechanism for the effects of temperature on ischemic outcome and support a key role for free radical-induced injury in the development of ischemic School of Medicine, Miami, Florida, U.S.A . 1250 damage . Key Words : Cerebral ischemia-Hydroxyl radicals-Microdialysis-Temperature .
Hemicraniectomy is an effective therapy in patients with malignant infarction of the MCA. However, a hemicraniectomy that is too small in diameter may cause the formation of additional lesions and adversely affect the risk of mortality and the quality of survival. In addition, the size and shape of the edges of the bone defect are important factors relating to its efficacy.
Previous infection has been shown to be a risk factor for acute cerebral ischemia. We tested the hypothesis that recent infection is also a risk factor for intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). We performed a case-control study with 56 consecutive patients with ICH, 44 consecutive patients with SAH, and 56 and 44 neurological control patients, respectively. Infection within 4 weeks was associated with SAH independently of hypertension and smoking (p = 0.049). There was no significant association between infection and ICH. Recent infection, primarily upper respiratory tract infection, may be a risk factor for SAH by contributing to the formation and rupture of aneurysms.
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