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目的：探讨大鼠脑梗死后急性期肾上腺皮质功能的改变以及地塞米松的干预作用。方法健康雄性SD大鼠60只，随机分为假手术组（对照组）、模型加生理盐水组（安慰剂组）和模型加地塞米松组（治疗组），每组20只。采用改进的线栓法建立大鼠脑缺血模型。治疗组应用小剂量地塞米松（0.8 mg/kg）替代治疗。各组分别于脑损伤后第3、12、24、72 h 4个时间点进行观察。给予小剂量促肾上腺皮质激素（ACTH）行刺激试验，应用ELISA法测定血清皮质酮（CORT）和ACTH含量。结果安慰剂组大鼠脑损伤后3 h外周血CORT和ACTH均明显高于对照组（P＜0.01），随后逐渐降低，72 h又有升高趋势；各时间点ACTH刺激后CORT上升值均低于对照组（P＜0.05或P＜0.01）。治疗组伤后所有时间点CORT均高于安慰剂组（P＜0.01或P＜0.05），ACTH仅24 h高于安慰剂组（P＜0.05）；各时间点ACTH刺激后CORT上升值均高于安慰剂组（P＜0.05或P＜0.01）。结论大鼠脑梗死急性期即存在肾上腺皮质功能不全，随着时间推移，肾上腺储备功能下降，对ACTH反应程度降低。小剂量短疗程肾上腺糖皮质激素可增强肾上腺皮质对ACTH刺激的敏感性。“,”Objective To study the changes in adrenal cortex function and protective effect of dexamethasone following acute cerebral infarction in rats. Methods 60 healthy male SD rats were randomly divided into three groups with 20 rats in each group: sham-operated group (control group), model group plus physiologic saline (placebo group) and model group plus dexamethasone (treatment group). The rat model was established by modified thread occlusion. A low dose of dexamethasone (0.8 mg/kg) was injected into the abdominal cavity 10 minutes after cerebral infarction. The related parameters were detected at four time points, 3 hours, 12 hours, 24 hours and 72 hours after cerebral infarction. The plasma ACTH and corticosterone (CORT) levels were measured after stimulated by 1 μg ACTH. Results The levels of ACTH and CORT at 3 hours of placebo group were increased remarkably compared to the control group (P<0.01), then reduced gradually and raised again at 72 hours post injury. The levels of CORT was lower than the control group at each time point after ACTH stimulation test (P<0.05 or P<0.01). The levels of CORT at each time point of treatment group were increased remarkably compared to the placebo group (P<0.05, P<0.01). However, only at 24 hours the ACTH levels of treatment group increased slightly than the placebo group (P<0.05). The levels of CORT were higher than the placebo group at each time point after ACTH stimulation test (P<0.05, P<0.01). Conclusion Adrenal dysfunction may occur early following acute cerebral infarction in rats, adrenal response to ACTH decreased as time goes by. A low-dose short-course of corticosteroids could increase the sensitivity of adrenal response to ACTH.