急性脑血管病应激状态下外周血皮质醇、淋巴细胞和T细胞亚群的变化

目的：探讨急性脑血管病患者应激状态下外周血皮质醇、淋巴细胞和T细胞亚群的变化及临床意义。 方法：将70例急性脑血管患者分为有应激反应组(A组，34例)和无应激反应组(B组，36例)，同时设立正常对照组(C组，38例)。应用IMMULITE自动定量免疫分析仪、HCP5200全自动血球分析仪及FACScalibur流式细胞仪检测外周血皮质醇、淋巴细胞及T细胞亚群。 结果：A组外周血皮质醇高于B组和C组(P<0.001)；A和B组外周血淋巴细胞绝对值、百分比低于C组(P<0.001)；A组淋巴细胞百分比与B组比较差异有显著性(P<0.01)；A组T细胞免疫功能失衡，CD4⁺和CD4⁺/CD8⁺降低，CD8 ⁺升高，B组无T亚群紊乱； 血皮质醇与淋巴细胞绝对值、百分比、CD4⁺以及CD4⁺/CD8⁺ 均呈负相关趋势，但仅与淋巴细胞百分比的相关有统计学意义(r=0.356，P=0.002)。 结论：急性脑血管病患者发病后机体存在严重的细胞免疫功能紊乱，与应激反应及程度有关；肾上腺质激素升高不是引起细胞免疫功能紊乱的惟一因素，可能还存在其他作用机制。

Changes of peripheral blood cortisol lymphocytes and T lymphocytes subsets in patients with acute cerebrovascular diseases in state of stress

Objective To investigate the changes of peripheral blood cortisol,lymphocytes count and percent,T lymphocytes subsets in patients with acute cerebrovascular diseases (ACVD) in a state of stress and the effect of cortisol on these immune markers so as to discuss the mechanism of cell-mediated immunity disorders. Methods Seventy ACVD patients were divided into two groups according to with stress reaction (group A,n=34) or without stress reaction (group B, n=36),while a normal control group (group C,n=38) was set up.Cortisol level,lymphocyte count and percent, T lymphocytes subsets (CD4~ , CD8~ , CD4~ /CD8~ ) were measured by IMMULITE automated quantitative immunoassay analyzer,HCP5200 whole blood cell auto-analyzied machine and FACS calibur fluid cell machine (direct immunofluroscent staining technique). Results The level of cortisol increased markedly in group A compared with those in group B and Group C (P<0.001). Lymphocyte count and percent decreased obviously in group A and B compared with group C (P<0.001), moreover, the lymphocyte percent in group A was significently decreased than that in group B (P<0.001). There were severe disorder of T lymphocyte subsets in group A with stress reaction.CD4~ ,CD4~ /CD8~ were remarkedly decreased, while CD8~ was obviously increased.Especially, although CD4~ ,CD4~ /CD8~ also slightly decreased in group B without stress reaction as compared with group C and normal control, there was not statistical significence (P>0.05). There was a negative correlation between cortisol and lymphocyte percent (r=-0.356, P=0.002).There were not statistical correlation between cortisol and other immune markers. Conclusion There exsits decline of cell immune function in ACVD both with stress and without stress, which may be assiociated with the degree of stress reaction and the level of periphral blood cortisol. Cortisol is not the only factor of cell-mediated immunity unbalance after ACVD, there may be other mechanisms that need better study.