摘要目的 探讨急性脑梗死(ACI)诱发全身炎症反应综合征(SIRS)及多器官功能障碍综合征(MODS)的发生率,以及血清中超氧化物岐化酶(SOD)含量变化在ACI诱发SIRS及MODS中的作用机制及临床意义. 方法 选取自2006年1月至2008年6月菏泽市立医院神经内科住院及门诊就诊的68例ACI患者.分为3组,其中急性单纯性脑梗死36例(SACI组),ACI诱发SIRS患者(SIRS组)32例,ACI诱发MODS患者(MODS组)24例,采用黄嘌呤氧化酶法测定血清SOD含量,另设28例到本院查体的健康人为正常对照组(NC组). 结果 (1)本组SACI诱发SIRS的发生率为88.9%,诱发MODS的发生率为66.7%;ACI诱发SIRS时MODS的发生率为75.0%.ACI诱发MODS时100%发生SIRS.(2)各组之间SOD含量比较差异有统计学意义(P<0.05),且血清SOD含量水平依次为MODS组<SIRS组<SACI组<NC组.ACI致MODS严重者(积分≥9分1血清SOD含量低于病情较轻者(积分<9分),差异有统计学意义(P<0.05);ACI致MODS死亡患者血清SOD含量低于存活患者,差异有统计学意义(P<0.05). 结论 (1)ACI易诱发SIRS,进而导致MODS的发生;(2)血清SOD水平可做为判断ACI诱发SIRS、MODS病变程度,预后及转归的一项指标.

abstractsObjective To investigate the incidences of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) in patients with acute cerebral infarction (ACI) and explore the role of serum superoxide dismutase (SOD) content in ACI-induced SIRS and its progression to MODS. Methods Sixty-eight ACI patients were in hospital and outpatient at the Heze Municipal Hospital from Jan.2006 to Jun.2008, including 36 with uncomplicated ACI (SACI group), 32 with ACl-induced SIRS (SIRS group), and 24 with ACI-induced MODS (MODS group) were enrolled in this study, with 28 healthy individuals from the hospital as the normal control group. Xanthine oxidase method was used to measure the serum SOD content in these subjects. Results SACI induced SIRS and MODS in 88.9% and 66.7% of these patients, respectively; in the ACI patients with SIRS, 75.0% had concurrent MODS, while all the patients with MODS showed the presence of SIRS. The serum SOD contents in patients with SACI, SIRS, and MODS were significantly lower than those in the normal control group (P<0.05). Patients with SIRS and MODS had significantly lower serum SOD contents than the SACI patients (P<0.05), and the MODS patients had significantly lower levels than the SIRS patients (P<0.05). The serum SOD content was significantly lower in patients with severe MODS (with a score no less than 9) than in those with milder MODS (with a score below 9) (P<0.05), and also significantly lower in fatal MODS cases than in surviving MODS cases (P<0.05). Conclusion ACI may initially trigger the occurrence of SIRS and then lead to MODS, and the abnormalities in serum SOD content in patients with ACI-induced SIRS can be a possible mechanism of MODS following ACI. The serum SOD levels may help estimate the severity of ACI-induced SIRS and MODS, and may serve as an indicator for predicting the prognosis and outcomes of the patients.