摘要
目的探讨乌司他丁对改善心脏骤停后综合征全身炎征反应的有效性。方法本研究采用前瞻、随机、对照等方法,对收入ICU的心脏骤停自主循环恢复(ROSC)后的昏迷患者(≥18岁)共40例进行研究。将患者随机分为综合治疗组(Z组:20例)和综合治疗+乌司他丁组(U组:20例),乌司他丁30万U/d,连续3d,两组均行心脏骤停后综合治疗,并于ROSC后1(使用乌司他丁前)、6、24、48、72h各时间点收集并比较两组患者临床资料、APACHEⅡ评分、INF-α、IL-6。结果两组患者在使用乌司他丁治疗前的临床资料、APACHEⅡ评分、INF-α、IL-6比较,差异无统计学意义(P>0.05);两组患者在6、24、48、72h的INF-α、IL-6浓度比较,U组均明显优于Z组,差异有统计学意义(P<0.05));两组患者在治疗72h时APACHEⅡ评分差异有统计学意义(P<0.05)。结论乌司他丁干预治疗对心脏骤停后综合征全身炎征反应有积极作用,所选用的治疗剂量和给药方法尚有待进一步探讨。
Objective To investigate the effect of ulinastatin on the improvement of systemic inflammatory response after post-cardiac arrest syndrome. Methods 40 cases of coma adult patients (≥ 18 years old) admitted to ICU with cardiac arrest of resumption of spontaneous circulation (ROSC) were investigated by prospective, randomized, and controlled method. They were randomly divided into comprehensive treatment group (Z group:20 cases) and comprehensive treatment+the ulinastatin group (300 000 U/day for three days;U group:20 cases ) .Both groups had PCAS comprehensive treatment. After ROSC, clinical data was collected at l hour (before using nlinastatin), after using ulinastatin at 6 hour, 24 hour, 48 hour and 72 hour.APACHE I score,levels of INF-α and IL-6 were compared between the two groups. Results APACHE Ⅱ score,levels of INF-α and IL-6 showed no significance between two groups before using ulinastatin significant(P 〉0.05), but the levels of INF-α and IL-6 at 6 hour, 24 hour, 48 hour and 72 hour after using ulinastatin were significantly above the indexes in the U group, significantly higher than those of the Z group (P〈O.05). The APACHE Ⅱ score at 72 hour was also significantly different between two groups (P〈0.05). Conclusions The ulinastatin intervention treatment for systemic inflammatory response after post-cardiac arrest syndrome has positive effect, but the therapeutic doses and dosage regimen remain need to be further studied.
出处
《热带医学杂志》
CAS
2012年第11期1344-1346,1349,共4页
Journal of Tropical Medicine
关键词
乌司他丁
心脏骤停后综合征
全身炎征反应
药物疗法
ulinastatin
post-cardiac arrest syndrome
systemic inflammatory response
pharmacotherapy