论文部分内容阅读
目的:观察金尔伦对急性脑梗死患者血浆β—内啡肽(β—EP)的影响及临床疗效。方法:49例急性脑梗死患者根据入院的先后顺序随机进入金尔伦组(25例)和常规治疗组(24例)。金尔伦组在常规治疗的基础上加金尔伦2mg静脉滴注,每日一次,连续14d。两组在用药前后均测定血浆β—EP含量,并观察其肢体功能的改变。结果:金尔伦组、常规治疗组和健康对照组治疗前血浆β—EP含量分别为(731.5±20.4)pg/L、(728.0±21.8)pg/L和(537.8±21.7)pg/L、治疗后分别为(563.7±24.2)pg/L和(631.4±23.6)pg/L。此外,临床症状和神经功能缺损的改善,金尔伦组均优于常规治疗组(P<0.01)。结论金尔伦可拮抗急性脑梗死患者β—EP的生物效应,改善临床症状。
Objective: To observe the effect of Huron on plasma beta-endorphin (β-EP) in patients with acute cerebral infarction and its clinical efficacy. Methods: Forty-nine patients with acute cerebral infarction were randomly divided into Hurun group (n = 25) and conventional treatment group (n = 24) according to the order of admission. The group of Huron was treated with intravenous infusion of 2mg per day on the basis of routine treatment, once a day for 14 days. Both groups were measured before and after treatment of plasma β-EP content, and observe the changes in limb function. Results: The plasma levels of β-EP before treatment in Jinren group, routine treatment group and healthy control group were (731.5 ± 20.4) pg / L, (728.0 ± 21.8) pg / L and 537.8 ± 21.7 pg / L, respectively, and were 563.7 ± 24.2 pg / L and 631.4 ± 23.6 pg / L, respectively. In addition, the improvement of clinical symptoms and neurological deficits was better in the Huron group than in the conventional treatment group (P <0.01). Conclusion Huron can antagonize the biological effects of β-EP in patients with acute cerebral infarction and improve the clinical symptoms.