静脉溶栓联合亚低温治疗对急性脑梗死患者疗效及可能作用机制的研究

目的观察重组人组织型纤溶酶原激活剂(recombinant tissue plasminogen activator,rt-PA)静脉溶栓联合亚低温治疗急性脑梗死患者的疗效,探讨该方案治疗的可能作用机制。方法纳入60例急性脑梗死患者,随机分为3组,各20例:1对照组:rt-PA静脉溶栓;2治疗组1:静脉溶栓联合局部亚低温治疗12 h;3治疗组2:静脉溶栓联合局部亚低温治疗24 h。记录各组患者治疗前后神经功能缺损量表(National institute of health stroke scale,NIHSS)评分,颅内压(intracranial pressure,ICP)变化,记录溶栓后并发症,并随访患者3个月的改良Rankin量表(modified Rankin scale,MRS)评分。收集患者溶栓前后血液样本,检测血浆中超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA)的水平。结果治疗后3个月治疗组1和治疗组2 MRS评分低于对照组(P0.05),其中治疗组2 MRS评分低于治疗组1(P0.05)。治疗72 h、7 d治疗组2 ICP较对照组降低,治疗7 d治疗组2 ICP低于治疗组1(P0.01)。治疗组1和治疗组2治疗24 h、72 h、7 d MDA浓度较溶栓前降低(P0.01),SOD浓度较溶栓前增高(P0.05)。治疗24 h、72 h、7 d治疗组1和治疗组2 MDA浓度较对照组均降低(P0.05),SOD浓度高于对照组(P0.05)。治疗72 h、7 d治疗组2 MDA浓度低于治疗组1(P0.01),治疗后7 d治疗组2 SOD浓度高于治疗组1(P0.05)。各组不良事件发生率及病死率差异无统计学意义(P0.05)。结论 rt-PA静脉溶栓联合亚低温治疗可改善脑梗死患者预后,静脉溶栓联合亚低温治疗24 h效果较12 h更优,未增加不良反应发生率,其作用机制可能是通过减轻患者氧化应激反应来实现的。

Clinical effect and possible mechanism of intravenous thrombolysis combined with mild hypothermia on acute cerebral infarction

Objective To examine the effects of intravenous thrombolysis with Tissue-type plasminogen activator (rt-PA) combined with mild hypothermia therapy on patients with acute cerebral infarction and further investigate under?lying mechanism for the treatment of cerebral infarction. Methods Sixty cases of cerebral infarction patients were random?ly divided into three groups with 20 patients in each group:①The control group was given rt-PA intravenous thromboly?sis;②The treatment group 1:intravenous thrombolytic therapy combined with local mild hypothermia treatment for 12 h;③The treatment group 2:intravenous thrombolytic therapy and local mild hypothermia in the treatment of 24 h. We col?lected NIHSS score before and after thrombolytic therapy, patient monitoring (ICP) changes during thrombolytic therapy, March (MRS) score and complications during follow-up after thrombolysis, The serum levels of SOD and MDA were as? sessed before and after thrombolytic therapy. Results NIHSS score was lower in both treatment group 1 and treatment group 2 than in the control group (P<0.05) at 72 h, 7 d, 14 d after thrombolysis. MRS was lower in both treatment group 1 and treatment group 2 than in the control group (P<0.05) at 3 months after thrombolytic therapy. MRS were lower in treat?ment group 2 than in the treatment group 1 (P<0.05). ICP in treatment group 1 and the concentration of MDA in treat?ment group 2 were lower, compared with control group (P<0.05) at 24 h, 72 h and 7 d after thrombolysis. ICP was lower in treatment group 2 than treatment group 1 at 7d after thrombolysis. The concentration of SOD was higher in treatment groups than in control group (P<0.05) at 24, 72 h and 7d after thrombolysis. ICP and MDA concentration were lower in treatment group 2 than in treatment group 1(P<0.05) at 72h and 7d after thrombolysis. The concentration of SOD was higher in treatment group 2 than in the treatment group 1 at 7 d after thrombolysis (P<0.05). There was no significant dif?ference in adverse events and mortality among groups (P>0.05). Conclusion Rt-PA intravenous thrombolysis combined with mild hypothermia treatment can improve the prognosis of patients with cerebral infarction without increasing the inci?dence of adverse reactions. In addition, thrombolysis combined with mild hypothermia 24 h has better effect than with mild hypothermia 12 h. The beneficial effects may be accomplished by reducing oxidative stress reaction.