静脉滴注尼莫地平治疗急性缺血性脑梗死

发病７２ｈ内的急性缺血性脑梗死６０例，分为２组。尼莫地平组３０例（男性２１例，女性９例；年龄５９±ｓ１０ａ）．ｗｋ１，２给支持疗法（脱水剂、维生素Ｃ等）和尼莫地平２ｍｇ／ｄ于５％葡萄糖液５００ｍＬ内静脉滴注，ｗｋ３，４改用扩容、改善微循环、细胞活性药，ｗｋ１－４口服尼莫地平６０ｍｇ，ｑｎ。对照组３０例（男性２３例，女性７例；年龄５８±９ａ），不给尼莫地平，其余同上。４ｗｋ后，前组神经功能缺损积分值较后组下降显著（Ｐ＜０．０１），与病情轻重、病灶大小、治疗早晚无关。＊Ｐ＜０．０１。讨论作者采用临床对照研究，静滴尼莫地平治疗发病７２ｈ内的缺血性脑梗死，无论病情分级或总体疗效，治疗前后的神经功能缺损的积分差，与对照组比较，差别均有非常显著意义（Ｐ＜０．０１），提示尼莫地平对急性缺血性脑梗死的近期疗效肯定。但是深部小梗死灶引起的中、重型患者，２组疗效差别无显著意义，可能与小梗死灶病理变化轻，不能充分发挥尼莫地平的阻止钙内流和细胞膜崩解、保护半暗带等作用有关［４］。动物模型局灶性脑缺血３０ｍｉｎ后开始用尼莫地平治疗即不能增加局部脑血流量［５］。用不同剂量的尼莫地平治疗发病４８ｈ内的急性脑梗死１０６４例，发现只有１２０?

Treatment of acute ischemic cerebral infarction with intravenous nimodipine

Sixty patients with acute ischemic cerebral infarction within 72 h were equally divided into 2groups.The nimodipine group 30 patients(M 21,F 9;age 59±s10 a) received nimodipine 2 mg/d intravenous infusion based on supported therapy(dehydrant,vit C)in 1-2 wk,oral nimodipine 60 mg every evening in 1-4 wk.Supported therapy was altered to improve hemodilution,microcirculation,and nervous cell activator in 3-4wk.Control group 30 patients(M23,F7,age 58±9 a) received only supported therapy.Irrespective of condition of patients or size of infarction, nervous functional defect scores of the nimodipine group decreased more than those of the control group(P<0.01).The effects of nimodipine showed no difference between those within 30h after onset and those within 31-72h.