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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?
60 cases of acute ischemic cerebral infarction in 72 hours, divided into two groups. Nimodipine group 30 patients (21 males and 9 females; age 59 ± s10a). wk1, 2 to supporting therapy (dehydration agent, vitamin C, etc.) and nimodipine 2mg / d in 500% glucose solution 500mL intravenous drip, wk3,4 switch to expansion, improve microcirculation, cell active drugs, wk1-4 Oral nimodipine 60mg, qn. Control group of 30 patients (23 males and 7 females; age 58 ± 9a), not to nimodipine, the rest ibid. After 4wk, the integral value of neurological deficit in the former group decreased significantly compared with the latter group (P <0.01), which was not related to the severity of the disease, the size of the lesion, and the treatment sooner or later. * P <0.01. Discussion The authors used a controlled clinical study of intravenous nimodipine within 72 hours of onset of ischemic cerebral infarction, regardless of disease grade or overall efficacy, neurological deficits before and after treatment, poor points, compared with the control group, the difference was significant (P <0.01), suggesting that nimodipine for the treatment of acute ischemic cerebral infarction in the near future. However, there were no significant differences between the two groups in the medium and heavy type of patients caused by deep small infarction, which may be related to the small pathological changes of small infarcts, which can not fully exert the effect of preventing nimodipine from preventing calcium influx and cell membrane disintegration and protecting the penumbra The role of [4]. Animal models of focal cerebral ischemia after 30min started with nimodipine treatment that can not increase the local cerebral blood flow [5]. With different doses of nimodipine in the treatment of acute cerebral infarction within 48h 1064 cases found that only 120?