Effect of nimodipine on cerebral functional and metabolic recovery following ischemia in the rat brain.

Effect of nimodipine on cerebral functional and metabolic recovery following ischemia in the rat brain.
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尼莫地平对大鼠脑缺血后脑功能和代谢恢复的影响。

DOI:
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发表时间:
1986
期刊:
影响因子:
8.3
通讯作者:
M. Ohno
M. Ohno
中科院分区:
医学1区
文献类型:
--
作者:
H. Mabe;H. Nagai;T. Takagi;S. Umemura;M. Ohno

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检查钙进入阻滞剂尼莫地平是否能防止缺血时游离脂肪酸浓度升高和代谢紊乱,并促进再循环后的功能和代谢恢复。四支血管闭塞伴轻度低血压引起大鼠严重前脑缺血。缺血30分钟后,通过移除动脉夹和将血压升高到缺血前水平来开始再循环。尼莫地平治疗组脑电图再循环后活动恢复优于对照组。在缺血期间,实验组和对照组之间游离脂肪酸的积累和ATP的消耗没有显著差异。再循环后120分钟,治疗组ATP水平的恢复明显好于对照组。因此,我们认为尼莫地平促进功能和代谢恢复不是由于防止游离脂肪酸的积累,也不是由于缺血期间ATP的消耗,而是由于改善缺血后低灌注或直接作用于再灌注期间的代谢过程。
Whether the calcium entry blocker, nimodipine, prevents the increase in the concentration of free fatty acids and metabolic disturbances during ischemia and promotes functional and metabolic recovery after recirculation were examined. Severe forebrain ischemia in rats was induced by four-vessel occlusion with mild hypotension. After 30 minutes of ischemia, recirculation was started by removal of the arterial clamps and by increasing blood pressure to the preischemic level. Recovery of EEG activity following recirculation was better in the nimodipine-treated group than in the control group. During the ischemic period, there were no significant differences in accumulation of free fatty acids or in depletion of ATP between treated and control groups. At 120 minutes following recirculation, recovery of the ATP level was significantly better in the treated group than in the control group. Therefore, the promotion of functional and metabolic recovery by nimodipine-treatment is suggested to be not due to the prevention of an accumulation of free fatty acids nor to the depletion of ATP during the ischemic period, but to either improvement of postischemic hypoperfusion or a direct action on metabolic processes during reperfusion period.
DOI: --
发表时间: 1982-05
期刊: Pathologie-biologie
影响因子: --
作者:
T. Wieloch;B. Siesjö
通讯作者: T. Wieloch;B. Siesjö
脑缺血中的离子转移。
DOI: 10.1016/0024-3205(82)90473-8
发表时间: 1982
期刊: Life sciences
影响因子: 6.1
作者:
Yanagihara,T;McCall,JT
通讯作者: McCall,JT