INTRACELLULAR CALCIUM AND PATHOPHYSIOLOGICAL CHANGES IN CEREBRAL-ISCHEMIA

被引:0
作者
GREENBERG, JH [1 ]
UEMATSU, D [1 ]
ARAKI, N [1 ]
REIVICH, M [1 ]
机构
[1] UNIV PENN,CEREBROVASC RES CTR,36TH & HAMILTON WALK,PHILADELPHIA,PA 19104
来源
ARZNEIMITTEL-FORSCHUNG/DRUG RESEARCH | 1991年 / 41-1卷 / 3A期
关键词
CALCIUM; INTRACELLULAR; CALCIUM CHANNELS; BLOCKERS; CAS-66085-59-4; CAS-77086-21-6; DIZOCILPINE; ISCHEMIA; CEREBRAL; NIMODIPINE;
D O I
暂无
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The role of calcium as a mediator in neuronal death during ischemia is now quite strong. Evidence supporting this link included studies in cell cultures, measurements of calcium accumulation in the mitochondria during ischemia as well as direct measurements of shifts in extracellular calcium using microelectrodes. Since high concentrations of intracellular free calcium have been hypothesized to lead to neuronal damage, direct in vivo measurements of this parameter in ischemia are important. The studies outlined demonstrate that changes in intracellular free calcium occur in focal ischemia and describe the time course of these changes. They indicate that cellular damage can be attenuated by the use of agents that block calcium channels (both voltage-sensitive and receptor-operated) and support the concept that these agents owe their beneficial effects to their ability to reduce the accumulation of intracellular calcium.
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页码:324 / 332
页数:9
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