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Intracellular calcium and pathophysiological changes in cerebral ischemia
J H Greenberg1, D Uematsu, N Araki
1Cerebrovascular Research Center, University of Pennsylvania, Philadelphia.
Arzneimittel-Forschung
|March 1, 1991
Summary
Calcium influx contributes to neuronal death during ischemia. Blocking calcium channels in vivo can reduce this cellular damage, highlighting calcium
Area of Science:
- Neuroscience
- Cell Biology
- Ischemic Stroke Research
Background:
- The link between calcium and neuronal death during ischemia is well-established.
- Previous evidence includes in vitro studies and mitochondrial calcium accumulation measurements.
- Direct in vivo measurements of intracellular free calcium during ischemia are crucial.
Purpose of the Study:
- To directly measure in vivo changes in intracellular free calcium during focal ischemia.
- To investigate the time course of these calcium shifts.
- To assess the efficacy of calcium channel blockers in mitigating ischemic neuronal damage.
Main Methods:
- Direct in vivo measurements of intracellular free calcium using microelectrodes during focal ischemia.
- Utilized studies involving calcium channel blockers (voltage-sensitive and receptor-operated).
Main Results:
- Demonstrated significant changes in intracellular free calcium levels during focal ischemia.
- Characterized the temporal dynamics of these calcium alterations.
- Showed that cellular damage could be attenuated by calcium channel blockers.
Conclusions:
- Intracellular calcium accumulation is a key mediator of neuronal damage in focal ischemia.
- Calcium channel blockers are effective in reducing ischemic neuronal injury.
- The beneficial effects of these agents are attributed to their ability to limit intracellular calcium overload.