Brain Regional Pharmacokinetics of 11C-Nimodipine in Patients with Acute Stroke: A Preliminary Account of a Positron Emission Tomographic Study

1991 
There are probably several explanations for the extraordinary sensitivity of the human brain to ischemia . An increased free intracellular calcium level is believed to promote the development of secondary damage after an acute ischemic event in the brain [4, 8]. The level of intracellular free calcium is normally regulated within extremely narrow limits, and this narrow regulation makes it possible to use Ca2+ ion as a mediator of intracellular signals and thereby as a regulator of intracellular chemical activity. The intracellular level is regulated both via pump mechanisms to the exterior and also via intracellular sequestration mechanisms (storing in mitochondria and endoplasmic reticulum). The regulation is in part directly energy dependent (Na+/Ca2+ ATPase) but mostly indirectly via the electroneutral Na+/Ca2+ antiporter [10].
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