Abstract
Publisher Summary It is commonly believed that calcium is intimately involved in the pathogenesis of ischemic damage to the brain. Morphological methods are used to gain insight into the kinetic alterations of calcium in ischemic brain. Using models of rat brain ischemia with reperfusion, intracellular calcium increased only slightly during 30 min of ischemia, but significantly during reperfusion, are reported. The results with forebrain ischemia in gerbils indicate that 30 min ischemia is more than enough to induce calcium overload in both neurons and glial cells. Bilateral carotid arteries of adult Mongolian gerbils were ligated for 5 or 30 min under ether anesthesia. Intracerebral calcium was precipitated as visible salt with the oxalate-pyroantimonate method. In normal brain, calcium deposits looked like small dots adhered onto membraneous structures. After interruption of blood supply, the small calcium deposited vanished gradually, whilst large deposits become visible. The kinetic change of calcium deposits suggested that, besides movement from the extra- to intracellular compartment, free calcium might be released from conjugated state, accelerating the ongoing pathological changes in neurons and glial cells.
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