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PubMedDate not supplied

Postischemic reperfusion causes a massive calcium overload in the myelinated spinal cord fibers.

The visualization of Ca binding in the myelinated axons of lumbosacral segments of rabbit was done at the electron microscopic level using the spinal cord ischemia model. To assess the calcium accumulation, the binding agent pyroantimonate was used. Nonsignificant Ca2+ binding was found in the myelinated axons after 40 min of ischemia followed immediately by perfusion fixation. A high concentration of calcium pyroantimonate deposits, seen as electron dense particles, was detected in the myelin interlamellar clefts and axoplasm. The paranodal region was the most affected site.

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PubMedDate not supplied

Short-term postischemic hypoperfusion improves recovery of protein synthesis in the rat brain cortex.

A cell-free system from rat brain cortex was used to follow changes in protein synthesis after ischemia and reperfusion (four-vessel occlusion). The experiment was focused to prevent a violent burst of free oxygen radicals creation during the first period of postischemic reperfusion by short-term hypoperfusion. After 30 min of ischemia, the authors applied hypoperfusion produced by releasing one (right) carotid for the first 5 min of reperfusion lasting from 30 min to 3 d. Results obtained by this procedure show that the activity of protein synthesis machinery from hypoperfused brains is higher than normovolemic ones; the left hemisphere, which is contralateral to direct blood flow during hypoperfusion, shows better results than the right hemisphere.

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