Cardiac arrest-induced complete cerebral ischaemia in the rat: dynamics of postischaemic in vivo calcium uptake and protein synthesis.

Dynamics of pathological changes following cardiac arrest induced cerebral ischaemia were related to the findings of double tracer autoradiography of 45Ca and 3H leucine uptake as respective indicators of ischaemic injury and metabolic disturbance. Abnormal calcium accumulation, determined by 45Ca uptake, was related to injured but still living neurons and to reactive glial elements. 45Ca autoradiography confirmed a high sensitivity to neuronal injury of the nucleus reticularis thalami (NRT), hippocampal CA1 pyramidal layer, inferior colliculus, ventral thalamic nucleus (VTN), caudate nucleus, and parietal cortex. 3H leucine incorporation revealed that an initially widespread inhibition of protein synthesis was followed by its considerable recovery. Observations concerning hippocampal CA1 sector and VTN suggested that a significant degree of protein synthesis, maintained at the late stage after postischaemic recovery, was related to survival and regeneration of neurons and not to the presence of glial elements.