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      Recovery of integrative central nervous function after one hour global cerebro-circulatory arrest in normothermic cat.

      Journal of the Neurological Sciences
      Animals, Brain, metabolism, pathology, Brain Ischemia, physiopathology, Cats, Central Nervous System, Cerebrovascular Circulation, Electroencephalography, Female, Follow-Up Studies, Nerve Tissue Proteins, biosynthesis, Xenon Radioisotopes, diagnostic use

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          Abstract

          Functional and metabolic recovery of a female cat is described which survived for 1 year following 1 hour global cerebro-circulatory arrest at normothermia. Ischemia was produced by intrathoracal occlusion of the innominate, the left subclavian and both mammary arteries. Following ischemia the animal was kept under intensive care for 46 h. EEG and evoked potentials began to recover after 3 h following ischemia, and spontaneous respiration returned promptly on the 2nd day when the animal was weaned from the respirator. The neurological deficit score declined from a maximum of 395 immediately after ischemia to 158 during the first week and to 40 within 4 weeks. At this time the animal was slightly ataxic but she was able to walk and to feed and clean herself. One year after ischemia EEG and evoked potentials were normal. Morphological studies and the autoradiographic evaluation of protein biosynthesis revealed an almost normal pattern in cortical structures but there was almost complete atrophy of dorsal hippocampus and striatum leading to enlargement of the ventricular system. These observations demonstrate that despite these lesions the central nervous system is able to recover integrative neurological function after cerebro-circulatory arrest in normothermia of as long as 1 h.

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          Calcium overload in selectively vulnerable neurons of the hippocampus during and after ischemia: an electron microscopy study in the rat.

          Light and electron microscopy has been used to study the cytopathological changes in the rat hippocampus directly after a 30-min period of forebrain ischemia and after 30 or 120 min of reperfusion. The fine structural localization of calcium has been demonstrated using the oxalate/pyroantimonate procedure. Cellular changes considered typical of ischemia (swelling of astrocytic processes, distention of mitochondria, condensation of cytoplasm, "ischemic cell change") are most prominent after 30 min of reperfusion. At this time, dense calcium pyroantimonate deposits are evident in swollen mitochondria in pyramidal and hilar neurons. After 120 min of reperfusion, substantial restitution has occurred; most mitochondria appear normal and there are few calcium deposits. However, a small number of selectively vulnerable neurons (hilar and pyramidal neurons) show dense condensation (ischemic cell change) with multiple vacuoles containing calcium deposits. The role of excessive calcium entry and mitochondrial calcium overload during the reperfusion period in determining the death of selectively vulnerable neurons is discussed.
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            Regional Cerebral Blood Flow in Man Determined by the Initial Slope of the Clearance of Intra-arterially Injected l33Xe

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              Recovery of monkey brain after prolonged ischemia. I. Electrophysiology and brain electrolytes.

              Adult normothermic monkeys were submitted to 1 h of total cerebral ischemia, followed by blood recirculation for 1.5-24 h. During ischemia EEG and evoked potentials were suppressed within 12 s and 3 min, respectively. Upon recirculation, high-voltage EEG bursts began to reappear after 82-125 min, followed by gradual return of continuous background activity and near normalization of EEG frequency pattern within 24 h. Somatically evoked potentials, in contrast, exhibited only partial recovery, and consciousness did not return during the observation period. At the end of the experiments, tissue contents of sodium, potassium, calcium, and magnesium were measured in the gray and white matter of parietal lobe by atomic absorption spectroscopy. Gray matter sodium content gradually increased by approximately 50% from 41.0 to 59.8 mumol/g wet wt during 24 h of recirculation. The other electrolytes including calcium did not change during the observation period. Postischemic recovery reported in this and the accompanying article is attributed to careful control of postischemic general physiological state and prevention or treatment of postischemic complicating side effects such as postischemic brain edema, hypotension, acidosis, pulmonary distress, and anuria. No specific drug treatment such as application of calcium antagonists or metabolic inhibitors was necessary to achieve this effect.
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