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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult rhesus monkeys were subjected to complete cerebral ischemia for one hour and subsequent recirculation for up to 24 h. Animals with signs of functional recovery (e.g. spontaneous EEG activity) exhibited a partial replenishment of cellular energy sources (ATP, phosphocreatine) and a progressive normalization of cerebral lactate levels. Glucose and pyruvate concentrations showed a transient increase over control values during the early stages of postischemic recirculation. Monkeys without functional recovery lacked a significant resynthesis of energy-rich compounds; adenine nucleotides continued to decrease and lactate concentrations were higher than in animals subjected to ischemia without recirculation. Cerebral polysome profiles remained unaltered during the ischemic period but in all animals a marked disaggregation of polyribosomes with a concomitant increase in ribosomal subunits occurred after the onset of recirculation. In monkeys with indications of functional recovery these changes were reversible but a normal polysome profile was only observed after 24 h of recirculation. The results obtained indicate a postischemic depression of protein synthesis due to an inhibition of peptide chain initiation. After recirculation of the brain for 3-6 h there was evidence for an induction of enzymes involved in polyamine synthesis (ornithine decarboxylase and S-adenosylmethionine decarboxylase). No changes in the activity of these enzymes were observed at the end of the ischemic period, indicating that during complete cerebral ischemia not only the synthesis but also the catabolism of proteins is inhibited.
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PMID:Resuscitation of the monkey brain after one hour complete ischemia. III. Indications of metabolic recovery. 115 69

Mongolian gerbils were anesthetized with halothane and forebrain ischemia was induced by occluding both common carotid arteries. After 2, 4, 6, 8, or 10 min of vascular occlusion clips were removed and animals allowed to recover for 8 or 24 h. At the end of the experiments animals were reanesthetized and their brains frozen in situ. Tissue samples were taken from the cerebral cortex, striatum, hippocampus, and thalamus for determination of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) activity by measurement of the release of 14CO2 from [14C]ornithine and S-[14C]adenosylmethionine, respectively. A transient increase in ODC activity was found after 8 h of recirculation following cerebral ischemia in all brain structures studied. ODC activity was significantly increased after 8 h of recirculation in the hippocampus of animals subjected to 4 min of ischemia, in the cortex and striatum after 6 min of ischemia, and in the thalamus after 8 min of vascular occlusion. ODC activity had already reached a plateau in the hippocampus after 4 min of vascular occlusion and in the cortex, striatum, and thalamus after 8 min, since there is no further increase in activity even after 10 min of ischemia. After cerebral ischemia and 24 h of recirculation ODC activity returned to control levels throughout the forebrain regardless of the duration of ischemia. SAMDC activity was significantly reduced after 8 h of recirculation following 4 to 10 min of ischemia in the cortex and 8 min of ischemia in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activity of ornithine decarboxylase and S-adenosylmethionine decarboxylase in transient cerebral ischemia: relationship to the duration of vascular occlusion. 149 93

Synthesis of the polyamines putrescine, spermidine, and spermine is controlled by the activity of the key enzymes ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC). Beside their function in cellular growth processes, polyamines and particularly putrescine play a role in calcium-related events at the cell membrane, coupling an extracellular stimulus to an intracellular response (second messenger-like reactions), modulate the calcium-buffering capacity of mitochondria (spermine), and, if present in the extracellular compartment, modulate the activity of the N-methyl-D-aspartate receptor (spermidine and spermine). Reversible cerebral ischemia triggers pathological disturbances in polyamine metabolism that are characterized by a sharp increase in ODC synthesis, even in the most vulnerable hippocampal CA1 subfield in which overall protein synthesis is severely depressed at the same time, and a marked suppression of SAMDC synthesis in parallel with the inhibition of overall protein synthesis. ODC immunohistochemistry has revealed that the observed changes are neuronal responses to reversible ischemia. These changes in enzyme activities result in an overshoot in the formation of putrescine, the product of ODC activity. Spermine levels are significantly reduced in vulnerable brain structures after prolonged recirculation. In addition, evidence is accumulating that polyamines may be released from the cell during ischemia and after prolonged recirculation at a time when cell necrosis is apparent. This review will summarize the major features of ischemia-induced disturbances in polyamine metabolism and the possible consequences for the cells involved, taking into account that the underlying changes may be indicative of either the activation of a recovery process of neurons from the metabolic stress produced by reversible ischemia or pathological disturbances resulting in the manifestation of neuronal necrosis. Elucidating the mechanisms responsible for the postischemic disturbances in polyamine metabolism may lead to a better understanding of the molecular mechanisms involved in the development of neuronal necrosis after different pathological stimuli.
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PMID:Polyamine metabolism in reversible cerebral ischemia. 156 52