Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients with good ventricular function undergoing coronary artery bypass surgery were studied to determine whether the pre-bypass use of nitrous oxide resulted in any differences in cerebrospinal fluid markers indicative of cerebral ischaemia. All patients were anaesthetised with diazepam, fentanyl and pancuronium, after which ten patients received 50-60% nitrous oxide in oxygen until commencement of bypass, and the remaining patients 100% oxygen. Because of the known effect of nitrous oxide in expanding gaseous bubbles, any neurological dysfunction of gaseous microembolic origin may be worsened in the presence of nitrous oxide. Patients were lumbar punctured 24 hours after cardiopulmonary bypass and cerebrospinal fluid analysed for the following markers of central nervous system ischaemia: creatine kinase, lactate, total protein, noradrenaline, adrenaline and adenylate kinase. There was a statistically significant difference in cerebrospinal fluid lactate between the two groups. There were no statistically significant differences in the other cerebrospinal fluid markers of ischaemia.
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PMID:Nitrous oxide and cerebrospinal fluid markers of ischaemia following cardiopulmonary bypass. 350 Dec 55

Adenylate kinase activity was found in 32 of 34 samples of cerebrospinal fluid (CSF) from 21 patients with stroke and seven patients with global cerebral ischaemia (GCI). The light absorbance values of the spectrum 400-650 nm revealed the scanty occurrence of haemoglobin products in the CSF in some patients. No correlation was found between the absorbance values at 415 nm, reflecting oxyhaemoglobin, and the adenylate kinase activities. Thus, a main contribution to the adenylate kinase activity in CSF by leakage of this enzyme from erythrocytes could be ruled out. Instead increased leakiness of the brain cells, having an impaired metabolism due to insufficient supply of oxygen and glucose, was the most plausible cause of the findings. The quotient between the adenylate kinase activity and the light absorbance at 415 nm seemed to reflect the extent of ischaemically deranged brain tissue in the GCI patients, while the CSF-lactate values were not correlated to the clinical outcome. Glutathione, an intracellular tripeptide, was more often found in the CSF from GCI patients than from stroke patients.
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PMID:Cerebrospinal fluid markers of disturbed brain cell metabolism in patients with stroke and global cerebral ischemia. 625 76

To investigate the possibility of improving the accuracy of prognostication in early hypoxic brain damage, 12 patients with global cerebral ischemia (GCI) due to circulatory arrest outside hospital were followed until death or for 1 yr. Five who survived for more than 2 weeks displayed better values on coma scoring from 16 h-3 days, compared to those who succumbed within 2 weeks. In 2 week-survivors, lumbar puncture revealed consistently lower adenylate kinase (AK) activity in cerebrospinal fluid (CSF) at 24 h than in the other patients, whereas glutathione and lactate values overlapped to some degree. The CSF-AK activity at 48--72 h was less correlated to clinical outcome. It is concluded that the results from coma scoring, based upon clinical observation, and from determination of AK activity in CSF at 24 h reinforce each other in discriminative power to predict prognosis in these patients.
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PMID:Cerebrospinal fluid markers in relation to outcome in patients with global cerebral ischemia. 684 7

Superoxide dismutase is well known to act as an effective antioxidant enzyme against cellular damage caused by oxidative stresses including ischemia/reperfusion-induced cerebral injury. However, it is still controversial whether or not the activity of endogenous superoxide dismutase changes during cerebral ischemia and reperfusion. In order to elucidate this phenomenon, we assayed the superoxide dismutase activity in the cerebral tissues of gerbils using the chemiluminescence method with a Cypridina luciferin analog. This method was demonstrated to be a sensitive and specific assay for the enzymatic activity of superoxide dismutase in cerebral tissues, which was not subject to interference from proteins or ascorbate. After 3 h of focal and global ischemia, there were no changes in the cerebral tissue superoxide dismutase activities. After 24 h of reperfusion following 1 h of ischemia, the superoxide dismutase activity decreased only approx 20%, whereas the adenylate kinase activities, measured in the same cerebral tissues as those used for superoxide dismutase assay, started to decline 1 h after reperfusion commenced and were approx 50% of the control levels after 24 h. These results show that almost all the activity of endogenous superoxide dismutase is maintained and does not decrease significantly as a result of ischemia/reperfusion-induced cerebral injury.
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PMID:The superoxide dismutase activities of cerebral tissues, assayed by the chemiluminescence method, in the gerbil focal ischemia/reperfusion and global ischemia models. 836 36

In order to provide a complete picture of pathogenesis in cerebral ischemia, cerebral cortex in MCAO rats were analysed for alteration in their proteomes. Comparative proteome analysis was used to compare signal corresponding to individual cerebral cortex proteins on a two-dimensional gel between MCAO rats and the normal control (NC) group. After sample preparation, two-dimensional electroghoresis separated proteins were stained with Commassie Brilliant Blue. The image data were analyzed on a Dell computer using Image Master v 3.01 software. In cerebral cortex, 30 proteins were differentially expressed in MCAO rats compared with NC. There were 11 spots significantly increased, 15 spots significantly decreased and Adenylate kinase isoenzyme 1 was detected only in NC group, biliverdin reductase B, small inducible cytokine A4 [Precursor] only in MCAO group. Peroxiredoxin 2 divided into two points in MCAO6h group. In the end, this approach may lay a foundation for the further investigation of pathogenic mechanisms in cerebral ischmic injury.
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PMID:[Comparative proteomic analysis of cerebral cortex between middle cerebral artery occlusion rats and normal controls]. 1646 49