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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incomplete ischemia of the spinal cord of rabbits was produced by a 40-min occlusion of the abdominal aorta followed by 1 and 4 days of recirculation. Regional evaluation of ATP-induced bioluminescence after 20 min of ischemia revealed ATP depletion mainly in the gray matter of the spinal cord. After 40 min of ischemia, ATP-induced bioluminescence was too faint to expose the photographic film. Within 1 and 4 days of recovery following 40 min of ischemia, restitution of ATP was regionally heterogeneous, reduced predominantly in the anterior horns of gray matter. Polysome profiles remained unaltered during the ischemic period, but a marked disaggregation of polyribosomes occurred after 10 min of recirculation. Protein synthesis in a cell-free system was inhibited by the addition of a postischemic cytosol or protein fraction isolated from cytosols on a DEAE column. The inhibition can be overcome by the addition of each initiation factor 2 (eIF-2), GTP and GDP exchange factor (GEF). Occlusion of abdominal aorta for 40 min results in decrease in monoamine oxidase accumulation in both proximal and distal ligature placed on sciatic nerve. Within 4 days of recovery the transport was progressively depressed to 22 and 21% in the proximal and distal direction, respectively.
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PMID:Molecular mechanisms of ischemic damage of spinal cord. 244 28

Rabbit spinal cords were subjected to 40 min of ischemia by abdominal aorta occlusion followed by 1 or 4 days of recirculation. Axoplasmic transport of mitochondria was investigated by monitoring the accumulation of monoamine oxidase activity (MAO, EC 1.4.3.4) at the proximal and distal ligatures placed on sciatic nerves. Within 1 day following ischemia, MAO accumulation was reduced to 45% and 34% at the proximal and distal ties, respectively. Within 4 days after ischemia, MAO accumulation was depressed still further to 22% in either direction. The substantial decrease in transport velocity appears to be the immediate cause for the observed decrease in MAO accumulation in sciatic nerve.
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PMID:Axoplasmic transport of monoamine oxidase after ischemia. 244 48

In vivo voltammetry is an electrical detection method by which dopamine and serotonin metabolism can be estimated in the brain of animals. In the present report preliminary and basic experiment were performed before its application to ischemic brain. Firstly, using voltammetry DPV-5 system in vitro, concentration/amplitude curve was obtained with various concentration of 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA) diluted in phosphate buffer (pH 7.4). DOPAC appeared at +150 mV (peak 2) while 5-HIAA appeared at +300 mV (peak 3). A linear relation was obtained in the concentrations ranging 5 x 10(-6)-10(-4) M for DOPAC and 10(-6)-10(-4) M for 5-HIAA. While a delay in oxidation potential was noticed for both peaks 2 and 3 by about 30 mV when the pH of solution was decreased by 1. Secondly the DPV-5 system was applied in vivo to the rat striatum. Peak 2 was observed at +150 mV which was increased by intraperitoneal injection of haloperidol, a dopamine receptor blocker and decreased by pargyline, a monoamine oxidase inhibitor. While peak 3 was observed at +300 mV and increased after probenecid and decreased by pargyline, which suggest that peak 2 and 3 correspond to DOPAC and 5-HIAA respectively. Thirdly DPV-5 system was applied to the rat striatum and rat's heart was arrested by KCl injection as a model of extreme brain ischemia. Shortly after cardiac arrest the heights of peak 2 was significantly increased to 600-900% while the increase of peak 3 was not significant, both of which subsided gradually toward 30 minutes after arrest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Measurements of monoamine neurotransmitter metabolism by in vivo voltammetry]. 245 32

The effects of total brain ischemia (decapitation) on striatal extracellular levels of dopamine (DA) dihydroxyphenyl acetic acid (DOPAC) and ascorbic acid (AA) in chloral hydrate anesthetized rats were monitored at 1-min intervals by differential normal pulse voltammetry (DNPV) with numerical deconvolution of the catechol peak. Changes in pH were assessed by the shift of AA oxidation potential and incorporated into the computational procedure. The AA peak showed a sharp, short-lived (less than 15 min) postdecapitation rise, followed by a slower secondary increase. The DA signal increased 100-fold in the first 20 min followed by a slow decline. DOPAC levels fell 80% within 15 min after death. The post-mortem changes in extracellular DA and DOPAC were verified by a similar experiment using microdialysis. These observations probably reflect massive release and impaired uptake of DA combined with reduced monoamine oxidase activity. Changes in membrane permeability to DOPAC as a consequence of a post-mortem drop in pH may also contribute to the decline in extracellular DOPAC levels.
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PMID:Post-mortem dopamine dynamics assessed by voltammetry and microdialysis. 259 Aug 45

Properties of monoamine oxidase (MAO) were investigated in mongolian gerbils brain mitochondria isolated from cerebral cortex, striatum and hippocampus during cerebral ischemia. 5 min of ischemia caused inhibition of MAO activity (kynuramine as a substrate), alterations in substrate specificity and in kinetic curves form deflexion from hyperbolic type in all the brain structures investigated. Alterations in properties of MAO were observed in hippocampus already after I min of ischemia.
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PMID:[Properties of monoamine oxidase in the brain of mongolian gerbils during cerebral ischemia]. 261 26

Changes in the activity of three mitochondrial enzymes in rat liver after in vitro ischemia have been determined by enzyme histochemical methods. The changes were correlated with the appearance in the electron microscope of flocculent densities in the mitochondria indicative of irreversible cell injury. The flocculent densities were observed in rat liver after about 2 h of ischemia in vitro at 37 degrees C. At the same time the activity of glutamate dehydrogenase, localized in the mitochondrial matrix, started to decrease. However, the activities of succinate dehydrogenase localized in the inner membrane of mitochondria, as well as monoamine oxidase of the mitochondrial outer membrane did not change at that stage. It is concluded from the results of this study and those of others that flocculent densities are formed by denaturation of proteins of the mitochondrial matrix in which glutamate dehydrogenase takes part. It should be considered more as a sign than as the cause of cell death.
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PMID:A histochemical study of changes in mitochondrial enzyme activities of rat liver after ischemia in vitro. 287 57

The effects of several concentrations of amines and reducing agents on the activity of creatine (CK) and adenylate (AK) kinases were determined in homogenates of the brain of the rat at 0 and 37 degrees C. The order of decreasing irreversible inhibition of the enzymes was peroxide, 6-hydroxydopamine, dopamine, norepinephrine, 5-hydroxytryptamine. At 37 degrees C, approx. 50% of the activity of creatine kinase was lost in 30 min in the presence of 20 microM dopamine. 5-Hydroxytryptamine was several orders of magnitude less toxic. The action of dopamine was not prevented by inhibition of monoamine oxidase, chelation of metals or the addition of a catalase, indicating that formation of peroxide by monoamine oxidase was not the primary cause of the loss of enzyme. Although auto-oxidation of dopamine to a toxic quinone was considered, the degree of inhibition of creatine kinase was not affected when auto-oxidation was prevented under anaerobic conditions. Glutathione (GSH), present during the incubation, protected the enzymes but could not restore activity after exposure to amine. Concentrations of glutathione above 5 mM and of oxidized glutathione as low as 10 microM inhibited creatine kinase. Ascorbate protected the enzymes even when present at a concentration much less than that of the amine, but ascorbate was itself toxic. The findings indicate that dopamine, at concentrations attained after drug-induced release or ischemia, can be toxic to a metabolic enzyme present in the synaptosomal membrane.
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PMID:Amine-mediated toxicity. The effects of dopamine, norepinephrine, 5-hydroxytryptamine, 6-hydroxydopamine, ascorbate, glutathione and peroxide on the in vitro activities of creatine and adenylate kinases in the brain of the rat. 300 2

The release of endogenous noradrenaline and its deaminated metabolite dihydroxyphenylglycol in the myocardium have been studied in the isolated perfused heart of the rat subjected to three models of energy depletion: ischemia, anoxia, and cyanide intoxication. Anoxia and cyanide intoxication were combined with substrate deficiency at constant perfusion flow. All three energy-depleting procedures caused a similar overflow of noradrenaline which, following a constant delay of 10 minutes without increased release, amounted to more than 25% of total heart content within 40 minutes. This noradrenaline overflow was not diminished in the absence of extracellular calcium and was inhibited by the uptake1 blocker desipramine in all three experimental models, indicating a common and nonexocytotic release mechanism. In the presence of glucose, neither anoxia nor cyanide intoxication resulted in a measurable noradrenaline overflow. Conversely, blockade of glycolysis or glucose depletion prior to ischemia or cyanide poisoning accelerated the noradrenaline overflow, demonstrating a key role of the sympathetic nerve cells' energy status in causing nonexocytotic catecholamine release. Blockade of energy metabolism in the presence of oxygen (cyanide model) resulted in the overflow of high amounts of dihydroxyphenylglycol that was not inhibited by uptake1 blockade. The release of the lipophilic dihydroxyphenylglycol by diffusion reflects deamination of axoplasmic noradrenaline by monoamine oxidase. Since saturation of the enzyme could be excluded in this model dihydroxyphenylglycol release can be taken as a mirror of cytoplasmic noradrenaline concentration. The results obtained by these studies indicate that nonexocytotic catecholamine release is a two-step process induced by energy deficiency in the sympathetic varicosity. In a first step, noradrenaline is lost from storage vesicles, resulting in increasing axoplasmic concentrations. The second step is the rate-limiting transport of intracellular noradrenaline across the cell membrane by the uptake1 carrier that has reversed its normal net transport direction.
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PMID:Nonexocytotic release of endogenous noradrenaline in the ischemic and anoxic rat heart: mechanism and metabolic requirements. 356 91

The behavior of cytoplasmic and mitochondrial enzymes has been studied in rat liver at 1, 5, and 24 hr after 60 min of ischemia using histochemical methods. This period of ischemia resulted 24 h after ischemia in liver cell necrosis in about 15% of the volume of the ischemic liver lobes. As early as after 1 hr reperfusion lactate dehydrogenase (LDH, cytoplasm) activity decreased in a certain proportion of the liver parenchymal cells, whereas glutamate dehydrogenase (GDH, mitochondrial matrix) activity started to decrease after 5 hr reperfusion; the activities of mitochondrial membrane enzymes, monoamine oxidase and succinate dehydrogenase, did not decrease before 24 hr of reperfusion. It has been concluded that the early decrease in LDH activity is caused by leakage into the blood and reflects reversible damage; when this decrease is accompanied by a decrease in GDH activity irreversible liver cell damage is assumed. Diminished activity of mitochondrial membrane enzymes, due to leakage and denaturation, is observed when real necrosis can be assessed.
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PMID:Changes in cytoplasmic and mitochondrial enzymes in rat liver after ischemia followed by reperfusion. 367 63

The effects of regional ischemia of the myocardium upon metabolism and catabolism of catecholamines were studied in the dog adrenal medulla. Regional ischemia was induced by ligating a small branch of the left anterior descending coronary artery for 1 or 24 hours. Sham-operated controls were run in parallel. Coronary ligation for 24 hours resulted in a decrease in the level of epinephrine and an increase in the level of dopamine in the adrenal medulla, and also resulted in an increase in the activities of the phenylethanolamine-N-methyltransferase (PNMT), monoamine oxidase, and catechol-O-methyltransferase. The results after coronary ligation for 1 hour were essentially the same as those after coronary ligation for 24 hours, except that the activity of PNMT decreased. These results suggest that both synthesis and catabolism of catecholamines in the adrenal medulla are accelerated during coronary ligation for a period of 1 to 24 hours.
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PMID:Myocardial ischemia stimulates catecholamine synthesis and catabolism in the dog adrenal medulla. 376 66


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