Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From all mammals investigated so far only in rabbits diamine oxidase could not be detected in any tissue except the gut. Thus this species was chosen for studying the physiological and pathophysiological function of this enzyme in the gastrointestinal tract. By gel filtration on Sephadex G 50 and G 200 the enzyme was purified 100-fold, separated from a soluble monoamine oxidase, and the properties of the two enzymes were determined. Diamine oxidase from rabbit small intestine deaminated putrecine (Km = 1.3 times 10(-4) M, pH-optimum 6.4-6.9) and histamine (Km = 8 times 10(-5) M, pH-optimum 7.5), but not serotonin, and was inhibited by aminoguanidine, but not by pargyline. Soluble monoamine oxidase from rabbit small intestine catabolized serotonin (Km = 1.8 times 10(-4) M, pH-optimum 8.8) but not putrescine and histamine, and was inhibited by pargyline, but not by aminoguanidine. Based on its properties in vitro intestinal diamine oxidase could inactivate the vasoactive biogenic amine histamine in vivo. To confirm this hypothesis, in rabbits the small intestine was damaged severely by inducing total intestinal ischemia, which occurs as mesenteric infarction also in human subjects and is accompanied by histamine release. Treatment with aminoguanidine and ischemia killed the animals 3-times faster than ischemia alone, which supported our hypothesis on a protective role of intestinal diamine oxidase against histamine.
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PMID:Diamine oxydase in rabbit small intestine: separations from a soluble monoamine oxidase, properties and pathophysiological significance in intestinal ischemia. 0 54

Bilateral occlusion of common carotid arteries in Mongolian gerbils was produced for the periods (up to 15 min) which were shown to be totally reversible. There was an initial increase of cyclic AMP and GABA levels and enhanced activities of adenylate cyclase and glutamate decarboxylase, as well as the reduction of norepinephrine level and decreased activities of monoamine oxidase, GABA-transaminase and Na+-K+-ATPase. Following these changes, decreased concentration of dopamine, serotinin and glutamate were found. The activities of total protein kinase and acetylcholinesterase were found to be reduced after longer periods of short-term ischemia. The data are consistent with the concept of increased non-controled release of putative neurotransmitters in ischemia.
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PMID:Alterations of putative neurotransmitters and enzymes during ischemia in gerbil cerebral cortex. 3 75

In tissue of ischemic kidney of rabbits a 5-hydroxytryptophan decarboxylase activity was decreased at first 15 min of ischemia; in contralateral kidney it was slightly increased. Then, within all the studied periods (24 hrs), activity of the enzyme was gradually decreased in both kidneys. The monoamine oxidase activity (substrates serotonin and p-nitrophenyl ethylamine) changed alternatively in early periods of ischemia; it tended to increase, especially in contralateral kidney, within 3 hrs after constriction of kidney artery.
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PMID:[Serotonin metabolism in acute renal ischemia in rabbits]. 113

Various doses of the neurotoxin 6-hydroxydopamine (6-OHDA) were infused into the substantia nigra-ventromedial tegmental area, caudateputamen nucleus, and red nucleus. A maximum of four successively occurring zones of neuropathology could by detected at all injection sites: (1) A zone of complete absence of neural, glial, and vascular elements due to tissue displacement by the cannula, (2) an area of glial cells, developing over time, which surrounded the cannula tract, (3) a region exhibiting virtually complete loss of neuronal elements, and (4) a zone of selective neuropathological reaction or cellular loss in which some neurons were affected and others were not. All investigators who have histochemically and/or histologically evaluated the effects of intracerebrally administered 6-OHDA agree on the existence and genesis, some non-selective process, of the first three zones. Although some scientists maintain that the fourth zone is where 6-OHDA operates selectively, data are presented in this report that other, well-established processes can account for neuropathology beyond zone 3. Prominent among these are retrograde and anterograde degeneration, ischemia as a function of interruption of blood supply, and nonselective traumatization. In addition, the topography of the injected site (e.g., morphology of affected neurons, degree of myelination) was found to be as important a determinant of the locus of tissue damage as the presumed selectivity of 6-OHDA's action. Furthermore, monoamine oxidase inhibition by nialamide did not appear to increase the neurotoxicity of 6-OHDA. Similarly, 1-(2,5-dihydroxy-4-methylphenyl)-2-aminopropane was not a more potent cytotoxin than 6-OHDA even though this new neurotoxin has a propane side chain which renders it immune to monoamine oxidase. These observations, taken together, suggest that considerable cautioon should be exercised in interpreting data from experiments in which 6-OHDA, or related neurotoxins, are used to uncover catecholaminergic mechanisms of behavior and other functional processes.
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PMID:Degenerative processes after punctate intracerebral administration of 6-hydroxydopamine. 118 65

Renal artery occlusion (RAO) for 30, 60 or 90 sec was found to reduce norepinephrine tissue levels in both the cortex and medulla of the rat, respectively, by 2 to 5%, 56 to 65% and 92 to 97%, but no significant change in dopamine tissue levels was found to occur. Similar effects were obtained with occlusion of the aorta proximally to the renal arteries for 90 sec. Administration of superoxide dismutase (40 mg/kg) immediately before RAO resulted in a marked protection of the norepinephrine depletion effect as caused by transient ischemia. The sodium-dependent formation of dopamine and 3,4-dihydroxyphenylacetic acid, the deaminated metabolite of dopamine, in renal slices loaded with L-3,4-dihydroxyphenylalanine (50 microM) was found to be similar in denervated and control kidneys. Type A and B monoamine oxidase activities were measured with the deamination of two specific substrates, respectively, [3H]-5-hydroxytryptamine and [14C]-beta-phenylethylamine, in homogenates of the renal cortex and renal medulla; neither type of monoamine oxidase, A or B, was found to be affected by denervation. The renal tissues collected for morphological observation were those in which RAO was performed for 90 sec. The general structure of the renal cortex was not affected by RAO, being similar in the control and the denervated kidney. In conclusion, the results presented suggest that the tissue damaging effect produced by RAO appears to be selective for the renal sympathetic innervation and seems to involve the generation of some reactive oxygen species, namely superoxide.
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PMID:Brief transient ischemia induces long-term depletion of norepinephrine without affecting the aromatic amino acid decarboxylase and monoamine oxidase activities in the rat kidney. 173 31

The effect of ischemia on myocardial noradrenaline concentration and endogenous noradrenaline output was studied in the isolated perfused rat heart. Following a 15-min stabilization period, regional ischemia was produced by coronary artery ligation. After 60 min of ischemia, noradrenaline concentrations were significantly reduced in the interventricular septum and left ventricle but not in the right ventricle. The reduction in tissue noradrenaline concentration was not prevented when the 60-min ischemia was replaced by a 10-min ischemia followed by a 50-min perfusion. No modification in noradrenaline output was observed during a 60-min ischemia. In contrast, reperfusion was accompanied by a washout of noradrenaline in the coronary effluent, corresponding to only 2% of the amount lost by the tissue. The effect of monoamine oxidase inhibition during the whole ischemic period was studied by perfusing the preparation with pargyline starting 10 min before the artery ligation. Although the administration of pargyline did not alter the noradrenaline output, it did prevent a reduction in myocardial noradrenaline concentration. It was concluded that monoamine oxidase may contribute to the elimination of the noradrenaline lost by the cardiac tissue during ischemia.
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PMID:Reduction of tissue noradrenaline content in the isolated perfused rat heart during ischemia: importance of monoamine oxidation. 178 1

Seven days after 30 min of ischemia, neuronal necrosis was observed in the striatum. Pretreatment with type A monoamine oxidase (MAO-A) inhibitors, clorgyline and RS-8359 ((+)-4-(4-cyanoanilino)-7-hydroxycyclopenta (3,2-e) pyrimidine) decreased significantly the number of necrotic neurons and inhibited changes in the dopamine metabolite contents during and after transient ischemia. An MAO-B inhibitor, deprenyl also decreased the neuronal necrosis, but it inhibited only the changes in 3,4-dihydroxyphenylacetic acid (DOPAC) content after reperfusion. The results suggest that the activation of dopamine metabolism after transient ischemia was mainly mediated by MAO-A and partly by MAO-B and suggest a possible role of dopamine deamination by MAO in the development of ischemic neuronal necrosis.
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PMID:Monoamine oxidase inhibitors prevent striatal neuronal necrosis induced by transient forebrain ischemia. 192 29

Changes in monoamine levels during and after ischemia and effects of RS-8359, a type A monoamine oxidase (MAO-A) inhibitor, were studied in the cerebral cortex, hippocampus, and striatum of rats killed by microwave irradiation. The patterns of the changes in norepinephrine (NE), dopamine (DA), and serotonin (5HT) levels were similar during ischemia: All these monoamines decreased in all three regions. After reperfusion, however, the three monoamines showed different patterns of changes: NE, except in the striatum, decreased further; DA increased over the controls; 5HT remained suppressed in all three regions. With regard to the metabolites of the monoamines, the changes during and after reperfusion were almost similar in all regions: O-methylated metabolites, normetanephrine and 3-methoxytyramine, markedly increased during ischemia; After reperfusion, the elevated levels of normetanephrine and 3-methoxytyramine returned to normal, while deaminated metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid, homovanillic acid (HVA), and 3-methoxy-4-hydroxy-phenylethyleneglycol clearly increased. RS-8359 pretreatment (30 mg/kg, p.o.) at an hour prior to ischemia elevated the levels of NE in the cortex and hippocampus during ischemia and inhibited the increases in DOPAC and HVA levels and the decrease in 3MT levels at 30 min after reperfusion. These results suggest that deamination of NE, DA, and 5HT is activated by the increases in the substrates for MAO in all three regions, except the noradrenergic system in the striatum, and that MAO-A participates in the activated deamination after reperfusion.
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PMID:Participation of type A monoamine oxidase in the activated deamination of brain monoamines shortly after reperfusion in rats. 208 1

Striatal microdialysis was performed in rats subjected to 20 min of transient forebrain ischemia produced by occlusion of the carotid arteries during hemorrhagic hypotension. Extracellular changes of dopamine, serotonin, and their metabolites were monitored before, during, and after the ischemic insult at 10-min intervals by on-line HPLC analysis. During ischemia, extracellular dopamine increased dramatically (156 times baseline), as did 3-methoxytyramine (3-MT), whereas 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) decreased (15-25% of baseline). Upon reperfusion, dopamine was cleared from the extracellular fluid within 40 min and reached a stable level (70% of baseline). DOPAC and HVA increased (250-330%) transiently and reached their maximum 1 h following reperfusion, whereas 3-MT decreased to undetectable levels within 20 min. Although baseline levels of serotonin were not detectable, serotonin and 5-hydroxyindoleacetic acid showed a qualitatively similar temporal pattern to dopamine and its acid metabolites. Killing rats by cervical dislocation produced changes in extracellular dopamine, serotonin, and their metabolites that were almost identical to those seen during ischemia. Pargyline pretreatment 2 h before ischemia had marginal effects on the postischemic clearing of dopamine. The pargyline pretreatment, however, did increase the survival rate of rats subjected to ischemia, and this protective effect might be due to the pargyline-induced blockade of the post-ischemic monoamine oxidase-mediated increase in dopamine metabolism and the concurrent production of the potentially neurotoxic molecule, hydrogen peroxide.
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PMID:Effects of transient forebrain ischemia and pargyline on extracellular concentrations of dopamine, serotonin, and their metabolites in the rat striatum as determined by in vivo microdialysis. 230 12

T4-induced endogenous monoamine oxidase (MAO) inhibitor in rat liver perfusate by perfusion with sucrose buffer and lipid peroxide (LPO) and superoxide dismutase (SOD) in rat liver tissues were investigated after pretreatment with total hepatic ischemia. When the gel filtration of these rats liver perfusate were carried out using Sephadex G-25, fraction 18-20 were found to inhibit MAO activity. LPO of these rats were increased, but SOD activity was decreased. The accumulation of lipid peroxides would partly result from decreased activity of SOD as a consequence of membrane disorders. These results suggest that T4-induced MAO inhibitor in rat cytosol was released into plasma by membrane disorder.
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PMID:Leakage of thyroid hormone-inducible monoamine oxidase inhibitor from rat liver cytosol. 234 6


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