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)

Hearts from rats fed low copper (1.3 mg copper/kg diet) or a copper-supplemented diet (243 mg copper/kg diet) were perfused for 90 min according to the Langendorff method. The perfusion protocol included 30 min normoxia, 30 min ischemia and 30 min reperfusion. After 90 min perfusion, hearts from the low copper group had gained more weight, had lower coronary perfusion pressure, developed less force of contraction and secreted less 6-keto PGF1 alpha into the perfusate than hearts from the copper-supplemented group. After perfusion, the major lipid change in the hearts from both groups was a 85-90% decrease in total triacylglycerol. In both groups, stearic acid and arachidonic acid (mg%) were increased in the triacylglycerol fraction after heart perfusion. The quantitative (mg/g) decrease in the triacylglycerol content of stearic acid and arachidonic acid was significantly less in the copper-supplemented group. After perfusion, dihomo-gamma-linolenic acid (mg/g) was lower in heart phospholipids from the low copper group. Dihomo-gamma-linolenic/arachidonic acid (microgram/mg) was significantly decreased after perfusion only in the hearts from the low copper group. Lipid and fatty acid changes in the hearts of the rats fed low dietary copper may contribute to abnormal heart function in this group.
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PMID:Copper intake affects rat heart performance during ischemia-reperfusion: possible relation to altered lipid and fatty acid metabolism. 323 64

The current status of superoxide dismutase (SOD) is that it is an enzyme with diverse ramifications. This review attempts an understanding of SOD as a structural, functional, and biological entity. Accordingly, the review is in three parts. The first part discusses SOD in terms of protein structure, proceeding from primary to secondary and three-dimensional structure for the three forms of SOD: copper/zinc SOD, manganese SOD, and iron SOD. This is the order of structural knowledge of the enzyme. Iron SOD is an enzyme of prokaryotes and some higher plants. Manganese SOD is an enzyme of prokaryotes and eukaryotes. Copper/zinc SOD is an enzyme of eukaryotes and certain prokaryotes. The evolutionary relationships of the three forms of SOD, the status of the copper/zinc SOD gene in prokaryotes, and the cloning and sequencing of SOD genes are discussed. The second part of the review deals with the catalytic mechanism of SOD in the three forms of the enzyme. Structural and mechanistic conclusions from various spectroscopic studies are critically considered. A detailed picture is given of the active site of copper/zinc SOD. The third part is a review of SOD in the general context of oxygen toxicity. After consideration of the question of superoxide toxicity and superoxide pathology, several areas in which SOD has been investigated or used as a tool in a biochemical, pharmacological, or clinical context are discussed, including population genetics; trisomy 21; development and senescence; the nutritional copper, zinc, and manganese status; hemolysis and anemia; oxygen toxicity in the lung and nervous system; inflammation, autoimmune disease and chromosome breakage, ischemia and degenerative changes; radiation damage; and malignancy. A comprehensive picture is given of measurements of SOD activity in disease states, and the question of superoxide-related disease is considered at several points.
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PMID:Aspects of the structure, function, and applications of superoxide dismutase. 331 61

Effects of complete ischemia on levels of antioxidative enzymes including copper-zinc (CuZn) superoxide dismutase (SOD), manganese (Mn)-SOD, and glutathione peroxidase (GSH-Px) were studied in rat brain regions at 30 and 60 min following decapitation. CuZn-SOD activities were significantly decreased in cerebral cortex and hippocampus at both time points whereas the enzyme activities were decreased at 60 min in cerebellum and caudate areas. The reduction of Mn-SOD activities followed the same pattern of CuZn-SOD in various brain regions. However, GSH-Px activities in these brain regions were not affected by decapitation ischemia. These data suggest that the reduction of CuZn-SOD and Mn-SOD activities during ischemia, in conjunction with the significant decrease in the contents of alpha-tocopherol and other endogenous antioxidants, may compromise the brain's ability to defend against the toxic effects of superoxide radicals formed by ischemia and by subsequent reoxygenation.
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PMID:Reduction of activities of superoxide dismutase but not of glutathione peroxidase in rat brain regions following decapitation ischemia. 335 97

The enzyme xanthine: acceptor oxidoreductase found in rat heart equilibrates between three forms differing in electron acceptor specificity. Form D transfers electrons exclusively to NAD+ and accounts for 85% of total oxidoreductase activity. Form O transfers electrons to molecular oxygen and accounts for 8%. The D/O form prefers NAD+, but without NAD+ transfers electrons to oxygen. Interconversion from D to O and O to D forms is catalyzed by sulfhydryl group-modifying reagents: Cd2+, Cu2+, disulfiram, and heating with dithiothreitol. This suggests that sulfhydryl groups participate in the first stage of enzyme conversion. The NADH/NAD+ concentration ratio may regulate the dehydrogenase activity of xanthine:acceptor oxidoreductase (NAD+-dependent activity of D and D/O forms). Accumulating NADH inhibits hypoxanthine hydroxylation. The amount of form O increases during cardiac ischemia, facilitating superoxide radical-ion generation. Also, NADH/NAD+ does not regulate form O, promoting adenylate nucleotide pool depletion, especially in the heart which has low de novo purine nucleotide synthesis.
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PMID:Three forms of xanthine: acceptor oxidoreductase in rat heart. 346 36

The ocular effects of intravitreally injected copper sulfate solutions were studied in New Zealand white rabbits. These injections resulted in uveitis characterized by prolonged ocular hypotony, increased protein concentrations and decreased ascorbic acid concentrations in both the vitreous and aqueous humors, and an apparent decrease in the transport function of the anterior uvea. The extent and the duration of these effects were dose-dependent. The lower doses used, 3 or 6 micrograms of Cu as CuSO4 per eye, produced reversible inflammation. The highest dose, 30 micrograms of Cu per eye, also produced some signs of ocular chalcosis: hemorrhage, vitreous liquefaction, prolonged hypotony and local iridial ischemia. Six hours after the intravitreal injection of 6 micrograms of Cu as CuSO4 per eye, the Cu concentration in the vitreous humor increased to approximately 100 times that in the vitreous of control eyes, and began to decline only 3 days later, with a half-time of approximately 8 days. The Cu concentration in the anterior chamber of these eyes never exceeded 1 ppm and returned close to control values within 3 days. Based on these findings, factors that affect ocular trace-metal distribution and kinetics are discussed, as are reasons for the apparent difficulty in diagnosing the presence of Cu-containing intraocular foreign bodies on the basis of the Cu concentration of the aqueous humor.
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PMID:The pathophysiology of the ocular microenvironment. II. Copper-induced ocular inflammation and hypotony. 372 Aug 74

Copper metabolism was studied in 82 patients with extravasal stenosis of the celiac trunk and in 14 patients with disturbed potency of the celiac trunk and inesenterial arteries of atherosclerotic etiology. The following parameters were analyzed: activity of ceruloplasmin and cytochromoxidase and copper content in the blood serum, copper and cytochromoxidase in the liver. It has been established that the level of the above elements in the blood and liver can be a diagnostic sign of chronic ischemia of the liver in patients with extravasal stenosis of the celiac trunk.
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PMID:[Copper metabolic disorder in extravasal stenosis of the celiac trunk]. 624 8

Male weanling rats were made copper deficient with a purified diet containing all known essential dietary nutrients except copper. Copper deficiency was verified by indirect (anemia, growth retardation, hypercholesterolemia, gross pathology, and abnormal electrocardiograms) and direct (tissue copper analysis) criteria. His bundle electrographic and electrocardiographic changes detected in the copper-deficient group consisted most notably of depressed His-Purkinje system conductivity and S-T segment depression. Phosphorus-31 nuclear magnetic resonance spectroscopic analysis of cardiac, renal, and hepatic tissue perchloric acid extracts revealed significant metabolic changes associated with the dietary copper deficiency, including a generalized marked decrease in ATP and phosphocreatine levels and a corresponding increase in inorganic orthophosphate and ADP levels in the various tissues. Tissue-specific changes consisting of elevated ribose 5-phosphate (heart), phosphocholine (heart), and inosine monophosphate (kidney) and decreased glycerol 3-phosphorylethanolamine (liver) and glycerol 3-phosphorylcholine (liver) levels were detected in copper-deficient rats. Microscopic examination of heart tissue from copper-deficient rats revealed extensive disruption of mitochondrial fine structure, including fragmentation of cristae and inner and outer mitochondrial membranes, which resulted in pronounced vacuolization throughout the tissue. Although the physiological and metabolic disturbances manifested in hearts from copper-deficient animals generally mimic myocardial responses to chronic ischemia, the observed changes are interpreted in a broader context to represent the appearance of a copper-dependent cardiomyopathy.
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PMID:Physiological and metabolic characterization of a cardiomyopathy induced by chronic copper deficiency. 663 5

To delineate beneficial effects of intracoronary thrombolysis on myocardial metabolism in vivo and their dependence on the interval after coronary occlusion prior to reperfusion, we studied 23 closed-chest dogs. Coronary occlusion was produced with a thrombogenic copper coil to performance of cardiac positron emission tomography with 11C-palmitate. Jeopardized zones were calculated by summation by myocardial regions exhibiting less than 50 percent of the peak left ventricular wall radioactivity, and residual metabolic activity within jeopardized zones quantified based on the average counts compared with average counts in normal myocardium. After tomography, streptokinase was infused into the coronary artery (4,000 units per minute), resulting in angiographically demonstrable restoration of patency. Repeat tomography performed 90 minutes after the initial study with a second injection of 11C-palmitate demonstrated reduction of jeopardized zones by 51 +/- 6.3 percent (SE) and by 21 +/- 1.8 (p less than 0.01 based on paired comparisons) when refusion was initiated 1 to 2 (in four dogs) or 2 to 4 (in six dogs) hours after occlusion. Metabolic activity in initially jeopardized regions increased by 111 +/- 24.3 percent and 61.8 +/- 12.6 (p less than 0.01 for each). When streptokinase was infused later after occlusion, significant salutary metabolic effects did not occur. These results indicate that positron tomography may be useful in the clinical delineation of the efficacy of thrombolytic therapy in restoring myocardial metabolism and underscore the marked dependence of such efficacy on the duration of the interval of ischemia prior to the onset of reperfusion.
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PMID:Temporal dependence of beneficial effects of coronary thrombolysis characterized by positron tomography. 698 98

The importance of metals in normal and pathologic cardiovascular function has been recognized. Significant derangements in myocardial Ca2+, Mg2+, and Cu2+ have been reported in ischemic heart injury. We studied 3 groups of hearts: 1) fifteen specimens obtained from patients who had no heart disease, 2) nine specimens from patients who had expired from cyanotic congenital heart disease, and 3) ten specimens from patients who had expired from acute rheumatic heart disease with carditis and severe heart failure. None of the patients had undergone cardiac surgery. Left ventricular lateral wall Mg2+, Ca2+, Cu2+, and Zn2+ contents were measured by atomic absorption spectrometry. The results showed a significant decrease in myocardial Mg2- (Group I 177.06 +/- 32.71; Group II 155.66 +/- 14.79; Group III 149.00 +/- 13.29, p less than 0.05 and p less than 0.01, respectively), and Cu2+ contents (Group I 3.22 +/- 0.37; Group II 2.94 +/- 0.22; Group III 2.56 +/- 0.32, p less than 0.02 and p less than 0.001, respectively), and a rise in myocardial Ca2+ content (Group I 36.06 +/- 10.72; Group II 43.22 +/- 7.01; Group III 46.30 +/- 4.85, p = not significant, and p less than 0.01, respectively). The myocardial Zn2+ content did not change significantly (Group I 26.53 +/- 3.99; Group II 26.00 +/- 4.15; Group III 26.40 +/- 3.53). The myocardial Mg2+/Ca2+ ratio was reduced markedly in both groups (Group I 5.328 +/- 1.879; Group II 3.685 +/- 0.735; Group III 3.135 +/- 0.291, p less than 0.001 for both Groups II and III vs Group I). The latter results correlated closely with the myocardial Mg2+/Ca2+ ratios reported in experimental models in peri-infarction zones. Thus, the myocardium of patients who had expired from cyanotic congenital heart disease and acute rheumatic carditis is jeopardized by ischemia, with metal contents similar to the border areas in myocardial infarction.
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PMID:Myocardial metal content in patients who expired from cyanotic congenital heart disease and acute rheumatic heart disease. 717 80

The serum levels and urinary excretion of magnesium and copper were studied in 66 patients with either acute myocardial ischemia or myocardial infarction. Serum for magnesium and copper determinations was obtained daily for three days. The initial serum magnesium levels were normal in patients with ischemia but were low in some patients with myocardial infarction. Patients developing ventricular arrhythmias with myocardial infarction showed the lowest levels of serum magnesium. Copper in the serum appeared elevated in patients developing acute congestive heart failure but the elevation was not statistically significant. These data indicate that a decrease in serum magnesium as evaluated may be associated with ventricular arrhythmias in patients with myocardial infarction; thus continued observations of magnesium levels in the myocardial infarction patient is warranted.
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PMID:Serum magnesium and copper levels in myocardial infarction. 746 38


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