Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effect of myocardial ischaemia on the bioantioxidants levels in the cat heart was evaluated. In addition, effect of curcumin, an anti-inflammatory and anti-thrombotic drug, and quinidine, a standard antiarrhythmic drug, was also studied in the cat. Myocardial ischaemia was induced by the ligation of left descending coronary artery. Quinidine (1 mg/kg, iv) was administered 15 min prior to while curcumin (100 mg/kg, ip) was given 30 min before ligation. Hearts were removed 4 h post coronary artery ligation. Levels of glutathione (GSH), malonaldelhyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT) and lactate dehydrogenase (LDH) were estimated in the ischaemic and non-ischaemic zones. Both the drugs protected the animals against decrease in the heart rate and blood pressure following ischaemia. In the ischaemic zone, after 4 h of ligation, an increase in the level of MDA and activities of MPO and SOD (cytosolic fraction) were observed. Quinidine and curcumin pretreatment prevented the ischaemia-induced elevation in MDA contents and LDH release. Curcumin pretreatment did not prevent the increase in MPO activity while quinidine did. Results obtained indicate alterations in the bioantioxidants following ischaemia and both curcumin and quinidine prevented ischaemia induced changes in the cat heart.
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PMID:Prevention of ischaemia-induced biochemical changes by curcumin & quinidine in the cat heart. 788 81

It is known that reperfusion of the ischemic myocardium may intensify damage and increase the extent of myocardial necrosis. Oxygen free radicals and their metabolites have been implicated as possible elements in myocardial ischemia-reperfusion injury. In this study in cyanotic patients undergoing open heart operation for tetralogy of Fallot, the myocardial tissue activities of catalase, superoxide dismutase, glutathione peroxidase, and lactate dehydrogenase were determined together with the tissue contents of malondialdehyde, oxidized glutathione, and total glutathione using the spectrophotometric assay method. The tissue activities of catalase, superoxide dismutase, and glutathione peroxidase increased significantly after myocardial reperfusion (p < 0.05) when compared with the tissue activities of the control group (myocardial tissue taken immediately after aortic cross-clamping). The tissue content of malondialdehyde increased significantly after reperfusion (p < 0.05), but the tissue activity of lactate dehydrogenase and the ratio of oxidized glutathione to total glutathione showed an insignificant difference after reperfusion. These data suggest that peroxidation of the cardiac lipids was triggered by the reperfusion of the hypoxic heart, but the myocardial cellular damage was not significant enough to decrease the myocardial lactate dehydrogenase and total glutathione levels. These results also suggest that oxygen free radicals may play an important role in in-vivo myocardial reperfusion stress, but endogenous self-defensive enzyme systems to protect the cell against the cytotoxic oxygen metabolites also were triggered, and the resulting myocardial cellular damage was insignificant.
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PMID:Changes in the antioxidative defensive system during open heart operations in humans. 803 18

The present work was conducted to evaluate the oxygen free radical system in 29 patients and comparing them with nine matched healthy controls of acute and chronic myocardial ischemic syndromes. The parameters assessed for oxidative stress were superoxide anion and malonyldialdehyde, and for the antioxidant defence system were superoxide dismutase, catalase and glutathione reductase. Both oxidative stress and the antioxidant defence system were altered in myocardial ischemia. Subset analysis revealed that in unstable angina and acute myocardial infarction, superoxide anion, malonyldialdehyde and glutathione reductase were elevated while superoxide dismutase and catalase levels were reduced. In stable angina only increased levels of superoxide anion and decreased levels of superoxide dismutase were found. However, this alteration was less marked than in unstable angina and acute myocardial infarction. In the post myocardial infarction group there was no alteration in any of these parameters.
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PMID:The free radical system in ischemic heart disease. 818 66

Oxygen free radical scavengers have been found to decrease infarct size in dogs subjected to myocardial ischemia-reperfusion injury. A baboon open-chest model was used to determine if superoxide dismutase (SOD), an oxygen free radical scavenger, together with catalase would be equally effective in subhuman primates (baboons). The left anterior descending coronary artery (LAD) was ligated for 2 hours. Before reperfusion, the animals received the following: Group 1 (low-dose SOD/catalase; n = 5) received 15,000 IU/kg of SOD and 55,000 IU/kg of catalase IV over 1 hour, 15 minutes before reperfusion. Group 2 (high-dose human SOD [h-SOD]/catalase; n = 5) received an intraatrial bolus of 400,000 IU of recombinant h-SOD and 27,500 IU/kg of catalase over 30 seconds, followed by 300,000 IU of h-SOD and 55,000 IU/kg of catalase over 1 hour, beginning 15 seconds before reperfusion. Group 3 (n = 8) were control animals. Baboons were put to death 22 hours after reperfusion. Their hearts were excised and sectioned after the perfusion bed distal to the site of ligation was delineated with microvascular dye. The infarct zone was determined histologically. Areas of the perfusion bed and infarct zone were measured by planimetry. Infarct size did not differ significantly between the three groups: control, 66 +/- 7%; low-dose SOD/catalase, 68 +/- 5%; and high-dose h-SOD/catalase, 74 +/- 4%. In this model, high- and low-dose SOD with catalase did not result in any significant reduction in infarct size.
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PMID:High- and low-dose superoxide dismutase plus catalase does not reduce myocardial infarct size in a subhuman primate model. 821 40

In spite of extensive research during the last decade it has not been possible to prove that endogenously generated hydrogen peroxide or any reduced oxygen species reaches sufficient concentration during reperfusion after myocardial ischemia to contribute significantly to irreversible cell injury. In an attempt to further test this hypothesis we subjected isolated perfused rabbit hearts to 30 min regional ischemia followed by reperfusion and supplied hydrogen peroxide in low levels with or without catalase during the first 30 min of reperfusion and thereafter continued the reperfusion for a total of 120 min. Five different groups were studied: controls, and hearts supplied with 2 microM H2O2, 1 microM H2O2, 1 microM H2O2 + catalase (IU/l) or catalase alone in the initial part of the reperfusion. At the end of 120 min reperfusion, area at risk was measured with fluorescent particles and infarct zone size with tetrazolium staining. The results were: in the control group 32 +/- 5.0% of the risk zone infarcted, in the 2 microM H2O2 group 16.3 +/- 5.6% and in the 1 microM H2O2 group 6.9 +/- 0.8% (P < 0.05 compared to control). The reduction in infarct size was not present when catalase was added to the hydrogen peroxide-containing solution (26.4 +/- 4.5) or if catalase was present alone (22.9 +/- 1.8% infarction). In conclusion, hydrogen peroxide, 1 microM, protected the heart during reperfusion and reduced the amount of cell death after 120 min of reperfusion. The study demonstrated reduction or delay in infarction based only on treatment in the reperfusion period. The mechanism behind this protection remains to be determined.
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PMID:Hydrogen peroxide as a protective agent during reperfusion. A study in the isolated perfused rabbit heart subjected to regional ischemia. 874 21

We previously demonstrated that cardiac sarcolemmal membranes bind [35S]ATP gamma S at both low and high affinity binding sites. In this study we examined the effects of some P2-purinoceptor antagonists as well as of two oxidants (H2O2 and HOCl) on the high affinity ATP-binding sites under in vitro conditions. It was found that putative P2-purinoceptor antagonists such as Cibacron blue, suramin, and 4,4'-diisothiocyanatostilbene 2-2 acid markedly inhibited specific ATP-binding with sarcolemmal membrane. H2O2 produced a biphasic effect (first increase and then decrease) on the specific ATP-binding with cardiac sarcolemma in a time- and concentration-dependent manner; these effects were prevented by catalase. On the other hand, HOCl markedly inhibited ATP-binding; this inhibition was prevented by l-methionine. These results suggest that the high affinity ATP-binding sites in cardiac sarcolemma may represent the P2-purinoceptors, which are susceptible to modification by oxidative stress under pathophysiological conditions including myocardial ischemia-reperfusion injury.
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PMID:Alteration in cardiac sarcolemmal ATP receptors by oxyradicals. 890 51

Alcohol is one of the most widely used addictive substances. It can be assumed that everybody encounters alcohol--ethanol in various forms and concentrations in the course of their lives. A global and social problem of our civilization is alcohol consumption which has a rising trend. Since 1989 the consumption of alcoholic beverages is rising and the mean annual consumption of concentrated ethanol per head is cea 10 litres. In ethanol abuse the organism is damaged not only by ethanol alone but in particular by substances formed during its metabolism. Its detailed knowledge is essential for the knowledge and investigations of the metabolic and toxic effect of ethanol on the organism. Ingested alcohol is in 90-98% eliminated from the organism by three known metabolic pathways: 1-alcohol dehydrogenase, 2-the microsomal ethanol oxidizing system and 3-catalase. Alcohol is a frequent important risk factor of serious "diseases of civilization" such as IHD, hypertension, osteoporosis, neoplastic diseases. Cirrhosis of the liver and chronic pancreatitis are the well known diseases associated with alcohol ingestion and also their most frequent cause. It is impossible to list all organs and diseases which develop as a result of alcohol consumption. It is important to realize that regular and "relatively" small amounts in the long run damage the organism and may be even fatal.
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PMID:[Alcohol]. 892 47

Parameters of antioxidant defense including superoxide dismutase, catalase and spontaneous chemiluminescence were studied in 68 patients with ischemic heart disease and 20 control patients. The above parameters decreased with the disease aggravation. Conventional therapy has improved antioxidant defense, the effect being dependent on effect of therapy irrespective of its variant.
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PMID:[Changes in indicators of the antioxidant defense system in patients with ischemic heart disease treated conventionally]. 892 95

Hyperthermia-induced cardioprotection during myocardial ischemia may involve increased activity of antioxidative enzymes. In this study we investigated the effects of 3-amino-1,2,4-triazole (3-AT), an irreversible catalase inhibitor, in heat-shocked (HS) rabbits subjected to ischemia-reperfusion injury. Rabbits underwent whole body hyperthermia at 42 degrees C for 15 min. Twenty-four hours later, rabbits were administered either saline vehicle or 3-AT (1 or 2 g/kg i.p.) 30 min before undergoing 30 min of regional coronary occlusion and 3 h reperfusion. Controls did not undergo whole body hyperthermia and were given either saline or 3-AT. Heart rate and left ventricular pressure were recorded continuously during these experiments. Infarct area (tetrazolium staining) was normalized to anatomic risk zone size (microsphere autoradiography). Expression of HSP 71 was verified using Western blot analysis; myocardial catalase activity was determined in tissue biopsies. Infarct size was significantly reduced in HS rabbits (25.1 +/- 2.8%, P = 0.2; means +/- SE) compared with controls (53.6 +/- 4.7%). Treatment with 1 g/kg 3-AT attenuated HS-mediated cardioprotection (36.9 +/- 4.9%, P = 0.063 vs. HS); protection was abolished with 2 g/kg 3-AT (48.9 +/- 6.6%). Myocardial catalase activities were higher in tissue biopsies from HS rabbits (47.0 +/- 4.5 U/mg protein, P < or = 0.02) compared with controls (33.4 +/- 1.9 U/mg protein); catalase activities were significantly reduced in rabbits treated with 3-AT. In conclusion, whole body hyperthermia increases expression levels of HSP 71; myocardial catalase activity is also significantly increased. Myocardial protection is HS rabbits subjected to ischemia-reperfusion injury was reversed with 3-AT. These data suggest that increased intracellular activities of catalase and possibly other antioxidant enzymes is an important mechanism for hyperthermia-mediated cellular protection.
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PMID:Effect of 3-aminotriazole on hyperthermia-mediated cardioprotection in rabbits. 896 53

Myocardial ischemia-reperfusion injury is at least partially mediated by oxygen-derived free radicals. Catalase is a major enzyme involved in the detoxification of hydrogen peroxide. The activity of catalase in the heart is very low, which may be a factor responsible for the high sensitivity of the heart to ischemia-reperfusion injury. The present study was undertaken to determine whether elevation of catalase specifically in the heart of transgenic mice can provide protection against ischemia-reperfusion injury. Hearts isolated from transgenic mice in which catalase in the heart was elevated approximately 60-fold higher than that in nontransgenic heart and from the non-transgenic littermates were subjected to 50 min of warm (37 degrees C) zero-flow ischemia followed by 90 min reflow. Compared with nontransgenic controls, transgenic hearts showed significantly improved recovery of contractile force (75 vs. 25% at the end of 90 min reperfusion, P < 0.01). Efflux of creatine kinase was reduced by approximately 50%, and the zone of myocardial infarction as demarcated by triphenyltetrazolium at the end of reperfusion was reduced by approximately 40% in transgenic hearts compared with nontransgenic controls. These findings support the view that hydrogen peroxide is an important cause of ischemia-reperfusion damage and suggest that protection may be provided by elevation of catalase activity.
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PMID:Catalase-overexpressing transgenic mouse heart is resistant to ischemia-reperfusion injury. 932 93


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