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)

Dietary effects of polyunsaturated fatty acids (PUFA) omega-3 on lipid peroxidation (LPO) and antioxidant system were studied in 73 patients with ischemic heart disease, hyperlipoproteinemia (HLPE) type IIa, IIb, IV and essential hypertension. Eiconol-enriched antiatherosclerotic diet has more potent hypolipidemic, hypotensive and thrombolytic action in association with inhibition of LPO, enhances SOD activity, keeps red cell catalase within normal. Vitamin E concentrations were not changed. It is suggested that eiconol addition to antiatherosclerotic diet causes no LPO induction and is pathognomonic for HLPE, hypertension and IHD patients.
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PMID:[Dietary effects of PUFA omega-3 on lipid peroxidation and antioxidant system in patients with IHD, hyperlipoproteinemia and hypertension]. 781 30

Paeonol 60 mg.kg-1 ip, was given to rats for 15 days. On the 16th day myocardial ischemia reperfusion injury was produced in the rat heart by occlusion of the left coronary artery and the release of the occlusion. The results showed that paeonol significantly improved myocardial SOD activity (5.8 +/- 0.6.mg-1 compared with reperfusion control 3.4 +/- 0.9, P < 0.01), reduced the MDA content (11.4 +/- 1.7 nmol.mg-1 versus 17 +/- 1.3, P < 0.01) and cardiac CPK release (1523 +/- 478.5 U.L-1 versus 2355 +/- 626.5, P < 0.01). The myocardial ultrastructure was also protected keeping them from the oxygen free radical damage. It appears that paeonol is an efficient protective agent against ischemia reperfusion damage in the rat heart.
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PMID:[Anti-ischemia reperfusion damage and anti-lipid peroxidation effects of paeonol in rat heart]. 804 13

Studies on the isolated rat heart perfusion model have proved that perfusion with high Ca2+ (4.5 mmol/L), high K+ (8.7 mmol/L) or free radical generating system (FRGS) significantly increases myocardial uptake of liposomes. Intravenous injection of liposomes covalently combined with antibody of rat myocardial cells obviously elevates the target action of liposomes to myocardium. Liposome-carried SOD for treatment of rat myocardial ischemia-reperfusion injury is much more effective than simple SOD. The results evidence that the liposome as drug carrier for treatment of ischemic heart diseases shows a broad prospect for its clinical use.
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PMID:Possibility of targeting treatment for ischemic heart disease with liposome (II). 821 41

Mice were used to make a comparative study of the biological distribution of intravenous preparations of native and monomethoxypolyethylene glycol-modified superoxide dismutase isolated from bovine liver, as well as native and aldehyde dextran. The study demonstrated that the biodistribution of the native enzymes from various sources was, however, equal, but in the mouse liver there was a higher accumulation of SOD isolated from the rat liver. AD-SOD was found to have a longer half-life in the blood and in the liver of mice, in particular, while MPEG-SOD showed 10, 15, and 16 times longer in the lungs, blood and heart of the animals examined, respectively. The elevated accumulation of MPEG-SOD in some organs was used for their treatment, particularly for experimental therapy of rat myocardial ischemia. A rat model of ischemia demonstrated that the intravenous bolus administration of MPEG-SOD reduced the size of a myocardial necrotic area by 40% as compared to a 13% decrease when the other compounds were assayed. The findings suggest that the MPEG-SOD preparation is promising for decreasing reperfusion injuries of the cardiovascular system and the lungs.
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PMID:[The modification of Cu, Zn-superoxide dismutase by monomethoxypolyethylene glycol improves the indices of the experimental therapy of the ischemic myocardium in rats]. 831

The cardioprotective effects of EGb 761 on the release of nitric oxide (NO), the concentration of serum thiobarbituric acid reaction substance (TBARS), the activity of creatine kinase (CK) and the incidence of ventricular arrhythmias were investigated in myocardial ischemia-reperfusion injury in vivo. Using sodium nitrite (NaNO2) as standard source of nitric oxide (NO), we compared the correlation coefficients of the three measuring methods used currently in the determination of NOFe2+(DETC)2 complex with that of the measuring method suggested in this study. The result showed that measuring the whole height of three splitting signals is the best linear correlation to the concentration of NO comparing with other methods in this system. Using this method, we observed the effects of EGb 761 on NOFe2+(DETC)2 complex in myocardial ischemia-reperfusion injury in vivo. The hearts of the Wistar rats were subjected to 30 min of ischemia and 10 min of reperfusion in vivo. Different doses of EGb 761 (25, 50, 100, 200 mg/kg i.p.), superoxide dismutase (SOD, 10(4) U/kg), l-arginine (50 mg/kg i.p.) and nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine (NNA, 50 mg/kg i.p.) were administered to the ischemia-reperfusion rats. EGb 761 under the dose of 100 mg/kg increased the signal intensity of NOFe2+(DETC)2 complex, while EGb 761 at 200 mg/kg showed an effect of decreasing the signal intensity of NOFe2+(DETC)2 complex. EGb 761 inhibited the formation of TBARS, the release of CK, and mitigated the incidence of ventricular arrhythmias in a dose dependent way. Both l-arginine and SOD increased the signal intensity of NOFe2+(DETC)2 complex and inhibited the formation of TBARS, the leakage of CK and the incidence of ventricular arrhythmia. NNA not only had no protective effects on myocardial injury, but also increased the incidence of reperfusion-induced arrhythmia. In conclusion, EGb 761 has cardiovascular protective effects by means of adjusting the level of NO and inhibiting oxygen free radicals induced lipid peroxidation in myocardial ischemia-reperfusion injury in vivo.
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PMID:Effects of EGb 761 on nitric oxide and oxygen free radicals, myocardial damage and arrhythmia in ischemia-reperfusion injury in vivo. 963 Jun 46

Oxygen-derived free radicals play an important role in myocardial injury associated ischemia and reperfusion. To investigate whether ginsenosides, as an additive agent of cardioplegic solution, can decrease toxicity of oxygen free radicals in myocardial injury, a heterotopic heart transplantation model in Wistar rats was employed. St. Thomas II cold cardioplegia containing ginsenosides 80 mg/l was used in the experimental group. St. Thomas II cold cardioplegia alone was used in the control group. After global ischemia for 60 minutes and reperfusion for 30 minutes of a transplanted heart, SOD activity in the myocardium treated with ginsenosides was significantly higher than that in the control group (N=10, p< 0.01), whereas the MDA in the myocardium treated with ginsenosides were markedly lower than that of the control group (p< 0.01). The amounts of oxygen free radicals in the myocardium treated with ginsenosides were significantly lower than that of the control group (p <0.001). This study demonstrates that ginsenosides, as a proper additive agent of cardioplegic solution, can decrease toxicity of oxygen free radicals, suggesting one of the mechanisms for its protective effects against myocardial ischemia and reperfusion injury.
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PMID:Experimental study on the scavenging effects of ginsenosides on oxygen free radicals using model of heterotopic heart transplantation in rats. 973 18

Lipid peroxidation is thought to be one of the major factors involved in atherogenesis. There is an increasing evidence is increasing that oxidation of LDL cholesterol may be instrumental in atherogenesis. Diabetics are known to be at increased risk of cardiovascular diseases, a phenomenon which has previously been linked to the lipid peroxidation process. As a result, a number of studies have been undertaken to evaluate the effects of antioxidant vitamins on coronary heart disease and risks factors of ischaemic heart disease such as diabetes mellitus. Lipid peroxidation and antioxidant status were studied in 51 patients with ischaemic heart disease and some of with having diabetes mellitus (18%). Results were compared before and after supplementation of 450 mg of tocopherol acetate for three months. SOD were found to be elevated in patients with diabetes and in whole groups of patients after supplementation of tocopherol acetate. Also, TAS was found to be elevated in a subgroup of patients without diabetes and no significant changes were found in glutathion-peroxidase after supplementation. We found statistically significantly decreased mean values of glucose after supplementation in all groups of patients. The monitoring of antioxidant parameters in diabetic patients could be of vital importance in the study of the disease.
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PMID:[Effect of vitamin E on erythrocyte enzymes and total antioxidant status in diabetic patients with ischemic heart disease]. 1108 30

We have reported that lecithin-conjugated recombinant human Cu, Zn-superoxide dismutase (lecithinized SOD) has greater pharmacological potency than unmodified SOD through an increase in cell membrane affinity and half-life in plasma. Recently, ischemia or hypoxia alone has been suggested to result in increased superoxide anions, which lead to apoptosis in cardiomyocytes. We tested the effect of lecithinized SOD in reducing the infarct size following prolonged myocardial ischemia without reperfusion. Rats were subjected to a 24-h left coronary occlusion. Lecithinized SOD, unmodified SOD, free lecithin derivative or PBS was administered intravenously 30 min before coronary occlusion. SOD concentration of the heart, measured by ELISA, was higher in the lecithinized SOD-treated group than in the other groups 24 h after administration. The infarct area ratio of the heart, assessed by TTC staining, in the lecithinized SOD-treated group was significantly smaller than those of the other groups. Both TUNEL-positive cardiomyocytes and DNA laddering were attenuated in the ischemic area of the heart treated with lecithinized SOD. Single bolus administration of lecithinized SOD had a cardioprotective effect against ischemia without reperfusion in the rat model of acute myocardial infarction, possibly due to its sustained high tissue concentration.
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PMID:Lecithinized copper, zinc-superoxide dismutase ameliorates ischemia-induced myocardial damage. 1148 6

Adrenochrome is an oxidative product of adrenaline and possesses cardiotoxic properties. As oxygen free radicals play a role in the cytotoxic effects of catecholamines, the role of superoxide anion radicals, as mediators of adrenochrome toxicity, was investigated using electrically-driven Langendorff rabbit hearts with depleted catecholamine stores. Repetitive regional myocardial ischemia (MI) was induced by coronary artery branch ligature, and MI was quantitated from epicardial NADH-fluorescence photography. Adrenochrome (10(-6) mol/l) was added to the perfusion solution after a reperfusion period of 20 min, 30 min before the 2nd coronary occlusion, with or without the additional application of SOD (30 U/ml). Left ventricular pressure was significantly enhanced by adrenochrome (p < 0.05), but it fell rapidly down below its initial value (p < 0.05). Coronary flow was significantly decreased by adrenochrome (p < 0.05). Whereas epicardial NADH-fluorescence was similar after repetitive coronary occlusions in untreated controls, it was significantly enhanced by adrenochrome (p < 0.05). The deleterious effects of adrenochrome on MI were not inhibited by SOD. Thus, there is no evidence for superoxide anion radicals as mediators of the deleterious effects of adrenochrome on MI in isolated rabbit hearts. The deleterious effects of adrenochrome on MI in isolated rabbit hearts might be caused by functional effects, impairing the oxygen consumption/oxygen supply balance.
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PMID:Studies on the role of superoxide anion radicals for the cardiotoxicity of adrenochrome. 1179 43

Without a doubt PEG-SOD has been the enzyme most studied in PEGylation. One can say that it represents the preferred model to assess chemistries for PEG activation, analytical procedures suitable for conjugate characterization, the influence of PEG size in conjugate removal from circulation and elimination of immunogenicity and antigenicity, and the effect of route of administration. The effect of PEG conjugation was studied in vitro and in vivo models in comparison with the free enzyme and the following conclusions may be drawn: (1) At the blood vessel level, PEG-SOD has been shown to provide a greater resistance to oxidant stress, to improve endothelium relaxation and inhibit lipid oxidation. (2) In the heart, PEG-SOD proved to be at least as effective as native SOD in treatment of reperfusion-induced arrhythmias and myocardial ischemia. (3) In the lung, PEG-SOD appeared to be able to reduce oxygen toxicity and E. coli-induced lung injury, but not in the treatment of lung physiopathology associated with endotoxin-induced acute respiratory failure and in the reduction of asbestos-induced cell damage. (4) On cerebral ischemia/reperfusion injuries the effect of PEG-SOD was uncertain, also due to the difficulty of cerebral cell penetration. (5) In kidney and liver ischemia both enzyme forms were found to ameliorate reperfusion damage. In view of so much positive research on PEG-SOD, it is surprising that no approved application in human therapy has been established and approved.
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PMID:Polyethylene glycol-superoxide dismutase, a conjugate in search of exploitation. 1205 16


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