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

1. Plasma, platelet and erythrocyte glutathione peroxidase activities and serum lipid concentrations were measured in patients with ischaemic heart disease and matched control subjects. 2. Mean plasma and platelet glutathione peroxidase activities were significantly lower in the patients with ischaemic heart disease. Erythrocyte glutathione peroxidase activities and serum lipid concentrations were similar in patients with ischaemic heart disease and control subjects. 3. No correlations between plasma, platelet and erythrocyte glutathione peroxidase activities were observed. 4. The combination of plasma and platelet glutathione peroxidase activities provided an 86% discrimination between patients with ischaemic heart disease and matched control subjects. 5. Our data suggest that plasma and platelet glutathione peroxidases may be significant risk factors for ischaemic heart disease. Plasma glutathione peroxidase is a previously unrecognized risk factor.
 ...
PMID:Plasma, platelet and erythrocyte glutathione peroxidases as risk factors in ischaemic heart disease in man. 132 53

Literature on the various manifestations of the selenium deficiency in humans and animals is presented. Mechanisms of the biological effects of selenium brought about by glutathione peroxidase are considered. Biogeochemical anomalies, parenteral nutrition, malabsorption syndromes as conditions for the development of hyposelenosis are characterized as well as their manifestations (white-muscular disease, myopathies, cardiomyopathies, Keshan disease, Kashin-Beck disease). Selenium deficiency facilitates the development of the ischemic heart disease, myocardium infarction, certain types of malignancy and so on. The attention is drawn to the link of the selenium deficiency with imbalance of other trace elements.
 ...
PMID:[Hyposelenoses]. 212 81

Primary (dienic conjugates) and secondary (malonic dialdehyde) products of plasma lipid peroxidation were measured and the activity of antioxidative enzymes (glutathione peroxidase and superoxide dismutase) in erythrocytes was determined in 96 patients with chronic heart failure due to ischemic heart disease and rheumatic heart disease. Heart failure was found to show elevated plasma lipid peroxidation product levels, mostly in Stages I and IIA. Whereas in Stage IIB, the product levels became lower and in Stage III, they reached the control values. Similarly, the activity of superoxide dismutase varied with the stages of heart failure. That of glutathione peroxidase increased with circulatory decompensation development, reaching the maximal level in Stage IIB, then decreased down to the values observed in the control groups of patients without heart failure. The changes detected were not related to the causes of heart failure.
 ...
PMID:[Changes in antioxidative enzyme activity in patients with chronic heart failure]. 238 Nov 25

Dietary fat-type and copper (Cu) deficiency have been independently identified as potentially important factors in the etiology of ischemic heart disease (IHD); a disease that has been linked to inflammation and oxygen free radical (OFR) mediated damage. Group (n = 6) of male, weanling, Wistar rats were provided ad libitum with deionized water and control or low Cu diets containing (200 g/kg) either saturated or polyunsaturated fatty acids (SFA or PUFA, respectively) for 56 d. Measurement of several indices of Cu status indicated that both groups fed the low Cu diets were Cu-deficient. SFA consumption resulted in significantly increased hepatic Cu (p less than 0.001) and iron (Fe) (p less than 0.001) concentrations and xanthine oxidase activity (p less than 0.05) and significantly decreased hepatic glucose-6-phosphate dehydrogenase activity (p less than 0.001). Although Cu deficiency resulted in significantly decreased hepatic copper-zinc superoxide dismutase (CuZnSOD) activity (p less than 0.01), no significant effect on the activities of the other hepatic antioxidant enzymes, manganese superoxide dismutase, catalase, and glutathione peroxidase, or glutathione reductase, were observed. Cu deficiency also resulted in significantly decreased hepatic Cu levels (p less than 0.001) and cytochrome c oxidase activity (p less than 0.01). No significant difference in hepatic thiobarbituric acid reactive substances (TBARS), a measure of lipid peroxidation, was found between groups consuming SFA or PUFA, but both Cu-deficient groups exhibited significantly increased hepatic TBARS (p less than 0.001), compared to controls. This was probably owing to the significantly decreased hepatic CuZnSOD activity observed in the Cu-deficient, compared to control animals.
 ...
PMID:Dietary saturated or polyunsaturated fat and copper deficiency in the rat. 248 34

We hypothesize that oxygen free radicals are involved in the genesis and maintenance of volume and pressure overload heart failure. Pressure and volume overload would produce myocardial ischemia. During ischemia there will be an increase in xanthine and xanthine oxidase; and a decrease in the superoxide dismutase and glutathione peroxidase activity leading to an increase in the oxygen free radicals. A decrease in the cellular pH during ischemia would release phospholipase which would, in turn, release arachidonic acid from phospholipids. Leukotrienes and prostaglandins will be synthesized through arachidonic acid metabolism. During this synthesis not only oxygen free radicals will be produced but also there will be formation of leukotriene, LTB4, which is known to activate neutrophil and hence increased secretion of oxygen free radicals. Increased circulatory catecholamines due to compensatory mechanism would also lead to an increase in the oxygen free radicals. Oxygen free radicals are known to depress Ca++ binding and uptake of sarcoplasmic reticulum which would lead to a decrease in the myocardial contractility. We have shown that oxygen free radicals depress cardiac function and cardiac contractility. It is, therefore, suggested that oxygen free radicals might be involved in the development of heart failure. The use of agents that reduce the amount of oxygen free radicals would be of value in the prevention and treatment of heart failure.
 ...
PMID:Oxygen free radicals and heart failure. 283 9

The pathways for the metabolism of molecular oxygen involve one electron-transfer reaction with the subsequent production of reduced-oxygen intermediates. These reduced-oxygen intermediates include the superoxide anion (.O2-), hydrogen peroxide (H2O2), and the hydroxyl radical (.OH), which are highly reactive, short-lived species. Normally intracellular enzyme systems that include superoxide dismutase, catalase, and glutathione peroxidase are responsible for "scavenging" these products of oxygen metabolism. However, in many pathological states such as inflammation, ischemia, and reperfusion, there is an increased production of these reduced-oxygen intermediates, which are capable of extensive tissue damage. It is the purpose of this symposium to examine, in depth, the role of oxygen free radical systems as mediators of myocardial dysfunction and expand our knowledge of myocardial ischemia, ischemia-reperfusion injury, and the inflammatory response of the myocardium.
 ...
PMID:The oxygen free radical system and myocardial dysfunction. 298 5

Oxygen free radicals and phospholipid degradation have been implicated in the pathogenesis of ischemia and reperfusion injury. The present study examines the involvement of such mechanisms in myocardial reperfusion injury in neonatal hearts. The isolated neonatal pig hearts from two different age groups, 0 to 2 days old (newborn) and 7 to 9 days old (week-old), were subjected to 60 min of normothermic global ischemia followed by 60 min of reperfusion. Although myocardial ischemia reduced superoxide dismutase, catalase, and glutathione peroxidase activities in both age groups, superoxide dismutase and catalase activities remained significantly lower in the newborn pig heart during ischemia and reperfusion. Oxidized glutathione release from the neonatal pig hearts was at minimum levels before ischemia, but it increased 10-fold at the onset of reperfusion and was significantly higher in the newborn heart. This indicates that generation of oxygen free radicals was enhanced in the newborn compared with that in the week-old heart. The increase in phospholipase A2 activity and decrease in acyl CoA synthetase and lysophosphatidylcholine acyl transferase activities during ischemia and reperfusion were associated with comparable loss of membrane phospholipids and accumulation of lysophosphatidylcholine and free fatty acids in both age groups, except that oleic acid content was significantly higher in the newborn heart during reperfusion. Myocardial damage appears to be potentiated in the newborn heart during reperfusion, as evidenced by higher release of creatine kinase and a lower content of high-energy phosphates. These results indicate that oxygen free radicals may play a crucial role in the occurrence of reperfusion injury in immature hearts.
 ...
PMID:The mechanism of myocardial reperfusion injury in neonates. 366 15

In the isolated and perfused rabbit heart ischemia induced a rapid decline of contractility, associated with a reduction of the content of tissue GSH with no significant changes in GSSG. Reperfusion induced a small recovery of contractility, a substantial release of total glutathione and a further decrease in the content of tissue GSH with a significant increase of tissue GSSG. Glutathione reductase and glutathione peroxidase activities were not affected by ischemia and reperfusion. This study suggests a possible role for glutathione in the determination of functional damage induced by myocardial ischemia and reperfusion.
 ...
PMID:Changes in the cardiac glutathione status after ischemia and reperfusion. 396 36

Protective effects of a perfluorooctylbromide emulsion on myocardial ischemia and reperfusion (MI/R) injury were evaluated in a modified Langendorff rat heart preparation. Isolated rat hearts were equilibrated in Krebs-Henseleit solution (KH) for 35 minutes and perfused with either cardioplegic solution (CPS) or a 100% perfluorooctylbromide (PFOB) emulsion in CPS for 3 minutes. Hearts were then bathed in the emulsion or CPS. Both groups were subjected to 30 minutes of ischemia. Following 30 minutes of ischemia and 30 minutes of reperfusion with KH solution, hearts subjected to the 100% PFOB emulsion showed improved recovery of left ventricular function. Tissue activities of the antioxidant enzymes glutathione peroxidase, superoxide dismutase, and catalase were not affected by the emulsion in this model. Activity of lactate dehydrogenase (LDH) in the bathing medium was elevated at the end of the experimental period in both control and PFOB-treated hearts. The PFOB emulsion reduced the decline in ATP and GSH levels produced by cardioplegia and subsequent reperfusion. No differences were noted in oxidized glutathione (GSSG) levels. These data suggest that the PFOB emulsion provides some protection for the myocardium against injury associated with cardioplegia.
 ...
PMID:Effects of a 100% perfluorooctylbromide emulsion on ischemia/reperfusion injury following cardioplegia. 758 37

Adaptation to various forms of stress has been found to be associated with increased cellular tolerance to myocardial ischemia. In this study, the effects of myocardial adaptation to oxidative stress was examined by injecting rats with endotoxin (0.5 mg/kg) and its non-toxic derivative, lipid A (0.5 mg/kg). Both compounds exerted oxidative stress within 1 h of treatment as evidenced by enhanced malonaldehyde formation. The oxidative stress disappeared steadily and progressively with time in concert with the appearance of the induction of glutathione and antioxidative enzymes that included superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. After 24 h of endotoxin or lipid A treatment, the amount of oxidative stress and antioxidant enzyme levels were significantly lower and higher, respectively, compared to those at the baseline levels. Corroborating these results, both endotoxin and lipid A provided protection against myocardial ischemia and reperfusion injury as evidenced by a significantly improved postischemic recovery of left ventricular functions. The data presented here demonstrates that a controlled amount of oxidative stress induces the expression of intracellular antioxidants that can result in enhanced myocardial tolerance to ischemia. This suggests that myocardial adaptation to oxidative stress may be a potential tool for reduction of ischemic/reperfusion injury.
 ...
PMID:Oxidative stress adaptation improves postischemic ventricular recovery. 779 47


1 2 3 4 5 6 7 8 9 10 Next >>