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)

It was established that in blood of patients with ischemic heart disease due to atherosclerosis of the coronary arteries (the diagnosis was verified in selective coronaroangiography) the content of acylhydroperoxides grows while the activity of glutathione-peroxidase II decreases. In blood of patients with no damage to the coronary vessels (according to the results of angiography), glutathione-peroxidase II activity does not differ significantly from the values in the control group. The decrease of glutathione-peroxidase II activity was most marked in patients with ischemic heart disease and hypercholesterolemia. It is suggested that the increase in the peroxide content in blood of patients with ischemic heart disease may be due to the sharp decrease in the activity of glutathione-peroxidase II.
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PMID:[Lipid peroxides and atherosclerosis. The enzymatic detoxication of lipid peroxides in the blood in ischemic heart disease due to coronary artery arteriosclerosis]. 45 35

The myeloperoxidase of peripheral blood neutrophils revealed by the cytochemical method was investigated in a group of patients with ischemic heart disease (24 men, mean age--51) treated with HBO (10 sessions, under 1.5-1.7 ata, for 60 min) prior to and after each HBO session. The ECG monitoring was performed during these sessions as well. A correlation analysis of the peroxidase index (mean enzyme content in 100 cells), total peroxidase activity and tension index (obtained by computer analysis of cardiac rhythm changes) was carried out in that group of patients. A close correlation was found between the total peroxidase activity and tension index.
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PMID:[Characteristics of cardiac rhythm and the peroxidase activity of blood in patients with ischemic heart disease treated by hyperbaric oxygenation]. 166 72

Afferent fibers mediating pain from myocardial ischemia classically are believed to travel in sympathetic nerves to enter the thoracic spinal cord. After sympathectomies, angina pectoris still may radiate to the neck and inferior jaw. Sensory fibers from those regions are thought to enter the central nervous system through upper spinal cord segments. We postulated that axons from nodose ganglion cells might project to cervical cord segments. The purpose of this study was to determine the density and pathway of vagal afferent innervation to the upper cervical spinal cord. Following an injection of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) into the upper cervical spinal cord, approximately 5.8% of cells in the nodose ganglion contained reaction product. Cervical vagotomy did not diminish the density of WGA-HRP labeled cells in the nodose ganglion. However, a spinal cord hemisection cranial to the injection site eliminated labeling of nodose cells. These data indicate that a portion of vagal afferent neurons project from the nodose ganglion to the upper cervical spinal cord. In addition, vagal afferent fibers reach the spinal cord via a central route rather than through dorsal root ganglia.
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PMID:Projection of nodose ganglion cells to the upper cervical spinal cord in the rat. 172 Jul 4

The localization of creatine kinase M (CK-M) in both normal and acute ischemic canine myocardial cells was studied by immunoelectron microscopy using the anti-CK-M Fab'-horseradish peroxidase conjugate. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery for 15, 60, or 180 minutes. In the normal myocardial cells, CK-M was localized mostly in the A-band and some in the Z-line, M-line, sarcolemmal membrane, and membrane of sarcoplasmic reticulum. Most CK-M in the A-band appeared to associate with thick fibers. This finding strongly suggests that the CK associated with thick fibers may be the enzyme to rephosphorylate ADP produced by myosin ATPase. In 15 minutes of myocardial ischemia, CK-M showed only minimal changes in its location, i.e., almost similar to normal, indicating that the CK in the A-band still has the ability to couple with myosin ATPase. However, in 60 and 180 minutes of ischemia, the A-band CK dissociated markedly from thick fibers, diffused to the I-band and leaked out to the intercellular spaces. These results suggest that the dissociation and disappearance of the A-band CK from thick fibers induced by progress of myocardial ischemia disrupt the myocardial energy transport system via CK reaction, and lead to the irreversible injury of myocardial cells.
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PMID:[Immunoelectron microscopic studies on the localization of creatine kinase M in normal and ischemic myocardial cells]. 240 81

Superimposition of cardioplegic arrest on acute low-cardiac-output states, as may occur after failure of percutaneous transluminal coronary angioplasty requiring emergency surgery, is associated with an increased operative risk. This increased risk is possibly attributable to reperfusion, which, after sequential episodes of myocardial ischemia, exacerbates tissue injury mediated by oxygen free radicals. One of the most cytotoxic of these active oxygen species is the hydroxyl radical, which is formed from superoxide anion and hydrogen peroxide through an iron-catalyzed reaction. This study assesses the effects of peroxidase, a hydrogen-peroxide scavenger, and of deferoxamine, an iron chelator, in isolated working rat hearts subjected to 30 minutes of low-flow ischemia (75% reduction in coronary flow) followed by 2 hours of cardioplegic arrest at 15 degrees C and by 30 minutes of normothermic reperfusion. Three groups of hearts (n = 7) were studied. Two groups were pretreated with either peroxidase (10,000 units/l) or deferoxamine (0.03 mM) during the last 15 minutes of the low-flow ischemic period. The third group received no prearrest intervention and served as a control group. In addition to hemodynamic determination, high-energy phosphate content [adenosine 5'-triphosphate (ATP)] and intracellular pH were monitored serially by 31P nuclear magnetic resonance spectroscopy. The two pretreated groups had better recovery of ATP levels and aortic flow values than did the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioplegic arrest superimposed on evolving myocardial ischemia. Improved recovery after inhibition of hydroxyl radical generation by peroxidase or deferoxamine. A 31P nuclear resonance study. 284 3

If myocardial ischemia always results from an imbalance between the needs and supplies in oxygen of the myocardium cells, the physiopathology of this process seems today infinitely more complex than the mere diminution or interruption of the output in a coronary artery. The extension of atheromatous lesions, the platelets aggregation, thrombosis, the coronary spasm, the release of products from the arachidonic cascade, the reactivity of the vascular endothelium, the profibrinolytic activity of the tissues are many of the intricate factors inducing myocardial ischemia. Cellular alterations, of which some are triggered by the release of oxygenated free radicals, lead then to an irreversible necrosis. The medications used until now in the treatment of angina are oxygen scavengers and research goes on in this direction with vaso-dilators beta-blockers, prolonged action nitro-compounds (nicorandil) or nitro-compounds with an action reinforced by N-acetyl-cysteine, bradycardiac derivates of alinidine and the new calcium antagonists dihydropyridine. However, the new physiopathological concepts of ischemia have opened new directions for the research: products which modify the arachidonic cascade by increase of synthesis or release of PGI2 (nafazatrom, defibrotide), by inhibition of TXA2 synthesis or blocking of TXA2 receptors, and similar products of PGI2 (iloprost); thrombolytic agents more specific of thrombin (PTA) or fibrinolysis activators (defibrotide), and anticoagulants with extended action; chelating agents of oxygenated free radicals (peroxide dismutase, catalase, peroxidase) or xanthine oxidase inhibitors; platelets anti-aggregates like ticlopidine which blocks the platelets receptors to fibrinogen, or inhibitors of the synthesis of pro-aggregating agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current therapeutic concepts in the treatment of myocardial ischemia. Current and future drugs]. 287 4

Myocardial ischaemia results from complex interrelated processes involving progression of atherosclerosis, thrombosis, coronary spasm, platelet aggregation and local release of products from the arachidonic acid cascade. Endothelium-dependent responsiveness contributes to the local regulation of coronary blood flow, and the presence of endothelial damage may result in enhanced contraction of the smooth muscle. Drugs which have been used for the treatment of angina pectoris are able to reduce myocardial oxygen consumption. This concept will further be developed in the near future with beta-blocking agents with vasodilating properties, potent long acting nitrates (nicorandil), bradycardic agents (AQA 39 or AS-AH 208), and new calcium antagonists. However, future prospects in the treatment of angina pectoris include: drugs modifying the arachidonic acid cascade by increasing synthesis or release of prostacyclin (nafazatrom) or decreasing prostacyclin degradation (almitrine), or blocking thromboxane A2 synthetase (dazoxiben) or thromboxane A2 receptors (BM 13177) or, blocking the lipoxygenase pathway (nafazatrom) or prostacyclin analogues (iloprost); more clot-specific thrombolytic agents and new oral anticoagulant drugs; free-radical scavengers such as superoxide dismutase, catalase or peroxidase and drugs inhibiting xanthine-oxidase; anti-platelet drugs such as ticlopidine which blocks the fibrinogen receptors of platelets; drugs preventing the progression of atherosclerosis lesions such as nifedipine or verapamil in animals fed high-lipid diets; drugs which could modify myocardial metabolism during ischaemia. In this context, trimetazidine acts through prevention of ischaemia-induced decrease in ATP cellular storages, inhibition of potassium leak, decrease in free-radical production and thromboxane A2 synthesis and increase in prostacyclin synthesis. These new concepts provide an important contribution to the understanding of the pathophysiology of myocardial ischaemia. This explains the considerable development of pharmacological research for new agents in the treatment of angina pectoris.
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PMID:[Treatment of angina pectoris. New perspectives]. 294 45

This study assesses the ability of the free-radical scavenger peroxidase to enhance cardioplegic protection when given during or before myocardial ischemia. Forty-four isolated isovolumetric buffer-perfused rat hearts were studied. In a first series of experiments that consisted of three groups, hearts were subjected to 90 min of normothermic global ischemia followed by 45 min of reperfusion. One group received a crystalloid cardioplegic solution given as a single dose at the onset of arrest. A second group received cardioplegic solution supplemented with superoxide dismutase (200,000 U/liter), and a third group received cardioplegic solution supplemented with peroxidase (6000 U/liter). Based on comparisons of postreperfusion coronary flow, left ventricular developed pressure, maximum dP/dt, and diastolic pressure, we found that the best protection was provided by peroxidase-enriched cardioplegia. A second series of experiments was then undertaken to assess the effects of the latter enzyme given as a pretreatment. Hearts were subjected to 3 hr of global ischemia, during which myocardial protection was provided by hypothermia (15 degrees C) along with multidose cardioplegia. The treatment group was given peroxidase (10,000 U/liter) added to the perfusate fluid for 15 min before the onset of cardioplegic arrest without further enzyme supplementation during ischemia or reperfusion. Hearts perfused with standard buffer for an equal period of time served as controls. While the two groups demonstrated the same degree of postischemic increase in myocardial stiffness, peroxidase-pretreated hearts had a significantly better recovery of contractile indexes at 30 and 45 min of reflow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of cardioplegic protection with the free-radical scavenger peroxidase. 302 57

A histopathological and histoimmunological comparison was performed on 143 fragments on coronary arteries taken from 43 patients who died of ischemic heart disease and from 20 patients who died of other diseases. The immunological study research of Ig (A, G, M) and C3 fraction of complement in the 3 coronary layers was done by the immuno-peroxidase technique. The fixation was essentially observed in fibromyocytes. A good correlation existed between atherosclerosis lesions and fixation of Ig and C3 fraction of complement in both the media and the intima. On the other hand, this correlation was not observed in the adventitia. Accumulation of immunoglobulins and of the C3 fraction of complement in atherosclerosis seemed specific and proportional to the degree of arterial well lesion. The significance and the role of this accumulation remains to be studied. It may be hypothesized that Ig and complement fixation on fibromyocyte cell receptors or on the fibrous tissue fundamental substance is followed by the formation of antigen-antibody complexes, which act as foreign bodies which are either responsible for (or a reflection) of the onset of lesions or, at least, of their increasing severity or their persistence.
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PMID:[Presence of immunoglobulins and complement in the walls of the coronary arteries in atherosclerosis]. 353 28

This report represents the first application of immunohistochemical methods for localizing an exogenously administered drug. Intravenously administered procainamide was localized in normal, ischemic, and necrotic myocardium in 23 dogs. Rabbit antiprocainamide antibodies were used in an avidin-biotin-peroxidase complex staining method. Normal myocardium demonstrated diffusely positive immunostaining for procainamide, as did the cardiac conduction system and vascular endothelial cells. Necrotic myocardium demonstrated markedly reduced to absent immunostaining. By contrast, in regions of myocardial ischemia without necrosis, immunostaining for procainamide was similar to that in the normal myocardium. Procainamide myocardial tissue levels were reduced in necrotic and ischemic zones compared to normal (p less than 0.05) only in those animals in which procainamide was administered after rather than before the onset of coronary occlusion. The demonstration of the absence of drug binding in the necrotic cells suggests that myocardial tissue levels or radiolabelled assessment of drug distribution can be misleading when nonhomogeneous tissue is sampled. The immunohistochemical technique provides additional information about the regional and cellular distribution of procainamide that is complementary to the information obtainable by radiolabelling microspheres and from biochemical assays.
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PMID:Immunohistochemical localization of procainamide in normal, ischemic, and necrotic canine myocardium during acute experimental myocardial infarction. 359 7


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