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)

Activation of lipid peroxidation during myocardial ischemia may be determined by the reduction of the enzymatic antioxidant cell protection. Such a conclusion has been drawn on the basis of an analysis of variation in the activity of superoxide dismutase, glutathion peroxidase and catalase in experimental myocardial ischemia in rats, induced by ligation of the left descending artery of the heart. In the early period of ischemia (1-3 h) the activity of superoxide dismutase and glutation peroxidase markedly decreases. In the periischemic zone, the fall in the enzymatic activity is not so pronounced. The activity of the enzymes does not reach the basic level 5 days after the operation.
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PMID:[Activity of antioxidative enzymes of the myocardium during ischemia]. 706 2

To determine whether liposomes (microscopic phospholipid vesicles) may be useful in delivering drugs to a region of myocardial ischemia, we studied the concentration of positively charged and neutral liposomes containing 131I-albumin and horseradish peroxidase in ischemic myocardium of 20 dogs during the first 4 hours of experimental myocardial infarction. We studied the interaction of liposomes containing fluorescent dyes and horseradish peroxidase with isolated contracting cardiac myocytes. We found that positively charged and neutral liposomes accumulated in poorly perfused myocardium and that positively charged liposomes accumulated in the ischemic region to a greater extent than neutral liposomes [138 +/- 21 vs. 81 +/- 9% (mean +/- SE) of the concentration of liposomes in uninvolved myocardium]. Electron microscopic examination of this myocardium showed liposome contents to be located in the vascular space, in endothelial cells, and in ischemic myocytes. We found high potassium environment and that liposomal contents were scattered throughout the interior of the cells in the electron micrographs of some of the isolated myocytes. Anoxia alone for 20-30 minutes did not modify the liposome-isolated myocyte interaction or cause depolarization of the cells. We conclude that liposomes may be useful as drug carriers to depolarized ischemic myocardium, although significant uptake by normal myocardial cells cannot be expected with lecithin, cholesterol, and octadecylamine liposomes we used.
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PMID:Liposome concentration in canine ischemic myocardium and depolarized myocardial cells. 724 77

To clarify the changes in creatine kinase M localization along with the progress of myocardial ischemia, immunoelectron microscopic studies were performed using rabbit anti-canine creatine kinase M Fab'-horseradish peroxidase conjugate in 21 dogs. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery for 15 (n = 5), 30 (n = 5), 60 (n = 5), or 180 (n = 4) minutes. Two dogs were used as normal controls. As we have already demonstrated, most creatine kinase M in normal myocardial cells was localized over the entire A band in association with the thick filament, suggesting that creatine kinase in this region (A-band creatine kinase) was the enzyme coupled with myosin ATPase. After 15 minutes of ischemia, creatine kinase M showed only minimal changes in its location, indicating that A-band creatine kinase still has the ability to couple with myosin ATPase (reversible injury). However, after 30 minutes of ischemia, A-band creatine kinase diffused markedly to the I band (transitional phase), and after 60 minutes of ischemia, it leaked out to extracellular spaces (irreversible injury). After 180 minutes of ischemia, most A-band creatine kinase disappeared from the myocardial cells (coagulation necrosis). These features of creatine kinase M localization seemed to reflect each stage of ischemic cell injury. We conclude that myocardial ischemia results in a dissociation of creatine kinase molecules from the thick filament, which leads the energy transport system to destruction.
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PMID:Changes in creatine kinase M localization in acute ischemic myocardial cells. Immunoelectron microscopic studies. 840 63

It is known that the peroxidation of LDL is a trigger for developing arteriosclerosis. The oxidized LDL is produced by either oxidative stress or a few oxidant. Selenium decreased in serum and some organs of stroke-prone spontaneously hypertensive rats (SHRSP), which is a cofactor of glutamine peroxidase. Serum magnesium decreased in patients with diabetes mellitus, with ischemic heart disease, with essential hypertension and with cerebral vascular lesions. Calcium to magnesium ratio was higher in some organs of SHRSP as compared to Wistar Kyoto rats (WKY). These changes accelerated vascular lesions in SHRSP.
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PMID:[Overview--suppression effect of essential trace elements on arteriosclerotic development and it's mechanism]. 858 7

This study was designed to investigate whether a new irreversible injury to the myocardium can occur 6 hours after reperfusion following ischemia. Conscious rabbits were subjected to myocardial ischemia for 30 minutes, followed by reperfusion. Horseradish peroxidase (HPR) tracing with TTC staining and histological quantification were used to study the histopathological changes in myocardial tissues. Necrotic myocardium at 6 hours after reperfusion gave positive HRP results and viable myocardium at 24 hours after reperfusion gave positive TTC results. Some myocardial tissue between the above two regions were found to be HRP negative as well as TTC negative, indicating that myocardial tissue death occurred between 6 to 24 hours after reperfusion. The myocardial infarct size at 24, 48, and 72 hours after reperfusion were 7.0%, 5.1% and 3.2% larger than that 6, 24 and 48 hours respectively. Therefore, new irreversible myocardial injury in the rabbit can still occur after 6 hours of reperfusion following myocardial ischemia for 30 minutes and cumulative myocardial injury from 6 to 72 hours after reperfusion can result in a marked extension of the size of myocardial infarct.
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PMID:[A pathologic study of delayed myocardial reperfusion injury]. 927 61

Red cell redox-status and hemodynamic changes were studied in 60 old patients with ischemic heart disease. The treatment consisted of standard therapy (ST), ST + amino acid composition (glutaminic acid, glycine, cysteine) or preductal (15, 30 and 15 patients, respectively). Glutathione levels, activity of glutathione-transferase, reductase, peroxidase, catalase, Cu-, Zn-superoxide dismutase, red cell levels of malonic dialdehyde, hemodynamic parameters according to echo-CG and ECG monitoring were estimated before the treatment and 20 days after it. Endogenic antioxidant defense/hemodynamic parameters correlation coefficients were calculated. Close correlations were not found. However, ST + amino acid composition demonstrated the weakest correlations between the antioxidant defense and hemodynamics, while ST + preductal produced the greatest number of correlations. It is suggested that amino acids promote search for the antioxidant system's optimum while ST + preductal promotes closer correlations between red cell redox status and hemodynamic parameters.
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PMID:[Parameters of hemodynamics and red cell redox-status in old patients with ischemic heart disease]. 1097 43

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

In this study, an animal model of early myocardial ischemia (EMI) was established by ligating the left anterior descending coronary artery of rats. The experimental animals were divided into five groups according to different intervals of MI (15, 30min, 1, 2, and 3h) and one control group. Tissues from the apex of the myocardium and the adjacent myocardium were taken for paraffin sections, followed by hematoxylin-eosin and streptavidin-biotin-peroxidase complex (SABC) staining. Results showed that the myoglobin (Mb) depletion and the fibrinogen (Fg) staining increase were detected in the 30min MI group. The wavy-like increasing extension of the size and the intensity of the Mb depletion and the Fg staining intensification from the subendocardial to the subepicardial cells were observed along with the prolongation of the ischemic period. Both changes had similar patterns and sensitivity, except Fg was less reliable than Mb as it is more easily contaminated by blood. After overcoming blood contamination, the SABC-Fg technique will provide a new method for the diagnosis of EMI.
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PMID:The contrast of immunohistochemical studies of myocardial fibrinogen and myoglobin in early myocardial ischemia in rats. 1293 92

Depletion of heart fatty acid binding protein (H-FABP) from cardiomyocytes with varying post-ischemia intervals was studied in acute myocardial infarction (AMI) model of rat, and 22 human autopsy cases were studied with streptavidin-peroxidase conjugated method (S-P). It was observed that as early as 15 min after ischemia, the depletion of H-FABP could be detected in model rats. With the ischemic time prolonged, the depletion of H-FABP was more and more evident. In all human cases with myocardial infarction, absent H-FABP staining could be found in infarcted area. And in some suspected early myocardial infarction cases, depletion of H-FABP staining could be demonstrated in areas that showed normal hematoxylin-eosin (HE) staining. The blood samples from model rats before ligation, at varying post-ischemia intervals and various postmortem time were measured for plasma concentration of H-FABP with enzyme-linked immuno-sorbent assay (ELISA) method. At 15 min after myocardial ischemia, the concentration of H-FABP was 4 times higher (546.0+/-85.3 microg/l) than that of the baseline level (103.7+/-94.1 microg/l). With the continuation of ischemic time, the concentration of H-FABP increased and peaked at 4 h (1953.5+/-405.3 microg/l), then decreased. The plasma concentration of H-FABP decreased slightly with postmortem time, but was still significant higher at any postmortem intervals than that of baseline level within 48 h after death. The results suggest that H-FABP staining can detect very early ischemic damages in human myocardium and the elevated plasma concentration of H-FABP in rat was an indicator of AMI, which was not affected by autolysis.
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PMID:Heart fatty acid binding protein as a marker for postmortem detection of early myocardial damage. 1618 85

Guan-Xin-Er-Hao (GXEH) is a Chinese medicine formula for treating ischemic heart diseases (IHD) and has a favorable effect. Our aim was to examine whether or not acute oral GXEH could protect the heart against myocardial infarction and apoptosis in acute myocardial ischemic rats. If so, we would explain the antioxidative mechanism involved. The left anterior descending coronary artery was occluded to induce myocardial ischemia in hearts of Sprague-Dawley rats. At the end of the 3h ischemic period (or 24h for infarct size), we measured the myocardial infarct size, myocardial apoptosis and the activities of antioxidative enzymes. GXEH reduced infarct size, myocardial apoptosis and the serum level of malondialdehyde (MDA), increased the activities of total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and GSH-peroxidase (GPX) activities and the serum level of glutathione (GSH). GXEH exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, likely through its antioxidation and antilipid peroxidative properties, and thus may be used as a promising agent for both prophylaxis and treatment of IHD.
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PMID:Chinese medicinal formula Guan-Xin-Er-Hao protects the heart against oxidative stress induced by acute ischemic myocardial injury in rats. 1895 Oct 1


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