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)

In a prospective multicenter study, 244 men with highly or moderately differentiated prostatic cancer in stage I, II or III (VACURG) were consecutively randomized to three groups of treatment: Group A (77 patients) received polyestradiol phosphate (Estradurin, Leo) 80 mg i.m. every fourth week + ethinyl estradiol (Etivex, Leo) 150 micrograms daily, group B (72 patients) estramustine phosphate (Estracyt, Leo) 280 mg twice daily, and group C (76 patients) no therapy. Only men without current or previous other malignancy and without cardiovascular disease were admitted to the study. After 4 1/2 years 125 of the 244 patients had left the study, 9 because of cancer progression (stage IV, VACURG). The most serious complications were cardiovascular, including ischemic heart disease, cardiac decompensation, cerebral ischemia and venous thromboembolism, which occurred in 24 patients from group A and 9 from group B as compared to only one patient in group C. The subgroup superficial or deep venous thrombosis comprised 11 group A and 2 group B patients. Estrogens (E + e) offered as palliative treatment to patients with non-generalized prostatic carcinoma is burdened with a high incidence of serious cardiovascular complications.
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PMID:Cardiovascular complications of estrogen therapy for nondisseminated prostatic carcinoma. A preliminary report from a randomized multicenter study. 352 68

The hypothesis that prostacyclin (PGI2) might have a direct cytoprotective action in ischaemic cardiac tissue was investigated. Myocardial ischaemia was induced in perfused rabbit hearts by ligating the left main coronary artery. Coronary flow, oxygen uptake, and turnover of lactate and purines were measured before and up to 120 min after coronary occlusion. After this, ischaemic tissue was separated from perfused myocardium, and levels of lactate, adenine nucleotides and creatine phosphate were determined in specimens from non ischaemic, ischaemic and border zones. PGI2 (final conc. 10(-7) M) was infused before or 30 min after ligation and the results were compared to those in control hearts. Coronary ligation reduced coronary flow and oxygen consumption by about 50%. The fractional extraction of lactate decreased from 20% to close to zero and purine release increased 5-fold. In the non-ischaemic area the tissue levels of ATP and creatine phosphate were high, with a low content of lactate, but in the ischaemic area the levels of ATP and creatine phosphate were considerably reduced and the content of lactate was high. Although coronary flow and oxygen uptake were elevated after treatment with PGI2, no change in lactate or purine turnover was observed. Neither the weight of the non-perfused myocardium nor the tissue levels of the adenine nucleotides, creatine phosphate and lactate were affected by PGI2 treatment. The data indicate that in this model, in which effects on cardiac work, collateral flow and platelets are eliminated, PGI2 does not limit ischaemic myocardial injury. Hence, the hypothesis of a direct cytoprotective action of PGI2 in ischaemic myocardial tissue was not supported.
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PMID:Effect of prostacyclin on the severity of ischaemic injury in rabbit hearts subjected to coronary ligation. 353 19

To evaluate the protective effects of L-carnitine on the ischemic myocardium, the effects of its administration on tissue levels of high energy phosphate and phospholipids were studied in ischemic dog hearts. Myocardial ischemia was induced by the ligation of the left anterior descending coronary artery for 40 min. In the experiment, L-carnitine (300 mg/kg) was administered intravenously prior to coronary artery ligation. Mitochondrial phospholipids were extracted from nonischemic and ischemic regions of the myocardium and subsequently analyzed. In ischemic myocardial tissues, levels of adenosine 5'-triphosphate (ATP) were reduced. The decrease was significantly elevated by L-carnitine pretreatment. The mitochondrial fractions obtained from ischemic myocardia had significantly lower levels of phospholipids than those obtained from nonischemic tissues. Moreover, the amounts of phosphatidylcholine, phosphatidylinositol and phosphatidylethanolamine were significantly decreased in ischemic myocardial tissues. L-carnitine-pretreatment prevented the reduction of these phospholipids. Lysophosphatidylethanolamine and sphingomyelin did not show statistically significant decreases. This may explain why the administration of carnitine has beneficial effects on ischemic myocardium.
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PMID:Effects of L-carnitine on phospholipids in the ischemic myocardium. 359 11

Risk factors for atherosclerosis are often associated with haemorheological changes. On this point, obesity (recently advocated as an independent risk factor) was not much studied and with not univocal results. We have studied 70 obese patients (BMI greater than 30) and 50 healthy subjects (BMI less than 25). Among obese 26 had no more pathologies, 29 had hypertension, 3 suffered from ischemic heart disease, 3 suffered from occlusive arteriopathy, 9 were hyperlipidemic, 10 were smokers. We determined plasma viscosity and whole blood viscosity (at haematocrit corrected to 45% too). Washed erythrocytes, poor in leucocytes and platelets and resuspended in phosphate-buffered saline, were used for study of erythrocyte viscosity and deformability. Obese patients showed raised mean blood viscosity values when compared to healthy controls (p less than 0.01); an even more significant increase (p less than 0.001) was found concerning plasma viscosity and fibrinogen. Erythrocyte viscosity and red blood cell filterability index did not show any significant difference. We found no significant correlation between viscosity values and presence of hypertension, hyperlipidemia and smoking habit among obese. In conclusion, the higher vasculopathy incidence might be caused by an increase in blood viscosity, mostly due to plasmatic component. This fact appears to be independent from the presence of atherosclerosis complications or other risk factors.
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PMID:[Hemorrheologic disorders in obese patients. Study of the viscosity of the blood, erythrocytes, plasma, fibrinogen and the erythrocyte filtration index]. 360 Nov 35

In this study of a canine heart model of localized reversible ischemia, a computer-based single-processing method is developed to detect and localize the epicardial projections of ischemic myocardial electrocardiograms (ECGs) during the cardiac activation, rather than the repolarization, phase. This is done by transforming ECG signals from an epicardial sensor array into the multichannel spectral domain and identifying three decision variables: (1) the frequency in hertz of the spectral peak (f0), its frequency band width 50% below the peak value (w0), and the maximum eigenvalue difference of the ECG signal's autocorrelation matrix (e0). With use of the histograms of the f0, w0, and e0 parameters of 3256 ECGs from normal and 957 from ischemic areas of myocardium obtained from 12 dogs, it was possible to predict ischemia in a new test group of nine animals from a Neyman-Pearson (NP) test in which the threshold probabilities of detecting ischemia for each decision variable are compared with those of detecting normality. Quantification of each sensor area by the NP tests revealed that, compared with the control, ECG spectra with decreased F0 and w0 and increased e0 relative to their respective thresholds had increased myocardial lactate (p less than 0.01), decreased adenosine triphosphate (ATP) (p less than 0.05), and reduced creatine phosphate (p less than 0.01). Prediction of f0 (p less than 0.0006) as a continuous variable could be obtained from the regression of the myocardial levels of ATP plus creatine phosphate, which demonstrated that this decision variable appears to directly reflect myocardial energetics. It appears that an advanced signal-processing method for ECG array data can be used to detect, localize, and quantify reversible myocardial ischemia.
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PMID:Advanced signal-processing method for the detection, localization, and quantification of acute myocardial ischemia. 361 12

Postreperfusion regional myocardial dysfunction may be associated with depletion of high energy phosphate compounds during ischemia and with their relatively slow repletion during reperfusion. However, few studies have correlated relatively rapid changes in regional myocardial function (sonomicrometers) and blood flow (microspheres) with high energy phosphate concentrations measured using phosphorus-31 nuclear magnetic resonance spectroscopy in intact large animal models of regional myocardial ischemia. The left anterior descending coronary artery of mongrel dogs was abruptly occluded for 17.1 +/- 1.9 minutes and then completely released; measurements were made for an additional 22 minutes. Transmural blood flow decreased from 1.07 +/- 0.25 to 0.25 +/- 0.10 ml/(min X g) and holosystolic expansion was observed in all dogs (segmental systolic shortening decreased from 9.3 +/- 3.7 to -6.3 +/- 6.0%). Phosphocreatine (PCr) measured during 4.4 minute sampling intervals decreased to steady state within the first sampling period after occlusion and was 45.9 +/- 17.0% of control at the end of the occlusion, whereas beta-adenosine triphosphate (beta-ATP) reached its lowest level early after reperfusion (72.7 +/- 13.3% of control). The ratio of PCr to inorganic phosphate (Pi) decreased during the occlusion (3.34 +/- 0.75 versus 1.01 +/- 0.61) but returned to control level early during reperfusion. The ratio of PCr to beta-ATP also decreased during coronary occlusion (2.16 +/- 0.39 versus 1.29 +/- 0.39) but did not return to control level during reperfusion. Significant correlations were observed between the intensity of ischemia (reduced blood flow) and reductions in regional contractile function, PCr, beta-ATP, myocardial pH and the increase in Pi during the coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional myocardial blood flow, function and metabolism using phosphorus-31 nuclear magnetic resonance spectroscopy during ischemia and reperfusion in dogs. 362 71

Phosphorus-31 nuclear magnetic resonance spectroscopy (31P NMR) was used to assess the temporal changes of high-energy phosphate metabolites in the region of acute myocardial ischemia of open-chest cats. Eight anesthetized cats were studied following ligation of the left anterior descending coronary artery. Creatine phosphate showed a 79 +/- 16% (mean +/- SD) reduction by 4 min after the onset of ischemia. Prominent qualitative reductions of the spectral peak of creatine phosphate occurred by 40 s after ischemia. Adenosine triphosphate measured under the beta spectral peak (beta-ATP) decreased 37 +/- 9% by 20-25 min after ligation of the left anterior descending coronary artery. These reductions developed more slowly and were of smaller magnitude than those of creatine phosphate. Intracellular pH decreased from 7.39 +/- 0.07 to 7.13 +/- 0.09 units by 40 s after ischemia. By 30 min, pH decreased to 6.07 +/- 0.40 units. The study shows, therefore, the temporal changes of high-energy phosphate metabolites during ischemia in localized regions of the myocardium of open-chest animals.
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PMID:In vivo evaluation of intracellular pH and high-energy phosphate metabolites during regional myocardial ischemia in cats using 31P nuclear magnetic resonance. 371 90

The purpose of this study was to compare the in vitro metabolic changes in mouse peritoneal macrophages exposed to sera of CHD patients and healthy donors. Oxidative (metabolic) burst was estimated by the activity of one of the limiting enzymes of hexose monophosphate shunt--glucoso-6-phosphate dehydrogenase. Pronounced enhancement of glucoso-6-phosphate dehydrogenase activity accompanied the exposure of macrophages to sera of patients with acute myocardial ischemia during the first two days after the onset of anginal pains. The correlation was established between the activity of creatine kinase in the sera of patients with acute myocardial infarction and the ability of these sera to enhance glucoso-6-phosphate dehydrogenase activity in mouse peritoneal macrophages.
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PMID:[Activation of glucose-6-phosphate dehydrogenase in mouse peritoneal macrophages by sera from patients with ischemic heart disease]. 373 May 42

In 34 patients with acute myocardial infarction (MI) plasma pyridoxal-5'-phosphate (PLP) levels were significantly lower (5.22 +/- 1.88 ng/ml) than those in an age- and sex-matched control group (11.5 +/- 2.03 ng/ml). In another group of patients who had clinical and angiographic evidence of ischaemic heart disease but had not had an MI plasma PLP levels were not significantly different from those in the control group (10.07 +/- 2.98 ng/ml). However, plasma high-density lipoprotein cholesterol levels in this group (0.75 +/- 0.28 mmol/l) as well as in the MI group (0.76 +/- 0.28 mmol/l) were significantly lower than those in the control group (1.26 +/- 0.23 mmol/l). On follow-up, all of 15 patients who had had an acute MI showed a continuous decrease in plasma PLP levels of approximately 50% during the first 48 hours after admission. Sixteen healthy volunteers subjected to a period of prolonged fasting (+/- 30 hours) displayed a decrease of approximately 43% over this period. We conclude that an acute reduction in plasma PLP levels occurred during the acute phase of MI. Other factors, for example prolonged acute starvation, may also produce a rapid decrease in plasma PLP levels.
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PMID:Plasma pyridoxal-5'-phosphate levels in myocardial infarction. 373 53

A procedure is described for estimation of aldolase of the type A-a tissue-specific enzyme of myocardium--in blood serum under conditions of myocardial infarction. The rate of the enzymatic reaction was estimated by monitoring production of heptulose-1,7-diphosphate. Erythrose-4-phosphate and dihydroxyacetone phosphate were used as substrates of the reaction. High rates of the reaction product accumulation was observed if the compounds, shifting the reaction K'equi, were not added into the experimental samples. Sensitivity of the test was 3-fold increased due to modifications of the original method. Clinical experience with the test showed that activity of aldolase of the type A was distinctly higher in blood serum of patients with myocardium infarction as compared with the healthy donors or with the patients with ischemic heart disease.
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PMID:[Determination of aldolase A activity in the serum of patients with myocardial infarction]. 377 21


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