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Biomedical subjects

I Edes

Publications and source records attributed to I Edes.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effect of thyroid status on phosphatidylinositols in rat heart.

The incorporation of 32Pi into phosphatidylinositols and inositol trisphosphates was studied in Langendorff-perfused hearts from hypothyroid, euthyroid and hyperthyroid rats. The hearts were perfused with modified Krebs buffer containing [32P]orthophosphate and the degree of 32P-labeling of phosphatidylinositol, phosphatidylinositol 4-monophosphate, phosphatidylinositol 4,5-bisphosphate, inositol trisphosphates and phosphatidic acid was measured. Hyperthyroidism was associated with increases in rates of rise and fall of left ventricular systolic pressure, sarcoplasmic reticular Ca(2+)-ATPase activity and 32P-labeling of phosphatidylinositols, inositol trisphosphates and phosphatidic acid. These measurements were significantly decreased in hypothyroid hearts. The tissue levels of inositol 1,4,5-trisphosphate isoform were found to be significantly higher in hyperthyroid hearts and lower in hypothyroid hearts than in euthyroid ones. Examination of phosphoinositide-specific phospholipase C activity in the perfused hearts revealed that hyperthyroidism was associated with an increase in the membrane-associated enzymatic activity, assayed at physiological calcium concentrations, while hypothyroidism was associated with a decrease in this activity as compared with control hearts. These findings indicate that alterations in the thyroid state of the myocardium may be associated with changes in basal phosphoinositide turnover which may contribute to alterations in myocardial contraction.

Animals↗
PubMed1991

[The significance of the dipyramidole echocardiography test in ischemic heart disease].

The diagnostic value of the dipyridamole echocardiography test was investigated in 46 patients who underwent coronary angiography due to suspected ischaemic heart disease. Twenty-two of 46 patients were found to have a narrowing of at least 70% one vessel. Twenty-four hour ECG monitoring was also performed on 19 patients on the day of the dipyridamole test. The sensitivity and specificity of the two-dimensional echocardiography test (new wall motion abnormality) were 72.7% and 62.5%. The ECG (V2-5-9) had a low sensitivity during the test (43.8%). Good agreement was found between the localization of the wall motion abnormalities and the site of anatomic narrowing in the ischaemic group. No significant ventricular arrhythmias were detected, and the sensitivity and specificity of ST-T changes were found to be 62.5% and 54.6% by means of Holter monitoring. The dipyridamole echocardiography test proved to be a suitable noninvasive method for the diagnosis of ischaemic heart disease and for the selection of patients for coronary angiography.

Coronary Angiography↗
PubMed1991

Effects of chronic alcohol ingestion on myocardial lipid and fatty acid composition in adult turkeys.

STUDY OBJECTIVE: The aim was determine whether alcohol induced left ventricular dilatation and myocardial lesions in turkeys are associated with changes in the phospholipid and fatty acid compositions of the cardiac tissue. DESIGN: Triglyceride, phospholipid, and cholesterol concentrations and the fatty acid compositions of phospholipids and triglycerides were measured in the myocardium of control and alcohol fed turkeys. Tissue samples were taken from the anteroapical wall of the left ventricle. SUBJECTS: Seven week old domestic Nicholas turkeys were used (10 controls and 10 ethanol fed); the alcohol, comprising more than 20% of the dietary energy, was given in the drinking water for 16 weeks. MEASUREMENTS AND MAIN RESULTS: Left ventricular function was assessed by echocardiography at the end of the treatment. Different phospholipid fractions were isolated by two dimensional thin layer chromatography, and individual fatty acids were identified by gas chromatography. Non-invasive evaluation of the cardiac function revealed a dilatation of the left ventricle and an impaired contractile function in the alcoholic birds. Increased amounts of triglyceride, phosphatidylinositol, sphingomyelin, lysophosphatidylcholine, and lysophosphatidylethanolamine were found in the left ventricle of the alcoholic turkeys. Examination of the fatty acid compositions of different phospholipids and the triglyceride fraction revealed an increase in the saturated/unsaturated ratio following ethanol treatment. In the phospholipid fractions of the alcoholic birds the arachidonic acid (20:4n-6) content was significantly decreased as were the linolic (18:1) and linoleic (18:2n-6) acid contents in the triglycerides. CONCLUSIONS: These alterations in the myocardial phospholipid and fatty acid compositions may contribute to the electrophysiological and functional derangements of the left ventricle in alcoholic cardiomyopathy.

Alcoholism↗
PubMed1991

Effect of alpha adrenergic agents and phorbol esters on phosphorylation of sarcolemmal proteins in beating guinea pig hearts.

STUDY OBJECTIVE: The aim was to determine whether activation of protein kinase C by alpha adrenergic agonists or phorbol esters would be associated with increased phosphorylation of the 15 kDa sarcolemmal protein in guinea pig hearts. DESIGN: Intact, beating guinea pig hearts were perfused with modified Krebs-Henseleit buffer containing [32P]Pi and freeze clamped in a control condition or at the peak of the inotropic response to noradrenaline. Membrane vesicles enriched in sarcolemma were isolated and then subjected to SDS polyacrylamide gel electrophoresis and autoradiography. Phosphorylated proteins were identified and 32P incorporation was quantitated. In some cases, hearts were perfused with phorbol 12-myristate, 13-acetate, or dioctanoyl-glycerol, which are known to be potent activators of protein kinase C. EXPERIMENTAL PREPARATIONS: Whole hearts from 55 anaesthetised guinea pigs weighing 500-600 g were used. MEASUREMENTS AND MAIN RESULTS: Perfusion of guinea pig hearts with noradrenaline resulted in increases in contractility and tissue inositol 1,4,5-triphosphate levels, but there were no increases in the phosphorylation of the 15 kDa sarcolemmal protein observed. Furthermore, perfusion with phorbol 12-myristate, 13-acetate, or dioctanoylglycerol failed to stimulate the phosphorylation of the 15 kDa sarcolemmal protein. CONCLUSIONS: These data indicate that the 15 kDa sarcolemmal protein, which may be phosphorylated by protein kinase C in vitro, is not a substrate for the same enzyme in beating guinea pig hearts.

Animals↗
PubMed1991

The effect of alpha-adrenergic agents and protein kinase C activators on protein phosphorylation in isolated guinea pig hearts.

The incorporation of [32P]Pi into sarcolemmal, sarcoplasmic reticular and myofibrillar proteins was studied in Langendorff-perfused guinea pig hearts treated with the alpha-agonist norepinephrine or with protein kinase C activators (phorbol 12-myristate 13-acetate (PMA) or 1,2-dioctanoylglycerol (D8G]. Norepinephrine was administered in the presence of propranolol and atropine, while the protein kinase C activators (PMA and D8G) were infused in the presence of propranolol, atropine and prazosin. Examination of 32P-incorporation into the various cardiac proteins revealed that there were no significant increases in the degree of phosphorylation of the: (1) 15 kDa sarcolemmal protein; (2) phospholamban in sarcoplasmic reticulum; and (3) troponin I and C protein in the myofibrils. In parallel control studies, stimulation of beating guinea pig hearts by isoproterenol was associated with a 4-5-fold increase in 32P-incorporation into phospholamban and troponin I and about a 2-fold increase in 32P-incorporation into C protein and the 15 kDa sarcolemmal protein. These findings indicate that the major cardiac regulatory phosphoproteins, which have been reported to serve as substrates for protein kinase C in vitro, are not phosphorylated by the same enzyme in perfused, beating guinea pig hearts.

Animals↗
PubMed1990

The role of phospholamban in the regulation of calcium transport by cardiac sarcoplasmic reticulum.

The calcium transport mechanism of cardiac sarcoplasmic reticulum (SR) is (SR) is regulated by a phosphoregulatory mechanism involving the phosphorylation-dephosphorylation of an integral membrane component, termed phospholamban. Phospholamban, a 27,000 Da proteolipid, contains phosphorylation sites for three independent protein kinases: 1) cAMP-dependent, 2) Ca2(+)-calmodulin-dependent, and 3) Ca2(+)-phospholipid-dependent. Phosphorylation of phospholamban by any one of these kinases is associated with stimulation of the calcium transport rates in isolated SR vesicles. Dephosphorylation of phosphorylated phospholamban results in the reversal of the stimulatory effects produced by the protein kinases. Studies conducted on perfused hearts have shown that during exposure to beta-adrenergic agents, a good correlation exists between the in situ phosphorylation of phospholamban and the relaxation of the left ventricle. Phosphorylation of phospholamban in situ is associated with stimulation of calcium transport rates by cardiac SR, similar to in vitro findings. Removal of beta-adrenergic agents results in the reversal of the inotropic response and this is associated with dephosphorylation of phospholamban. These findings indicate that a phospho-regulatory mechanism involving phospholamban may provide at least one of the controls for regulation of the contractile properties of the myocardium.

Animals↗
PubMed1990

Phospholamban and troponin I are substrates for protein kinase C in vitro but not in intact beating guinea pig hearts.

The incorporation of [32P]inorganic phosphate into membranous, myofibrillar, and cytosolic proteins was studied in Langendorff-perfused guinea pig hearts treated with phorbol 12-myristate 13-acetate (PMA) or 1,2-dioctanoylglycerol (D8G), which are potent activators of protein kinase C. Control hearts were perfused with an inactive phorbol ester (4 alpha-phorbol 12,13-didecanoate), which does not cause activation of protein kinase C. To ensure the blockade of different receptor systems, the perfusions were carried out in the presence of prazosin, propranolol, and atropine. Perfusion of hearts with either PMA (4 microM) or D8G (200 microM) was associated with a negative effect on left ventricular inotropy and relaxation. Examination of the 32P incorporation into various fractions revealed that there were no increases in the degree of phosphorylation of phospholamban in sarcoplasmic reticulum, and troponin I and C protein in the myofibrils, although these proteins were found to be substrates for protein kinase C in vitro. However, in the same hearts, there were significant changes in the 32P incorporation into a 28-kDa cytosolic-protein. Examination of the activity levels of protein kinase C in hearts perfused with PMA indicated a redistribution of this activity from the cytosolic to the membrane fraction, suggesting the activation of the enzyme in vivo. These findings indicate that cardiac regulatory phosphoproteins, which may be phosphorylated by protein kinase C in vitro, are not substrates for protein kinase C in beating hearts perfused with phorbol esters or diacylglycerol analogues.

Animals↗
PubMed1990

The effect of phorbol esters and diacylglycerol analogues on the basal phosphoinositide turnover in isolated guinea pig hearts.

Langendorff perfusion of guinea pig hearts with phorbol 12-myristate, 13-acetate or 1,2-dioctanoylglycerol caused a progressive impairment of contraction and relaxation of the left ventricle. Exposure of the hearts to 4 microM phorbol 12-myristate, 13-acetate or 200 microM 1,2-dioctanoylglycerol for 3 minutes resulted in a redistribution of protein kinase C activity and increased phosphorylation of a 28 kDa cytosolic protein. Examination of the incorporation of [32P]Pi into phosphatidylinositols and inositoltrisphosphates, under identical conditions, revealed that the degree of 32P-labeling of phosphatidylinositol, phosphatidylinositol 4-monophosphate and phosphatidylinositol 4.5-bisphosphate was significantly increased. However, the degree of phosphate labeling of inositol trisphosphates was decreased. The effects of phorbol 12-myristate, 13-acetate and 1,2-dioctanoylglycerol on the intermediates of the phosphatidylinositol cycle were observed in the presence of prazosin, propranolol and atropine. Examination of the activity of phosphoinositide-specific phospholipase C in the perfused guinea pig hearts revealed that treatment with phorbol 12-myristate, 13-acetate was associated with a decrease in the membrane-associated enzymatic activity, assayed at low concentrations of calcium. Control hearts, perfused with a phorbol ester (4 alpha-phorbol 12,13-didecanoate) which does not activate protein kinase C, did not show any changes in cardiac contraction and relaxation or in the intermediates of the phosphatidylinositol cycle. The findings suggest that the basal production of inositol phosphates may be down-regulated by agents which activate protein kinase C in guinea pig hearts.

Animals↗
PubMed1989

Changes in phosphoinositide turnover in isolated guinea pig hearts stimulated with isoproterenol.

The incorporation of 32Pi into phospholamban, troponin I, phosphatidylinositols, and inositol trisphosphates was studied in Langendorff-perfused guinea pig hearts stimulated with isoproterenol. Hearts were perfused with Krebs-Henseleit buffer containing [32P]Pk and freeze-clamped at different times during the positive inotropic response. Exposure of the hearts to 0.1 microM isoproterenol for up to 1 minute was associated with significant (up to threefold) increases in phospholamban and troponin I phosphorylation, but there was no significant increase in 32P incorporation into phospholipids. However, longer exposure (2 minutes or more) to isoproterenol was associated with increases in the degree of 32P labeling of phosphatidylinositols and phosphatidic acid. Examination of 32P labeling of inositol trisphosphates in the same hearts revealed that the radioactivity associated with these compounds decreased with time. The decreases were significant at times of exposure of 2 minutes or longer to beta-adrenergic stimulation. The tissue levels of the inositol 1,4,5-trisphosphate isoform were also measured in hearts perfused with isoproterenol for 3 minutes, and they were found to be significantly lower compared with values obtained in control hearts. The effects of isoproterenol on 32P incorporation into phospholipids and proteins were observed in the presence of prazosin, and they were completely abolished by the beta-receptor blocker propranolol. Examination of the phosphoinositide-specific phospholipase C activity in the perfused hearts revealed that isoproterenol stimulation was associated with a decrease in the membrane-associated enzymatic activity at physiological calcium concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effects of long term alcohol ingestion on glutathione metabolising enzymes and taurine contents in the myocardium of rats.

The effects of long term intake of dietary alcohol on myocardial glutathione metabolism and taurine content were studied in rats. Alcohol, comprising more than 30% of the dietary calorie content, was administered to male CFY rats for six weeks. Compared with the controls, the left ventricle of the alcohol treated animals had an increased taurine content (18.4(2.6) vs 13.1(2.5) mumol X g wet weight-1) and a slightly, but not significantly, decreased reduced glutathione content. To assess the glutathione metabolism in the myocardium, the activities of glutathione reductase, glutathione peroxidase, glutathione-S-transferase, gamma-glutamylcysteine synthetase, and glutathione synthetase were measured. Significant increases were found in the activities of glutathione reductase (0.65(0.03) U.g wet weight-1 in the controls and 0.80(0.05) U.g wet weight-1 in the alcohol treated rats) and glutathione-peroxidase after six weeks of alcohol ingestion. Only slight, non-significant changes were found for the other enzymes investigated. It is thus apparent that in the myocardium of rats treated long term with ethanol the previously observed enhanced lipoperoxidation is not necessarily associated with severe glutathione depletion, and an increase in the activity of glutathione reductase might be responsible, at least in part, for the preservation of glutathione.

Alcoholism↗
PubMed1986

Myocardial lipid peroxidation in rats after chronic alcohol ingestion and the effects of different antioxidants.

The effects of chronic intake of dietary alcohol on myocardial peroxidation (measured as formation of diene conjugates), reduced glutathione content, and morphology and the protective actions of different antioxidant compounds (vitamin E and (+)-cyanidanol-3) were studied in rats. Alcohol, comprising more than 30% of the dietary calorie content, was administered to rats for six weeks. Compared with the controls, the left ventricle of the alcoholic animals had an increased diene conjugate content (5.4(0.5) vs 4.3(0.6) optical density X g wet weight-1) and a slightly, but not significantly, decreased glutathione content (1.62(0.05) vs 1.66(0.07) mumol X g wet weight-1). Simultaneous administration of antioxidants (vitamin E or (+)-cyanidanol-3) prevented the pathological changes in diene conjugates and significantly increased the glutathione content compared with the alcoholic rats. Electron microscopy showed remarkably few ultrastructural abnormalities in the myocardium of alcoholic animals fixed by vascular perfusion. The data are consistent with the hypothesis that reactive oxygen radicals are involved in the ethanol induced biochemical changes and that the antioxidants could prevent the increased formation of peroxides in the myocardium.

Animals↗
PubMed1986

The effect of chronic alcohol ingestion on the contractile proteins of the rat heart.

With increasing duration of alcohol consumption the amounts of total myofibrillar proteins in CFY rats decreased slightly, but significantly (from 63.3 +/- 5.7 mg X g wet muscle weight to 54.9 +/- 5.9 mg X g-1 after 12 weeks on alcohol). Similar slight changes could be observed in the case of sarcoplasmic proteins. No significant changes were observed in the composition of the myofibrillar proteins. The densitiometrically calculated percentage ratios of myosin/actin, myosin light chains (LC1/LC2) and troponin components remained the same in the alcoholic animals. The same distribution of native myosin isoenzymes was found in the ventricles of the alcoholic animals as in the controls. We found no electrophoretically detectable evidence that a change in the composition of the myofibrillar proteins is responsible for the decreased contractility of the rat heart following chronic alcohol ingestion.

Alcoholism↗
PubMed1984

Bile enzyme activities following choledochotomy and the effect of steroid treatment.

The alkaline phosphatase (AP) and gamma-glutamyl-transpeptidase (GGT) activities and the effect of steroid treatment were studied in human bile and serum following choledochotomy. Activity of the two enzymes in the bile changed in parallel. Following the operation the enzyme activities initially decreased, but after 3 days they showed a progressive increase and reached their maximum on day 6. It appears that the bile is a major route for the elimination of both enzymes from the damaged liver. 60 mg Prednisolone on the day of operation and 2 days after surgical intervention prevented the initial decline in enzyme activity and significantly increased the excretion of enzymes. The possible pathogenesis of enzymatic changes after choledochotomy is discussed.

Alkaline Phosphatase↗