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Biomedical subjects

I Edes

Publications and source records attributed to I Edes.

At least 19 recordsLinked to original sources
PubMed2000

Differences in the changes of allergen-specific IgE serum levels and the chemiluminescence of peripheral blood phagocytes in patients with allergic rhinoconjunctivitis during the ragweed season.

The objective of this study was to compare the changes in the values of allergen-specific serum IgE levels and zymosan-induced whole blood chemiluminescence (CL) in 41 patients who had exclusively only ragweed allergy in the season of acute symptoms of disease in July, August and September. All patients had allergic rhinitis or rhinoconjunctivitis. Each patient was investigated as a self-control. The ragweed-specific IgE levels were measured by enzyme immunoassay (EIA). The luminol amplified zymosan-induced CL of whole human blood was detected. The allergen-specific serum IgE levels showed slight, but not significant, gradually increasing elevations during the whole season. On the other hand, significant increases were found in the values of the basal but especially in the zymosan-stimulated CL of peripheral blood phagocytes during the acute phase of allergy. Both the basal and the zymosan-induced CL reflected significantly the activated state of the immune system. These observations clearly show that there are well detectable signs of the systemic activation of the immune system in allergic rhinoconjunctivitis beside the local alterations. In addition, the measurements of the basal and zymosan-induced CL of peripheral phagocytes could clearly reflect the clinical state of disease in vitro.

Adult↗
PubMed1999

[Improvement of myocardial perfusion following left ventricular resection].

Left ventricular aneurysm had detected at the 55-year-old woman after extensive anterior myocardial infarction in association with progressive ventricular dilatation and symptoms of heart failure. Coronary angiogram revealed a serious lesion in the proximal segment of the left anterior descending coronary branch with a poor run off tract. 18FDG-PET and 99mTc-MIBI-SPECT investigation were performed in order to differentiate the scarred regions from the viable myocardial segments. Taking into consideration the results an aneurysm resection was performed without revascularisation procedure. After the surgery not only the ejection fraction and the left ventricular dilatation had improved but the tissue perfusion in the segments surrounding the resected aneurysm had also showed a significant increase at the follow up MIBI-SPECT imaging.

Coronary Angiography↗
PubMed1999

The effect of isoproterenol on phospholamban-deficient mouse hearts with altered thyroid conditions.

The aim of the present study was to determine the effects of beta -adrenergic stimulation in wild-type and phospholamban-deficient mouse hearts with altered thyroid conditions. Hypothyroidism was associated with significant decreases in heart/body weight ratio in wild-type and phospholamban-deficient mice, whereas hyperthyroidism was associated with significant increases in heart/body weight ratio in both groups. Hypothyroid hearts of wild-type and phospholamban-deficient mice exhibited similar increases in beta -myosin heavy chain protein levels and decreases in alpha -myosin heavy chain protein levels. In hyperthyroidism, there were increases in the alpha -myosin heavy chain protein levels and these were similar in wild-type and phospholamban-deficient hearts. There were no detectable levels of beta -myosin heavy chain protein in the hyperthyroid hearts. The relative tissue level of phospholamban in wild-type hearts was increased (133%, P<0.01) in hypothyroidism, and decreased (69%, P<0.01) in hyperthyroidism, when compared to euthyroid controls (100%). Similar increases and decreases in SR Ca(2+)-ATPase protein levels were observed between phospholamban-deficient and wild-type hearts in hyperthyroidism and hypothyroidism, respectively. The basal contractile state of wild-type and phospholamban-deficient hearts was significantly depressed in hypothyroidism. On the other hand, the basal contractile state of wild-type and phospholamban-deficient hearts was significantly increased in hyperthyroidism. During beta -agonist stimulation of wild-type hearts, the responses in the rates of contraction and relaxation were highest in the hypothyroid group, followed by the euthyroid, and lastly by the hyperthyroid groups. There was a close linear correlation between the magnitude of the contractile parameter responses and the phospholamban/SERCA2 ratios in these hearts. However, the phospholamban-deficient hypothyroid, euthyroid, and hyperthyroid hearts did not exhibit any responses to isoproterenol, indicating that the alterations in the thyroid states of these hearts do not influence the effects of isoproterenol on cardiac function. These findings suggest that phospholamban is an important regulator of the heart's responses to beta -adrenergic stimulation under various thyroid states.

Animals↗
PubMed1999

The effects of levosimendan on the left ventricular function and protein phosphorylation in post-ischemic guinea pig hearts.

The widely accepted theories for the decreased function in the stunned myocardium relate to Ca2+ desensitization and free radical-mediated tissue damage of the myofilaments. The aim of the present study was to examine whether the depressed contractile function and Ca2+ responsiveness of the stunned myocardium may be restored by a new Ca2+ sensitizer (levosimendan), which has been shown to improve the Ca2+ response of the myofilaments. The effects of levosimendan on the left ventricular function and the in vivo protein phosphorylation were examined in both the non-ischemic and the stunned myocardium. Myocardial stunning was induced in Langendorff-perfused guinea pig hearts by suspending the circulation for 8 min, followed by a 20-min reperfusion period. Perfusion of post-ischemic guinea pig hearts with levosimendan (0.03-0.48 microM, 6 min) was associated with dose- and time-dependent increases in both dP/dtmax (contractility) and dP/dtmin (speed of relaxation). When the effectiveness of levosimendan was compared in non-ischemic and post-ischemic hearts, no significant differences were noted in the relative stimulatory effects on contractility and relaxation, at any given time point (time-response curve) or concentration (dose-response curve). Perfusion of the guinea pig hearts with a high (0.3 microM) levosimendan concentration did not reveal any qualitative or quantitative difference in the phosphodiesterase inhibitory potential of the compound (elevation of tissue cyclic AMP levels and characteristics of protein phosphorylation) between the non-ischemic and the post-ischemic myocardium. However, when isoproterenol was administered to induce maximal in vivo phosphorylation of cardiac phosphoproteins, an attenuation of the 32P-incorporation into troponin I was noted in the post-ischemic hearts. The decrease in isoproterenol-induced 32P-incorporation into troponin I was associated with similar alterations in the tissue level of this protein. We conclude that the Ca2+ sensitizer levosimendan exerts dose- and time-dependent positive inotropic and lusitropic effects on the post-ischemic myocardium, lending support to the hypothesis tha Ca2+ desensitization of the myofibrils is involved in myocardial stunning.

Animals↗
PubMed1998

Thyroid hormone-induced alterations in phospholamban-deficient mouse hearts.

Alterations in the expression levels of the sarcoplasmic reticulum (SR) Ca2+-ATPase and its regulator, phospholamban, have been implicated in the effects of thyroxine hormone on cardiac function. To determine the role of phospholamban in these effects, hypothyroidism and hyperthyroidism were induced in phospholamban-deficient mice and their isogenic wild types. Hypothyroidism resulted in significant decreases of left ventricular contractility, which could be moderately stimulated by increases in preload or afterload, in both phospholamban-deficient and wild-type mice. However, the basal contractile parameters in hypothyroid phospholamban-deficient hearts were at least as high as those exhibited by hyperthyroid wild-type hearts. In hyperthyroidism, there was no further enhancement of the hyperdynamic contractile parameters in phospholamban-deficient hearts, although the wild-type hearts exhibited significantly increased contractile function compared with their respective euthyroid groups. Furthermore, increases in preload or afterload did not enhance contractility in either phospholamban-deficient or wild-type hyperthyroid hearts. Examination of the relative tissue levels of cardiac SR Ca2+-ATPase revealed increases in hyperthyroidism and decreases in hypothyroidism compared with euthyroidism, and these changes were similar between phospholamban-deficient and wild-type hearts. An opposite trend was observed for phospholamban expression levels in the wild-type group, which were depressed in hyperthyroid hearts but increased in hypothyroid hearts. These findings indicate that (1) thyroid hormones induce similar changes in the cardiac SR Ca2+-ATPase levels in either the presence or absence of phospholamban, (2) the thyroxine-induced increases in SR Ca2+-ATPase levels are not associated with any further stimulation of the hyperdynamic cardiac function in phospholamban-deficient mice, and (3) the decreased contractile parameters in hypothyroid phospholamban-deficient hearts associated with decreases in SR Ca2+-ATPase levels and myosin heavy chain isoform switches are at least as high as those of the stimulated hyperthyroid wild-type hearts. Thus, alterations in the phospholamban level or its activity may be a critical determinant of the contractile responses to altered thyroid states in the mammalian heart.

Animals↗
PubMed1998

Phospholamban ablation and compensatory responses in the mammalian heart.

Phospholamban is a low molecular weight phosphoprotein in cardiac sarcoplasmic reticulum. The regulatory role of phospholamban in vivo has recently been elucidated by targeting the gene of this protein in embryonic stem cells and generating phospholamban-deficient mice. The phospholamban knockout hearts exhibited significantly enhanced contractile parameters and attenuated responses to beta-agonists. The hyperdynamic cardiac function of the phospholamban knockout mice was not accompanied by any cytoarchitectural abnormalities or alterations in the expression levels of the cardiac sarcoplasmic reticulum Ca(2+)-ATPase, calsequestrin, Na(+)-Ca2+ exchanger, or the contractile proteins. Furthermore, the attenuation of the cardiac responses to beta-agonists was not due to alterations in the phosphorylation levels of the other key cardiac phosphoproteins in the phospholamban knockout hearts. However, ablation of phospholamban was associated with down-regulation of the ryanodine receptor, which suggests that a cross-talk between cardiac sarcoplasmic reticulum Ca2+ uptake and Ca2+ release occurred in an attempt to maintain Ca2+ homeostasis in these hyperdynamic phospholamban knockout hearts.

Adrenergic beta-Agonists↗
PubMed1997

[Prediction of the result of high-risk coronary bypass surgery by positron emission tomography].

Coronary angiography revealed three-vessel disease in a 56-year-old male with two previous myocardial infarctions. Coronary bypass surgery was initially ruled out by cardiac surgeon because of the poor left ventricular function (EF: 23%), despite moderate viability signs during conventional isotope techniques. Positron emission tomography with 18FDG indicated a large periinfarction area of hibernating myocardium. Accordingly, coronary bypass grafting was performed. Postoperatively, the symptoms disappeared, the left ventricular wall motion abnormalities (with the exception of the scarred region demonstrated by PET) improved, and the global left ventricular function increased significantly. This case and the role of cardiac PET study for prediction of the result of revascularization are discussed.

Coronary Angiography↗
PubMed1997

Postinfarction left ventricular pseudoaneurysm.

Left ventricular wall rupture after myocardial infarction is a mechanical complication that may result in a pseudoaneurysm. Between January 1994 and October 1996, false or pseudoaneurysms were detected in 6 (0.0026%) of 2,600 consecutive patients (4 women, 2 men; mean age 59.4 years) undergoing cardiac catheterization at University Medical School, Debrecen, Hungary. All patients had a history of cardiovascular disease, with diagnosis of pseudoaneurysm confirmed by echocardiography. The average time from the occurrence of acute infarction to diagnosis was 37.0 days (range 3-80 days). All patients were in New York Heart Association functional class IV congestive heart failure; in four patients cardiogenic shock was present. Five patients underwent coronary angiography, which demonstrated multivessel disease and occlusion of the infarct-related artery (TIMIO) without adequate collateral circulation (grade 0-1). Five patients had surgical repair of the false aneurysm, and, in three patients, concomitant coronary bypass grafting was performed. The 2-year mortality rate for all patients was 50%. Early diagnosis of false aneurysm is facilitated by echocardiography, and coronary angiography is required before surgery. Early surgical correction with coronary revascularization is advised.

Aged↗
PubMed1997

beta-Adrenergic regulation of cAMP and protein phosphorylation in phospholamban-knockout mouse hearts.

The stimulatory effects of beta-adrenergic agonists reflect increases in intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels and phosphorylation of key regulatory proteins in the heart. One of these phosphoproteins is phospholamban (PLB) in sarcoplasmic reticulum, and ablation of PLB is associated with attenuation of the contractile responses to beta-adrenergic stimulation in the mouse heart. To determine whether this attenuation of beta-stimulation is due to altered phosphorylation characteristics of the other key cardiac phosphoproteins and/or to compensatory responses occurring in the absence of PLB, PLB-knockout and wild-type hearts were perfused and their protein phosphorylation patterns examined. The beta-adrenergic receptor density, adenylyl cyclase activity, tissue cAMP levels, and the basal phosphoprotein pattern were similar between PLB-knockout and wild-type hearts. Isoproterenol perfusion resulted in similar increases in the tissue cAMP levels and the degree of phosphorylation of troponin I, C protein, and the 21-kDa microsomal protein in wild-type and PLB-knockout hearts. These findings indicate that the attenuation of isoproterenol-mediated increases in contractility of the PLB-knockout hearts is not due to alterations in the beta-adrenergic signal transduction pathway or the degree of phosphorylation of the key cardiac regulatory phosphoproteins in myofibrils and sarcolemma.

Animals↗
PubMed1995

[Angiographic findings in postinfarction cardiac rupture].

The hemodynamic and angiographic findings were examined in 16 patients with myocardial rupture following acute myocardial infarction. The patients (9 men, mean age 55.8 years, and 7 women, mean age 64.0 years) had suffered an extensive transmural infarction, all but 2 cases involved first cardiac events. The diagnosis of myocardial rupture was made on clinical grounds, and confirmed by the results of noninvasive (echocardiography) and invasive (left ventriculography) investigations. The average time from the infarction to the appearance of cardiac rupture was 4.6 days (range: 1 hour to 16 days). The patients receiving thrombolytic therapy mainly suffered an early rupture (less than 72 hours following the infarction), while the group receiving conventional therapy mainly had a late rupture (between 4 and 16 days). 7 patients had single-vessel, 3 two-vessel and 6 three-vessel disease. Examination of the infarct-related vessel revealed a total occlusion in the proximal or medial part of the coronary in 75% of the cases. Angiography demonstrated no manifest collateral circulation to the infarct-related artery in 10 cases, and only limited collateral blood flow in 6 patients. It is concluded that cardiac rupture depends on the management of the myocardial infarction, the abrupt cessation of flow in the infarct-related vessel and the absence of adequate collateral circulation supporting the infarcted zone. 15 patients underwent cardiac surgical correction and in 8 cases additional coronary artery bypass grafting was performed. After the operative intervention, 9 patients exhibited a significant improvement, and there was no sign of cardiac failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Effects of Levosimendan, a cardiotonic agent targeted to troponin C, on cardiac function and on phosphorylation and Ca2+ sensitivity of cardiac myofibrils and sarcoplasmic reticulum in guinea pig heart.

A new cardiotonic agent, (R)-[[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)-phenyl] hydrazono]propanedinitrile (Levosimendan), has been developed and screened for its ability to bind to cardiac troponin C. In perfused hearts, low concentrations of 0.03 or 0.1 mumol/L Levosimendan increased +dP/dt, but did not affect the speed of relaxation and produced only a slight increase in spontaneous heart rate in the hearts perfused with 0.1 mumol/L of the drug. In these same hearts, perfusion with 0.03 mumol/L Levosimendan did not alter the 32P incorporation into troponin I or C protein, whereas a slight but significant increase was noted for phospholamban, with no detectable change in tissue cAMP levels. Administration of 0.1 or 0.3 mumol/L Levosimendan significantly increased myocardial cAMP levels as well as the phosphorylation of phospholamban, troponin I, and C protein. Levosimendan (0.03 to 10 mumol/L) reversibly increased force generated by detergent-extracted fiber bundles over a range of submaximally activating free Ca2+ concentrations with no significant effect on maximum force or on Ca2+ binding to myofilament troponin C. There was no direct effect of Levosimendan on Ca2+ uptake by vesicles of sarcoplasmic reticulum (SR). In contrast, under conditions optimal for cAMP-dependent phosphorylation, Levosimendan slightly but significantly lowered the concentration of Ca2+, yielding half-maximal uptake rates by the SR vesicles. Our results indicate that at low concentrations Levosimendan acts preferably as a Ca2+ sensitizer, whereas at higher concentrations its action as a phosphodiesterase inhibitor contributes to the positive inotropic effect.

Analysis of Variance↗
PubMed1994

Thyroid hormone-induced alterations in phospholamban protein expression. Regulatory effects on sarcoplasmic reticulum Ca2+ transport and myocardial relaxation.

The aim of the present study was to determine the changes in phospholamban protein levels and their regulatory effect on sarcoplasmic reticulum (SR) Ca2+ uptake and left ventricular function in hypothyroid and hyperthyroid rat hearts. Hypothyroidism was associated with decreases in basal left ventricular function (+dP/dt and -dP/dt), whereas in hyperthyroidism these parameters were elevated compared with values for euthyroid hearts. The maximal SR Ca2+ uptake rates were 12.8 +/- 1.1, 15.5 +/- 1.2, and 21.4 +/- 1.4 nmol Ca2+ per milligram per minute, and the EC50 values for Ca2+ were 0.76 +/- 0.09, 0.41 +/- 0.07, and 0.30 +/- 0.05 mumol/L assayed in homogenates from hypothyroid, euthyroid, and hyperthyroid hearts, respectively. The relative tissue level of phospholamban was increased (135%) in hypothyroidism and decreased (75%) in hyperthyroidism compared with euthyroidism (100%). An opposite trend was observed for the SR Ca(2+)-ATPase, which was depressed (74%) in hypothyroid hearts but increased (134%) in hyperthyroid hearts. Consequently, the relative ratio of phospholamban to Ca(2+)-ATPase was highest in hypothyroid and lowest in hyperthyroid hearts, and these changes correlated with changes in the EC50 of the SR Ca2+ uptake for Ca2+. Stimulation of hearts with 0.1 mumol/L isoproterenol revealed that the relaxant effects were lower in hyperthyroid hearts and higher in hypothyroid hearts compared with euthyroid hearts, consistent with the alterations in the phospholamban levels. The maximal increases in the speed of relaxation, elicited by isoproterenol stimulation, correlated with the changes in the relative ratio of phospholamban to Ca(2+)-ATPase in these hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1994

Effect of thyroid status on basal phosphorylation of cardiac myofibrillar phosphoproteins in rats.

The effect of thyroid status on myocardial function and accompanying alterations in the expression of specific genes has been well defined in animals. However, the effects of thyroid hormones on the basal phosphorylation of key cardiac regulatory proteins, which may also contribute to alterations in myocardial function, have not been defined. The present study concerns the phosphorylation status of myofibrillar proteins in hearts from hyperthyroid, euthyroid and hypothyroid rats. Hyperthyroidism was produced by daily subcutaneous injections of L-triiodothyronine, while hypothyroidism was induced with an iodine-deficient diet and KClO4. Two different approaches were used to study changes in the basal phosphorylation levels of troponin I and C protein: 1) direct measurement of the 32P-label associated with these proteins, using intact, beating hearts perfused with [32P]orthophosphate-labeled Krebs buffer; 2) indirect measurement by the back-phosphorylation technique with [gamma-32P]ATP and the catalytic subunit of cAMP-dependent protein kinase in vitro. Measurements of left ventricular contraction (+dP/dt and -dP/dt) were significantly higher in hyperthyroid than in euthyroid animals and this was associated with increases in basal phosphorylation levels of both troponin I and C protein in the myofibrils. In hypothyroid animals, both +dP/dt and -dP/dt were significantly lower than in euthyroid animals and this was associated with decreases in basal phosphorylation levels of troponin I and C protein. The changes in the phosphorylation status of troponin I or C protein correlated with the changes in the speed of myocardial relaxation (-dP/dt) in response to the altered thyroid states.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Intracellular mechanisms mediating reversal of beta-adrenergic stimulation in intact beating hearts.

The changes in 32P labeling of phosphoproteins were studied in Langendorff-perfused guinea pig hearts during reversal of the stimulatory effects of isoproterenol. Exposure of the hearts to isoproterenol was associated with significant increases in adenosine 3',5'-cyclic monophosphate (cAMP) levels and in the phosphate incorporation into phospholamban in sarcoplasmic reticulum, the 15-kDa protein in the sarcolemma, and troponin I in the myofibrils. Phospholamban was phosphorylated on serine and threonine residues, both of which are sites for cAMP-dependent and Ca(2+)-calmodulin-dependent protein kinases, respectively. Termination of isoproterenol infusion was associated with reversal of the mechanical effects of isoproterenol stimulation and reversal of the increases in tissue cAMP levels. However, the decreases in cAMP levels correlated only with dephosphorylation of phosphoserine in phospholamban. Dephosphorylation of phosphothreonine in phospholamban, the 15-kDa sarcolemmal protein, and troponin I occurred at a slower rate. These findings suggest that cAMP-dependent phosphorylation of phospholamban (phosphoserine) may play a prominent role during beta-adrenergic stimulation of intact hearts.

Amino Acid Sequence↗
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↗