Fasting blood taken from 34 patients with myocardial infarction, 19 with unstable angina and 40 healthy controls, was analysed for malondialdehyde and erythrocyte detoxification enzymes, superoxide dismutase and glutathione peroxidase. Malondialdehyde concentration was raised in the patients with myocardial infarction during the initial 48 h after an attack, and correlated with the severity of the attack. 12 days after the infarct, malondialdehyde concentrations were lower but still raised. Superoxide dismutase activity was below normal during the initial 48 h post infarct and raised twelve days after. Glutathione peroxidase was reduced after 12 days. Similar, but less marked changes were seen in the patients unstable angina.

Aged↗

PubMed1991

The evolution of oxidative stress indicators in the course of myocardial ischemia.

Two studies were carried out in patients suffering from Unstable Angina (UA) and Myocardial Infarction (MI). The first study investigated the variations of the Malondialdehyde (MDA) rate at 1st, 5th, 12th day of treatment in 27 patients (15 UA and 12 MI), compared to 15 controls. This rate varied in a different way, with a first peak and a rapid decrease in UA, where it regularly decreases in MI. The second study focused on the variations of MDA, Superoxide Dismutase (SOD), Glutathion Peroxydase (GPX) rates at 2nd, 12th days in 53 patients (19 UA and 34 MI), compared to 35 controls. Here again, the rate of MDA was high on day 2 and decreased on day 12. The rate of GPX showed similar evolution while the SOD rate had an opposite evolution. These two studies confirm the evidence of oxidative stress in acute coronary deficiency.

Aged↗

PubMed1988

Study of fatty acids in atheroma induced in rabbits by an atherogenic diet with or without silicon i.v. treatment.

Fifty-two rabbits were submitted for two months to an atherogenic diet with or without addition of silicon in the form of an I.V. silicon organic compound and compared to a control group of 21 rabbits. Out of the 26 rabbits receiving cholesterol alone, 23 showed atheromatous lesions; out of the 26 rabbits receiving cholesterol + silicon, only 8 had lesions. Free fatty acids, total fatty acids and esters were studied in the plasma and in the aorta. During atheroma, saturated fatty acids decrease, in particular 18:0, unsaturated fatty acids increase, in particular 18:1, 18:2, 20:4; with added silicon the variations are less important: in free fatty acids in plasma, there is a decrease of 20:4; in cholesterol esters in plasma and aorta an increase of 18:0 and a decrease of 18:2. There is a negative correlation between atheromatous lesions and myristic and stearic acids, and a positive correlation between oleic, linoleic and arachidonic acids and atheroma. Arachidonic acid, involved in phenomena of lipid peroxidation, decreased in the silicon treated rabbits.

Animals↗

PubMed1987

[Pathogenesis of atherosclerosis].

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Animals↗

PubMed1986

[Study of a marker of free radical activity in myocardial infarction and in the prodromal syndrome].

Myocardial ischemia is accompanied by a release of free radicals (FR) derived from oxygen, elements having an important cytotoxic activity. These FR react with unsaturated lipids from the membrane fatty acids, leading possibly to a lysis of the membrane. This lipidic peroxidation of the fatty acids generates, in fact, endoperoxides, unstable lipid by-products and also with a cytotoxic activity. At the end of these reactions, cyclical compound and aldehydes are formed, and it is possible to titrate one of them, the malondialdehyde (MDA) which represents a marker of the aggression of the radicals on the membranes. We have therefore studied the appearance of MDA in the systemic venous blood and compared 10 patients with a threat syndrome (group I) to 8 other patients with acute myocardial infarction (group II). The plasma MDA level is measured upon admission (D1), on the 5th day (D2) and on the 12th day (D3) of the evolution. We have therefore found a significant elevation of MDA in the two groups of patients at D1 and D2, in comparison with the results obtained in a reference group of 15 normal patients (p less than 0.01). In the infarction group, the level of MDA on the 12th day (189 +/- 41 ng/ml) drops significantly as compared to the highest level noted upon admission and on the 5th day, called MDA peak (258 +/- 62 ng/ml, p less than 0.01). The MDA drop is less marked in group I of the threat syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

[Study of lipid peroxidation by the assay of malondialdehyde in human and experimental atheroma].

Malondialdehyde is a marker for the oxidation of membrane unsaturated fatty acids. This biochemical process, called lipid peroxidation, occurs in the biosynthesis of leukotrienes, prostaglandins and other cytotoxic and chemotactic lipid peroxides. It may play a part in the genesis of atheroma from lipids stored in the arterial wall. Plasma malondialdehyde levels were found to be different in hyperlipidemic subjects with or without arterial lesions, and in rabbits under an atherogenic diet with or without added silicon. The same positive correlation was found in rabbit aorta between atheromatous lesions and high levels of malondialdehyde. These data would support the hypothesis that lipid peroxidation plays a role in atherogenesis.

Animals↗

PubMed1986

[Membrane lipid peroxidation in coronary insufficiency].

Malondialdehyde (MDA) as lipid peroxidation marker was studied in 27 patients with acute coronary insufficiency. Significantly elevated plasma levels as compared with controls were found in patients with myocardial necrosis and with preinfarction syndrome. No correlation was found between MDA and creatine phosphokinase, and a significant MDA decrease was observed at day 12: plasma MDA reached normal levels in the myocardial necrosis group. The MDA decrease was also significant in the preinfarction group, but the MDA level remained high in 4 patients with unstable angina. MDA is not a prognostic index. No correlation was found between MDA and plasma lipid levels or patients' ages. These data confirm that myocardial ischemia is associated with abnormal production of oxygen-derived free radicals which react with the membrane unsaturated fatty acids, resulting in toxic endoperoxides. This is thought to be one of the physio-pathological pathways which aggravate ischemic myocardial tissue damage.

Animals↗

PubMed1986

[Free radical toxicity in coronary insufficiency].

A number of experimental models have shown abnormally high concentrations of cytotoxic oxygen derived free radicals (FR), and decreased concentrations of protecting anti-oxidising enzymes during myocardial ischaemia. These FR react with the unsaturated lipids of the cell membrane, a phenomenon known as membrane lipidoperoxidation (MLP) to produce very cytotoxic endoperoxides. We studied an intermediary product of MLP, malondialdehyde (MDA) in 10 patients with a preinfarction syndrome (Group 1) and 8 patients in the acute phase of myocardial infarction (Group 2). Plasma MDA was measured on admission (P2) and 12th day (P3). There was a significant elevation of MDA in both groups at P1 and P2 (p less than 0.01) compared with results obtained in 15 normal control subjects of the same age. The MDA concentration on the 12th day in the infarct group was significantly lower (189 +/- 41 ng/ml, p less than 0.01) compared with the highest value observed either on admission or on the 5th day (peak MDA 258 +/- 62 ng/ml). The difference between MDA concentrations on the 12th day and peak MDA was less striking in Group 1. None of the patients in Group 2 had a recurrence of chest pain after the initial phase of infarction and the residuals MDA concentration (P3) was similar to control values (181 +/- 27 ng/ml). On the other hand, in the preinfarction syndrome group, 4 patients had persistent unstable angina on the 12th day and their MDA concentrations remained high (250 +/- 42 ng/ml). This was interpreted as reflecting continuing MLP in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1986

[HDL2 and HDL3 cholesterol in men and women in different forms of hyperlipidemia without arterial involvement].

The investigation was carried out in one hand on 54 hyperlipidemic men without arterial injury compared to 54 normolipidemic men, on the other hand on 50 hyperlipidemic women compared to 50 normolipidemic women. The hyperlipidemic subjects were separated in IIa, IIb and IV groups, according to WHO classification. Lipoprotein's separation was carried out by sequently ultracentrifugation and HDL2-HDL3 were isolated at a solvant density of 1.125 and 1.21; cholesterol was measured by enzymatic method. We observed a significant decrease of: (Formula: see text) ratio in all hyperlipidemic subjects compared to controls; but no significant variation of HDL2 and HDL3 cholesterol appeared in the three groups of hyperlipidemic subjects compared to controls; on the other hand we noted a HDL2 cholesterol greater in women than in men and this fact seems to prove a favorable action of this fraction in preventing atherosclerosis. The (Formula: see text) ratio remains the most discriminant factor of hyperlipidemia, but the: (formula: see text) ratio seems interesting and HDL2 cholesterol is always higher in women during hyperlipidemia with high risk, IIa and IIb.

Arteriosclerosis↗

PubMed1985

[Hemodynamic effects of an inhibitor of the vascular effects of vasopressin in patients with congestive heart failure].

To assess the role of vasopressin (AVP) in congestive heart failure (CHF), we investigated 10 patients with CHF refractory to conventional treatment, before and 60 minutes after intravenous administration of 5 micrograms/kg of d(CH2)5Tyr(Me)AVP, a specific antagonist of AVP at the vascular receptor level. Heart rate, systemic arterial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac index by thermodilution, and cutaneous blood flow by laser-Doppler technique were measured. In 9 patients there was no significant hemodynamic and cutaneous blood flow response to the AVP antagonist. Plasma AVP was 2.3 +/- 0.8 pg/ml and plasma osmolality 284 +/- 14 mosm/kg H2O. The tenth patient had the most severe CHF. His plasma AVP was 55 pg/ml and plasma osmolality 290 mosm/kg. He responded to the AVP antagonist with a marked decrease in systemic arterial pressure from 115/61 to 79/41 mm Hg, in pulmonary arterial pressure from 58/31 to 33/13 mm Hg and in pulmonary capillary wedge pressure from 28 to 15 mm Hg. Simultaneously cardiac index increased from 1.1 to 2.21 X min-1 X m-2 and cutaneous blood flow rose 5-fold. Thus, most patients with CHF have only moderately elevated plasma AVP and its role in determining peripheral vascular resistance appears to be limited. AVP may become important in rare patients presenting with marked hemodynamic instability and very high plasma AVP.

Adult↗

PubMed1984

Munchausen's registry.

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Australia↗

PubMed1984

[Fatty acids and lipid peroxidation in experimental atheroma in the rabbit. Role played by silicon].

Free fatty acids (FFA) and esterified fatty acids (EFA), lipid peroxidation were analysed in experimental atheroma. Among rabbits receiving cholesterol (formula; see text) compared with controls group in FFA and EFA on plasma and aortas: arachidonic acid in plasma and malonaldehyde (MDA) in plasma and aorta are increased with atheroma and there is a positive correlation between arachidonic acid, MDA, and arterial injury; organo silicic compounds when added to atherogenic diet, had a favorable action about these variations, organic silicon having an antiatheromatous action. Therefore it seems possible that unsaturated fatty acid's peroxidation had an injurious action on arteries in atheroma by discharging toxic endoperoxides; arachidonic acid is probably involved in thromboxane's generation, and consequently in aggregability of blood platelets.

Animals↗

PubMed1983

[Fatty acid and lipid peroxidation in human atherosclerosis].

Plasma fatty acids and lipid peroxidation were studied in human atherosclerosis. Analysis of fatty acids in 16 controls and 32 hyperlipidemic patients showed, in the latter, a decrease in saturated fatty acids, especially palmitic and stearic acids, and an increase in unsaturated fatty acids, especially arachidonic acid. Compared to hyperlipidemic patients without arterial injury, patients with arterial injury exhibit a significant increase in malonaldehyde (MDA). In the former, MDA concentrations are significantly increased compared to controls. Therefore, peroxidation of unsaturated fatty acids may have a deleterious effect on arteries in atheroma, through the release of toxic endoperoxydes and the metabolization of arachidonic acid into thromboxane, which is a platelet aggregator. Lipid peroxidation can also be demonstrated in other diseases: we found very high MDA concentration in 11 alcoholic patients (alcoholic hepatitis, cirrhosis) and 6 patients with inflammatory conditions such as Crohn disease.

Adult↗