arachidonate/infarction

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Leukotriene B4 production in healthy subjects carrying variants of the arachidonate 5-lipoxygenase-activating protein gene associated with a risk of myocardial infarction.

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Leukotrienes are implicated in the pathogenesis of coronary artery disease. Recently two haplotypes (HapA and HapB) in the gene encoding ALOX5AP (arachidonate 5-lipoxygenase-activating protein), the main regulator of 5-lipoxygenase, have been associated with a doubling of the risk of myocardial

Genetic variants of arachidonate 5-lipoxygenase-activating protein, and risk of incident myocardial infarction and ischemic stroke: a nested case-control approach.

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OBJECTIVE Recent findings have implicated specific gene polymorphisms of arachidonate 5-lipoxygenase-activating protein (ALOX5AP), and 2 at-risk haplotypes (HapA, HapB) in myocardial infarction and stroke. To date, no prospective data are available. METHODS We evaluated 10 specific Icelandic ALOX5AP

Attenuation of neutrophil function by inhibitors of arachidonate metabolism reduces the extent of canine myocardial infarction.

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To assess the role of neutrophils and arachidonate metabolites in evolving myocardial infarction, the effect of inhibitors of arachidonate metabolism on the extent of myocardial damage and neutrophil function was examined in a 90-minute occlusion/5-hour reperfusion model of canine myocardial

Increased production of arachidonate metabolites in an occlusion-reperfusion model of canine myocardial infarction.

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To define the role of arachidonate metabolites in evolving ischaemic myocardial damage 10 anaesthetised open chest dogs underwent 90 min occlusion of the left anterior descending coronary artery followed by 5 h reperfusion. Tissue extracts from ischaemic myocardium incubated in vitro were subjected

Genetic variation in the arachidonate 5-lipoxygenase-activating protein (ALOX5AP) is associated with myocardial infarction in the German population.

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Genetic variation in the genes ALOX5AP (arachidonate 5-lipoxygenase-activating protein) and LTA4H (leukotriene A4 hydrolase) has previously been shown to contribute to the risk of MI (myocardial infarction) and stroke in Icelandic and Scottish populations. Both genes encode proteins playing a role

Exaggerated atrial arachidonate metabolism in rabbit left ventricular myocardial infarction.

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Isolated perfused rabbit hearts that have previously been subjected to in vivo left ventricular myocardial infarction respond to N-formylmethionyl-leucyl-phenylalanine (fMLP) or bradykinin (BK) administration with the synthesis of large quantities of eicosanoids. To anatomically localize these

[A quantitative measurement of the cerebral infarct focus induced by arachidonate infusion and the relationship between measured values and stroke signs].

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A method for measuring the organic infarct focus induced by arachidonate infusion into rat brain was devised, and the statistical relationship between the measured values and stroke signs in the rat was studied. By the infusion of arachidonate, a high incidence of cerebral infarction was found in

Arachidonate 5-lipoxygenase (5-LO) promoter genotype and risk of myocardial infarction: a case-control study.

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BACKGROUND Leukotrienes are inflammatory mediators derived from arachidonic acid via the 5-lipoxygenase pathway. Both experimental and clinical studies implicate the 5-lipoxygenase pathway in the pathophysiology of atherosclerosis. In a previous study, a microsatellite polymorphism in the

Acute myocardial infarction: measurement of arachidonate end-products in whole blood as an index of platelet cyclo-oxygenase activity in vivo.

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The endogenous arachidonic acid metabolism was investigated ex vivo, in separated serum from clotted whole blood, soon after the onset of acute myocardial infarction (3.3 +/- 0.7 hr). A group of eight consecutive male patients was selected, since no evidence was obtained of any associated disease

Arachidonate-induced experimental nerve infarction.

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Despite the clinical importance of ischemia in the pathogenesis of many human neuropathies, little is known about the effect of circulatory compromise on the structure of peripheral nerves. This results in part from the lack of an entirely satisfactory model in which to study ischemic neuropathy. We

Arachidonate versus ADP-induced platelet aggregation in acute myocardial infarction.

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The sodium arachidonate-induced cerebral infarct in the rat: a model for the study of drugs.

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Protective effect of FR35447 on experimental cerebral infarction.

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The protective effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline [FR35447] on cerebral infarction was examined in animal models. FR35447 in p.o. doses of 1 mg/kg or more caused a marked reduction of arachidonate-induced cerebral infarction in rats. Since FR35447 (10(-6) M) inhibited platelet

Common Polymorphisms in the 5-Lipoxygenase Pathway and Risk of Incident Myocardial Infarction: A Danish Case-Cohort Study.

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BACKGROUND The 5-lipoxygenase pathway (5-LOX) has been implicated in the development of cardiovascular disease and studies have suggested that genetic polymorphisms related to key enzymes in this pathway may confer risk of myocardial infarction (MI). This study investigated the association of

Arachidonate 5-lipoxygenase-activating protein (ALOX5AP) gene and coronary heart disease risk in familial hypercholesterolemia.

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OBJECTIVE To investigate the arachidonate 5-lipoxygenase-activating protein (ALOX5AP) gene as a potential modifier gene for coronary heart disease (CHD) in patients with familial hypercholesterolemia (FH). BACKGROUND The ALOX5AP gene is required for the synthesis of leukotrienes, a protein family

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