phospholipase/infarzierung

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The effects of phospholipase A2 inhibition on experimental infarct size, left ventricular hemodynamics and regional myocardial blood flow.

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It has been reported that activation of phospholipase A2 and the subsequent degradation of membrane phospholipids are responsible for irreversible myocardial injury. Thus, we examined whether a phospholipase A2 inhibitor 1-(benzylmethyl-amino)-3-[(alpha, alpha, alpha-trifluoro-m-tolyl)oxy]-2-

Reduction in infarct size by the phospholipase inhibitor quinacrine in dogs with coronary artery occlusion.

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It has been suggested that activation of tissue phospholipases may contribute to the development of ischemic cell injury. In the present study we sought to assess whether administration of the phospholipase inhibitor quinacrine would reduce the extent of myocardial necrosis after coronary artery

Increased plasma group II phospholipase A(2) concentrations in patients with acute myocardial infarction: correlation with tumor necrosis factor-alpha.

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OBJECTIVE Group II phospholipase A(2) (PLA(2)) is thought to play an important role in inflammation and tissue injury. It has been suggested that the inflammatory process is important in the setting and progression of myocardial ischemia or reperfusion. We measured plasma PLA(2) as well as

Association between the Ala379Val variant of the lipoprotein associated phospholipase A2 and risk of myocardial infarction in the north and south of Europe.

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Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) has been identified as a coronary heart disease (CHD) risk predictor. Both its anti-inflammatory role by hydrolysing platelet activating factor, and pro-inflammatory generation of atherogenic mediators may influence CHD risk. We investigated the

The association between the D166E polymorphism of the lipoprotein associated phospholipase A2 and risk of myocardial infarction.

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Although numerous studies have evaluated the association between lipoprotein associated phospholipase A2 (Lp-PLA2) gene polymorphisms and coronary heart disease, the conclusions are still inconsistency. Here we detected the correlation between D166E polymorphism of Lp-PLA2 and

Admission lipoprotein-associated phospholipase A2 activity is not associated with long-term clinical outcomes after ST-segment elevation myocardial infarction.

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BACKGROUND Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity is a biomarker predicting cardiovascular diseases in a real-world. However, the prognostic value in patients undergoing primary percutaneous coronary intervention (pPCI) for ST-segment elevation myocardial infarction (STEMI) on

Elevated Lipoprotein-Associated Phospholipase A2 is Valuable in Prediction of Coronary Slow Flow in Non-ST-Segment Elevation Myocardial Infarction Patients

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Background Coronary flow is a determinative factor of non-ST-segment elevation myocardial infarction (NSTEMI) patients. Lipoprotein-Associated Phospholipase A2(Lp-PLA2) as a vascular specific inflammatory cytokine might relate to coronary slow flow in these patients. Methods 105 NSTEMI patients and

Plasma lipoprotein-associated phospholipase A2 mass is elevated in STEMI compared to non-STEMI patients but does not discriminate between myocardial infarction and non-cardiac chest pain.

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BACKGROUND Plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) mass predicts future cardiovascular events in the non-acute setting. We tested the extent to which Lp-PLA2 is elevated in patients with acute coronary syndrome. METHODS A total of 231 consecutive patients referred for acute chest

Lack of phospholipase A2 receptor increases susceptibility to cardiac rupture after myocardial infarction.

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BACKGROUND Recent evidence indicates that the biological effects of secretory phospholipase A2 (sPLA2) cannot be fully explained by its catalytic activity. A cell surface receptor for sPLA2 (PLA2 receptor 1 [PLA2R]) and its high-affinity ligands (including sPLA2-IB, sPLA2-IIE, and sPLA2-X) are

Secretory type II phospholipase A2 in culprit coronary lesions is associated with myocardial infarction.

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BACKGROUND Secretory type-II phospholipase A(2) (sPLA(2)-II) is a cardiovascular risk marker since higher levels of this acute phase protein imply an increased risk for coronary artery disease. Moreover, it is hypothesized that local activity of sPLA(2)-II in the atherosclerotic plaque facilitates

Ambient air pollution and lipoprotein-associated phospholipase A₂ in survivors of myocardial infarction.

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BACKGROUND Increasing evidence suggests a proatherogenic role for lipoprotein-associated phospholipase A₂ (Lp-PLA2). A meta-analysis of published cohorts has shown that Lp-PLA2 is an independent predictor of coronary heart disease events and stroke. OBJECTIVE In this study, we investigated whether

Lipoprotein-associated phospholipase A2 and prognosis after myocardial infarction in the community.

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OBJECTIVE We evaluated the role of lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory biomarker, in defining risk after myocardial infarction (MI). RESULTS Olmsted County, Minn, residents who experienced an MI meeting standardized criteria between 2003 and 2005 (n = 271) were

The phospholipase A2 inhibitor, quinacrine, reduces infarct size in rats after transient middle cerebral artery occlusion.

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The present study was conducted to evaluate the role of phospholipases in neuronal injury after transient focal ischemia. The phospholipase A2 (PLA2) inhibitor, quinacrine (5 mg/kg) or saline (of equal volume), was administered upon reperfusion to rats that underwent 2 h of middle cerebral artery

[Disorder of the contractile function of the nonischemic portion of the heart in experimental infarct and its prevention by the phospholipase inhibitor chloroquine].

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Contractility of an isolated rat right auricle was studied one day after producing one day after producing experimental infarction in the left cardiac region, there was a pronounced decrease in elasticity, and contractility was depressed, which manifested in an approximately two-fold decline in the

Inhibition of secretory phospholipase A2 activity attenuates acute cardiogenic pulmonary edema induced by isoproterenol infusion in mice after myocardial infarction.

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Several types of secretory phospholipase A2 (sPLA2) are expressed in lung tissue, yielding various eicosanoids that might cause pulmonary edema. This study examined whether inhibition of sPLA2 activity attenuates acute cardiogenic pulmonary edema in mice. Acute cardiogenic pulmonary edema was

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