proteinase inhibitor/infarction

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[Clinical significance of alpha 1-proteinase inhibitor in myocardial infarct].

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The authors analyze data of determination of alpha 1 proteinase inhibitor in patients with myocardial infarction depending on the severity of the disease. It is suggested that the quantitative values of alpha 1 proteinase inhibitors of the blood plasma may be used in the diagnosis and prognosis of

[The effect of proteinase inhibitors in the early stage after experimental myocardial infarction (author's transl)].

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Our experiments have shown that in cats in the early phase after experimental myocardial infarction, the volume of extravascular fluid increases in the lungs while the intravascular volume decreases. A hemoconcentration developed with increased hematocrit and a fall in plasma volume. The thrombocyte

[Clinical implication of plasma PMN elastase (alpha 1-proteinase inhibitor-elastase complex) in patients with early stage of acute myocardial infarction].

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Effect of the proteinase inhibitor Trasylol on the mortality and infarct size in dogs with acute myocardial infarction.

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Role of PMN elastase on ischemic myocardial injury in evolving myocardial infarction: correlation with clinical parameters and intervention by protease inhibitor ulinastatin.

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The purposes of this study were to investigate the sequential changes of PMN elastase during evolving myocardial infarction, and also to ascertain whether or not ulinastatin (UL), a clinically useful protease inhibitor, would affect the extent of ischemic myocardial injury. The levels of plasma PMN

Circulating Serpina3 levels predict the major adverse cardiac events in patients with myocardial infarction.

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Serine proteinase inhibitor A3 (Serpina3), initially discovered as an acute phase plasma protease inhibitor, has been demonstrated in the pathology of complex human disorders, but it is yet to be discovered following acute myocardial infarction (AMI) in clinical practice. Therefore, we

Granulocyte elastase in acute myocardial infarction.

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Plasma concentrations of polymorphonuclear granulocytes elastase (PMN elastase) in complex with alpha-1 proteinase inhibitor are a marker of neutrophil activation. The latter complex, creatine kinase and cardiac troponin T, were measured in peripheral venous blood samples serially drawn in 39

Degradation of myocardial structural proteins in myocardial infarcted dogs is reduced by Ep459, a cysteine proteinase inhibitor.

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The purpose of this study is to clarify whether cysteine proteinases play an important role in the degradation of myocardial proteins in the infarcted tissue. We studied the effects of a cysteine proteinase inhibitor, Ep459, on degradation of cardiac structural proteins caused by ischemia due to

Role of cellular proteinases in acute myocardial infarction. I. Proteolysis in nonischemic and ischemic rat myocardium and the effects of antipain, leupeptin, pepstatin and chymostatin administered in vivo.

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To test the hypothesis that cellular proteinases contribute to ischemic myocellular death, measurements were made of tyrosine release (an index of overall proteolysis) from incubated slices of nonischemic and ischemic myocardium obtained at various times after coronary artery occlusion in rats.

Multi-locus candidate gene polymorphisms and risk of myocardial infarction: a population-based, prospective genetic analysis.

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BACKGROUND Polymorphisms in candidate genes related to lipid metabolism, thrombosis, hemostasis, cell-matrix adhesion, and inflammation have been suggested clinically useful in risk assessment of cardiovascular disease. METHODS We evaluated a panel of 92 candidate gene polymorphisms, using a

Determination of amyloid beta protein precursors harboring active form of proteinase inhibitor domains in cerebrospinal fluid of Alzheimer's disease patients by trypsin-antibody sandwich ELISA.

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beta-Amyloid protein precursors (APP) having proteinase inhibitor domains (APPI) were quantified by a new sandwich enzyme linked immunosorbent assay for detection of active (free) form of proteinase inhibitors by using trypsin in place of the first antibody and by denaturation of APPI-trypsin

[Kinin-modifying therapy of patients with myocardial infarction].

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According to clinical characteristics and serum levels of alpha 1-proteinase inhibitor in the acute period (1-3 days), four groups of patients with myocardial infarction were identified. The most severe myocardial infarction was observed in patients from Groups 1 and 4. It was found that the serum

[Changes of Nonspecific Proteinases and Proinflammatory Cytokines in the Clinical Course of Acute Myocardial Infarction of Various Severity].

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OBJECTIVE to study changes of serum levels of nonspecific proteinases, their inhibitors, and proinflammatory cytokines during short term observation of patients with acute myocardial infarction (MI). METHODS We included in this prospective short-term study 82 patients (27 with uncomplicated non-Q

Effect of metalloproteinase inhibitor on early postinfarction remodeling in the most acute phase of myocardial infarction.

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Echocardiography in control narcotized rats (n=12) revealed that acute single-stage ligation of coronary artery induced a rapid and significant decrease in systolic function of the heart, which attained minimum to postischemic minutes 10-20 and then gradually restored during 60 min after coronary

Neuroserpin reduces cerebral infarct volume and protects neurons from ischemia-induced apoptosis.

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Neuroserpin, a recently identified inhibitor of tissue-type plasminogen activator (tPA), is primarily localized to neurons within the central nervous system, where it is thought to regulate tPA activity. In the present study neuroserpin expression and its potential therapeutic benefits were examined

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