elastase/infarction

To elucidate the involvement of activated polymorphonuclear neutrophil (PMN) proteolytic activity in the pathophysiology of cerebrovascular stroke, we measured internal jugular venous and femoral arterial levels of PMN elastase in 6 patients with acute stroke from the day onset (day 0) to 7 days

In a group of young subjects with acute myocardial infarction (AMI) (68 men and 7 women; mean age 39.6+/-5.7 years) we examined the plasma concentration of elastase, the thiobarbituric acid-reactive substances (TBARS) and the total antioxidant status (TAS) at the initial stage of AMI. In this group

We investigated the potential of inhibition of elastase, a granulocyte-derived proteolytic enzyme, in ameliorating the effects of myocardial stunning caused by repetitive ischaemia (RI) and myocardial infarction (MI) for the first time in an in situ, perfused, rat heart model. The effects of the

Many recent studies demonstrate that neutrophils may be involved in the genesis and propagation of myocardial ischemia and reperfusion injury. Clinical value of PMN elastase activity before reperfusion which is released from activated polymorphonuclear leucocyte were evaluated in 30 patients with

Neutrophils, a source of proteolytic enzymes and oxygen free radicals, have been shown to participate in animal models of myocardial ischemic injury. To characterize neutrophil activation in human ischemic heart disease, a specific neutrophil elastase-derived fibrinopeptide in plasma was measured in

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

Angiotensin II (Ang II), whose generation largely depends on angiotensin-converting enzyme (ACE) activity, mediates most of the renin-angiotensin-system (RAS) effects. Elastase-2 (ELA-2), a chymotrypsin-serine protease elastase family member 2A, alternatively generates Ang II in rat arteries.

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

Neutrophil elastase contributes to the severity of cardiac damage following coronary ischemia and reperfusion. We evaluated the effects of 2-(9-(2-piperidinoethoxy)-4-oxo-4H-pyridol[1,2-a]pyrimidin-2-yloxymethyl)-4-(1-methyethyl)-6-methoxy-1,2-benzisothiazol-3(2H)-one-1,1-dioxide hemihydrate

Inflammatory responses have been known to contribute to the development of neuronal damage after brain ischemia in experimental animals. Also, neutrophil elastase activity in the plasma has been elevated in the patients with acute cerebral infarction. In order to clarify whether neutrophil elastase

OBJECTIVE Polymorphonuclear leukocytes (PMNL) are involved in the pathogenesis of acute cerebral ischemia and atherosclerosis. Elastase is one of the proteolytic enzymes released by activated PMNL. We evaluated whether plasma levels of elastase-inhibitor complexes (EIC) are related to acute cerebral