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coronary occlusion/protease
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Страница 1 от 16 полученные результаты
Effect of NCO-700, an inhibitor of protease, on myocardial pH decreased by coronary occlusion in dogs.
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During myocardial ischemia in dogs effects of NCO-700, a protease inhibitor on myocardial pH, were investigated. Ischemia was produced for 90 min by partial occlusion of the left anterior descending coronary artery (LAD). Myocardial pH was measured by a micro glass pH electrode inserted in the
Calcium-activated neutral protease inhibitor (E-64c) and reperfusion for experimental myocardial infarction.
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We examined the efficacy of the combination of coronary reperfusion and calcium-activated neutral protease (CANP) inhibitor (E-64c) for the treatment of acute myocardial infarction in dogs. In 34 dogs, the left anterior descending artery (LAD) was occluded and reperfused after 1 hour (Groups A and
Caspase-dependent and serine protease-dependent DNA fragmentation of myocytes in the ischemia-reperfused rabbit heart: these inhibitors do not reduce infarct size.
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Some infarcted myocytes undergo caspase-dependent DNA fragmentation, but serine protease-dependent DNA fragmentation may also be involved. There is controversy regarding whether caspase inhibitors can reduce infarct size, so the present study investigated whether serine protease inhibitor can reduce
Warm ischemia provokes inflammation and regional hypercoagulability within the heart during off-pump coronary artery bypass: a possible target for serine protease inhibition.
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OBJECTIVE
Accumulating evidence suggests that a hypercoagulable state influences early graft failure after off-pump coronary artery bypass (OPCAB). We hypothesized that regional myocardial ischemia caused by obligatory periods of coronary occlusion during OPCAB is an important trigger for this
Histamine release in acute coronary occlusion-reperfusion in isolated guinea-pig heart.
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It has been shown that plasma histamine significantly increases during myocardial infarction in the dog. Histamine is also released when the isolated guinea-pig heart is reperfused after 30 minutes of low flow perfusion. The release of histamine and lactate dehydrogenase (LDH) after left anterior
Ca2+ sensitivity change and troponin loss in cardiac natural actomyosin after coronary occlusion.
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Ca2+ sensitivity of natural actomyosin (NAM) isolated from both the intact left ventricular free wall and an area of myocardial infarction (MI) was analyzed by use of superprecipitation response from 2 to 48 h after left anterior descending coronary artery ligation in the dog. NAM from the intact
Reduction of myocardial infarct size by doxycycline: a role for plasmin inhibition.
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Myocardial ischemia-reperfusion (I/R) is associated with the activation of matrix metalloproteinases (MMPs) and serine proteases. We hypothesized that activation of MMPs and the serine protease plasmin contribute to early cardiac myocyte death following I/R and that broad-spectrum protease
Coronary thrombolytic properties of a novel recombinant plasminogen activator (BM 06.022) in a canine model.
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We studied the thrombolytic dose-response relationship of a recombinant plasminogen activator (rPA) (BM 06.022) compared with alteplase in a canine model of coronary artery thrombosis. BM 06.022 consists of the kringle 2 and protease domains of human tissue PA (tPA) and lacks oligosaccharide side
Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction.
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BACKGROUND
Erosion and rupture of coronary atheromas are the events preceding the vast majority of acute coronary syndromes. The shoulder regions of atheromas, the sites at which erosion or rupture is most likely to occur, are the sites at which mast cells accumulate. These cells are filled with
Role of locally formed angiotensin II and bradykinin in the reduction of myocardial infarct size in dogs.
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OBJECTIVE
The aim was to investigate the role of local formation of angiotensin II and bradykinin in the reduction of myocardial infarct size.
METHODS
Bilaterally nephrectomised male mongrel dogs were used. Effects were compared of pretreatment with three inhibitors of angiotensin II forming
A tissue plasminogen activator/P-selectin fusion protein is an effective thrombolytic agent.
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BACKGROUND
P-selectin is expressed on the surface of activated endothelial cells and platelets. We hypothesized that a tissue plasminogen activator (TPA)/P-selectin fusion protein would have not only thrombolytic activity but also might target TPA to the thrombi. In addition, it seemed possible that
Calpain inhibitor-1 reduces infarct size and DNA fragmentation of myocardium in ischemic/reperfused rat heart.
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Myocardial ischemia/reperfusion activates a calcium-dependent protease, calpain, in the ischemic myocytes. It is not known whether calpain is involved in the mechanism of ischemia/reperfusion injury in hearts. Thus the purpose of this study was to clarify the effect of a selective calpain inhibitor
Rivaroxaban Suppresses the Progression of Ischemic Cardiomyopathy in a Murine Model of Diet-Induced Myocardial Infarction.
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Mitochondrial m-calpain opens the mitochondrial permeability transition pore in ischemia-reperfusion.
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OBJECTIVE
Opening of the mitochondrial permeability transition pore (mPTP) is involved in ischemia-reperfusion injury. Isoforms of Ca(2+)-activated cysteine proteases, calpains, are implicated in the development of myocardial infarction in ischemia-reperfusion. Growing evidence has revealed the
Attenuation of ischemia/reperfusion injury in rats by a caspase inhibitor.
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BACKGROUND
Z-Val-Ala-Asp(OMe)-CH2F (ZVAD-fmk), a tripeptide inhibitor of the caspase interleukin-1beta-converting enzyme family of cysteine proteases, may reduce myocardial reperfusion injury in vivo by attenuating cardiomyocyte apoptosis within the ischemic area at risk.
RESULTS
Sprague-Dawley rats
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