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mesenteric ischemia/protease

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Activated protein C attenuates intestinal mucosal injury after mesenteric ischemia/reperfusion.

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BACKGROUND Activated protein C (APC) is a serine protease with anticoagulant and ant-inflammatory activities. APC has been shown to attenuate deleterious effects of ischemia/reperfusion (I/R) injury in many organs. In this study, we aimed to investigate the effects of APC on intestinal mucosal

Chronic atherosclerotic mesenteric ischemia that started to develop symptoms just after anaphylaxis.

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An 83-year-old woman was referred to our emergency department with acute urticaria and sudden shortness of breath approximately 30 min after taking rectal diclofenac potassium for lumbago. After treatment with adrenaline and corticosteroids, the patient became hemodynamically stable and left the

Case report. Intestinal infarction due to vascular catastrophe in an HIV-infected patient.

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A 40-year-old HIV-infected woman developed nausea, vomiting, and epigastric pain and died following her third dose (per study protocol) of interleukin (IL)-2. Her HIV infection was diagnosed in 1996. Her last CD4 cell count was 390/microL, and her viral load was negligible (as of November 28, 1998).

Antithrombin III attenuates pulmonary tissue injury caused by mesenteric ischemia-reperfusion.

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BACKGROUND Mesenteric ischemia-reperfusion (I/R) is a well-known event causing both local and remote organ injuries, including the lungs. Recently, several studies indicated that activated leukocyte-endothelial cell interactions play an important role in the mechanisms of these injuries. As a
OBJECTIVE Severe acute pancreatitis is poor prognosis. Continuous regional arterial infusion of protease inhibitors and antibiotics were developed in Japan. We evaluated whether arterial infusion both celiac artery and superior mesenteric artery for this disease would reduce

Antishock and endothelial protective actions of a NO donor in mesenteric ischemia and reperfusion.

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Splanchnic artery occlusion (SAO) of the celiac, superior mesenteric, and inferior mesenteric arteries for 2 hr, followed by a 2-hr reperfusion period in cats produces a severe form of circulatory shock characterized by endothelial dysfunction, increased lysosomal leakage, and severe hypotension

Pathophysiology of mesenteric ischemia/reperfusion: a review.

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During ischemia, the cell structures are progressively damaged, but restoration of the blood flow, paradoxically, intensifies the lesions caused by the ischemia. The mechanisms of ischemia injury and reperfusion (I/R) have not been completely defined and many studies have been realized in an attempt
BACKGROUND Activated protein C (APC) is a serine protease with anticoagulant and antiinflammatory activities. The delaying effects of remote reperfusion injury on the wound-healing process in colonic anastomoses have been previously shown. In this study, we aimed to investigate whether APC protects

Hypoxia/reoxygenation of human endothelium activates PMNs to detach endothelial cells via a PAF mechanism.

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Our previous in vivo studies have implicated phospholipase A2 activation and platelet-activating factor (PAF) production as an important mediator of neutrophil (PMN) priming after mesenteric ischemia/reperfusion. Furthermore, our in vitro studies demonstrate that PAF priming of PMN enhances PMN
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