Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antithrombin III (AT III) supplementation has proven to be effective in the treatment of disseminated intravascular coagulation. Administration of AT III is also useful for prevention of organ failure in animals challenged with endotoxin or bacteria and it increases the survival rate of such animals. Since inhibition of coagulation abnormalities failed to prevent organ failure in animals given bacteria, AT III may exert a therapeutic effect independent of its anticoagulant effect. This therapeutic mechanism of AT III has been explored using an animal model of septicemia. AT III prevented pulmonary vascular injury by inhibiting leukocyte activation in rats given endotoxin. This effect is mediated by the promotion of endothelial release of prostacyclin which inhibits leukocyte activation. Interaction of AT III with heparin-like glycosaminoglycans (GAGs) on the endothelial cell surface appears to be important for this effect. Heparin inhibits these therapeutic effects of AT III by preventing AT III from interacting with the cell surface heparin-like GAGs. This activity of AT III may explain why AT III prevents organ failure as well as coagulation abnormalities in patients with sepsis. This antiinflammatory activity of AT III may be useful for the treatment of organ failure such as in ischemia/reperfusion-induced organ dysfunction, in which activated leukocytes play a critical role.
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PMID:The anti-inflammatory properties of antithrombin III: new therapeutic implications. 951 77

We investigated the effect of antithrombin III on 60 min warm intestinal ischemia-reperfusion (IR) injury in rats. Sprague-Dawley rats, weighing 220-250 g, were divided into three groups: group 1 sham-operated group (no IR injury, n = 8), group 2 ischemic control group (control, Ringer's lactate infused, n = 8), group 3 Antithrombin III treated group (250 U/kg before ischemia, n = 8). Intestinal ischemia was induced in rats by occluding the superior mesenteric artery for 60 min. Malondialdehyde (MDA) levels, myeloperoxidase activity (MPO) and mucosal damage were investigated after 120 min reperfusion. Elevated MDA levels and MPO activity and severe histopathological damage were observed in the control group compared with the sham group (P < 0.05). Decreased MDA levels and MPO activity and less histopathological damage were detected in group 3 compared with the control group (P < 0.05). Accumulation of lipid peroxidation products and neutrophils in mucosal tissues were significantly inhibited by antithrombin III treatment. We conclude that treatment with antithrombin III before intestinal ischemia prevents histological damage in rats.
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PMID:Antithrombin III prevents 60 min warm intestinal ischemia reperfusion injury in rats. 1020 59

Few studies have pointed out the relationship between ischemia-reperfusion (IR) injury and the coagulation system. Antithrombin III (AT) has anti-inflammatory effects in IR injury. We investigated the effect of AT supplementation on renal IR injury in rats achieved by clamping of the left renal pedicle for 60 min and subsequent 24-h reperfusion after right nephrectomy. Sprague-Dawley rats were divided into three groups: sham-operated (no IR injury), ischemic controls, and an AT-treated group (250 U/kg before reperfusion). Creatinine values, tissue malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and histopathological damage were investigated after 24 h of reperfusion. In addition, the 7-day survival rates in each group were evaluated. Creatinine and MDA levels and MPO activity were significantly elevated and histopathological damage was more severe in controls than in the sham group (P<0.05). Creatinine and MDA levels and MPO activity were significantly lower and there was less histopathological damage in the AT group than in controls. Accumulation of lipid peroxidation products and neutrophils were significantly inhibited by AT treatment. We conclude that AT may attenuate renal IR injury in rats.
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PMID:Antithrombin III reduces renal ischemia-reperfusion injury in rats. 1142 71

Hepatic microcirculation after warm hepatic ischemia in rats can be significantly enhanced by Antithrombin III. The number of sinusoidal stickers as a tool for characterizing the leukocyte-endothelial cell interaction was significantly reduced. The peak of serum transaminases as an indicator of hepatocellular damage was significantly decreased after the AT III application. It has to be concluded that AT III application before Pringle maneuver might significantly reduce the reperfusion damage after liver resection.
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PMID:[New aspects of anti-inflammatory potential of AT III: reduction of reperfusion injury after warm liver ischemia]. 1451 80