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)

The last few years have clarified the tight link between inflammation and coagulation. In addition to the identification of new regulatory mechanisms of the coagulation system and of an explosive number of mediators of inflammation, it is now clear that the existence of a positive feed-back between inflammation and coagulation leads to reciprocal activation of both pathways. Plasma levels of acute phase proteins involved in coagulation and fibrinolysis are elevated during inflammation, while natural anticoagulant mechanisms are depressed. Pro-inflammatory cytokines "activate" cell membranes exposed to flowing blood (endothelium, platelets, monocytes, neutrophils) which from physiologically inert or anticoagulant become procoagulant. Increased tissue factor expression results in increased thrombin formation within the microcirculation. Thrombin is central to fibrin deposition but it also plays a key role in cell-mediated mechanisms involving inflammation, cell proliferation and activation of the natural anticoagulant protein C. Depression of natural anticoagulant mechanisms, occurring in severe sepsis, results in uncontrolled thrombin formation, with pro-inflammatory activity prevailing, and the feed-back loop of inflammation and coagulation ultimately leading to multi-organ failure. However, both in the clinical setting and in animal experiments, heparin or direct anticoagulants have shown no effect on survival even if blocking fibrin deposition. Organ failure is only partially due to the thrombotic occlusion of the microcirculation, while other mechanisms of endothelial damage are probably more relevant in the development of ischemia. The endothelium is central to the maintenance of the natural anticoagulant mechanisms (TFPI, antithrombin, protein C). The protein C system, in addition to dumping thrombin formation, specifically modulates inflammation by cell signaling. This system is markedly depressed in severe sepsis. The infusion of activated protein C, or restoring normal levels of protein C within the circulation - depending on the individual bleeding risk are powerful tools to treat the endothelitis responsible for the clinical sequelae of severe sepsis.
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PMID:[Protein C and coagulation in sepsis]. 1518 14

Acute mesenteric ischemia is a highly morbid affliction which requires urgent care. Acute mesenteric ischemia consists in an ischemia injury of the small bowel, secondary to vascular insufficiency, either occlusive (thrombosis, embolism, arterial, venous) or non-occlusive (low flow or vasospasm). Given that the superior mesenteric artery supplies the small bowel as well as the right part of the colon, any ischemic process involving the right colon should be considered an acute mesenteric ischemia until proven otherwise. Acute mesenteric ischemia should always be suspected in the setting of a sudden, unusual and intense abdominal pain requiring opioids. Chronic mesenteric ischemia can also be revealed by postprandial abdominal pain associated with significant weight loss. The clinical presentation of mesenteric ischemia is nonspecific. Thus, a suspected diagnosis must be confirmed by imaging usually consisting in an abdominal computed tomography scan. Imaging will also provide guidance with regards to treatment decision. Organ failure, serum lactate elevation as well as bowel loop dilationper imaging are predictive of irreversible intestinal necrosis. In the presence of any of these predictive factors, surgical management should be considered. The modern treatment of mesenteric ischemia in Intestinal Stroke Centers has allowed rates of resection-free survival in nearly two-thirds of patients. The management of mesenteric ischemia relies in a combination of: (1) a medical protocol including oral/enteral antibiotics; (2) the revascularization of viable bowel and (3) the surgical resection of necrosic, non viable intestinal tissue. The inception and development of Intestinal Stroke Centers has been the cornerstone of significantly improved management and survival rates as well as crucial asset in research, specifically in the field of biomarkers associated with early diagnosis.
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PMID:[Modern treatment of mesenteric ischemia]. 2977 90

The shortage of donor organs is a major global concern. Organ failure requires the transplantation of functional organs. Donor's organs are preserved for variable periods of warm and cold ischemia time, which requires placing them into a preservation device. Ischemia and reperfusion damage the organs, due to the lack of oxygen during the ischemia step, as well as the oxidative stress during the reperfusion step. Different methodologies are developed to prevent or to diminish the level of injuries. Preservation solutions were first developed to maximize cold static preservation, which includes the addition of several chemical compounds. The next chapter of organ preservation comes with the perfusion machine, where mechanical devices provide continuous flow and oxygenation ex vivo to the organs being preserved. In the addition of inhibitors of mitogen-activated protein kinase and inhibitors of the proteasome, mesenchymal stem cells began being used 13 years ago to prevent or diminish the organ's injuries. Mesenchymal stem cells (e.g., bone marrow stem cells, adipose derived stem cells and umbilical cord stem cells) have proven to be powerful tools in repairing damaged organs. This review will focus upon the use of some bone marrow stem cells, adipose-derived stem cells and umbilical cord stem cells on preventing or decreasing the injuries due to ischemia-reperfusion.
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PMID:Therapeutic Properties of Mesenchymal Stem Cell on Organ Ischemia-Reperfusion Injury. 3169 40