Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the anticoagulants, heparin and low molecular weight heparin (LMWH), and the antiplatelet agents, prostaglandin E1 (PGE1) and aspirin, on endotoxin-induced renal insufficiency not induced by prerenal factors, were investigated using rabbits to evaluate the clinical usefulness of these drugs and their possible involvement in the activation of hemostasis in renal insufficiency. The intravenous administration of PEG1, at 0.4 microgram/kg/min, or aspirin, at 5 mg/kg, significantly restored all the parameters of renal function measured in the present study, namely, effective renal plasma flow, glomerular filtration rate and urine N-acetyl-beta-D-glucosaminidase, as well as histological renal ischemic changes. On the other hand, neither heparin nor LMWH, even at a high dose, improved any parameter. As the antiplatelet effect is the common property of PGE1 and aspirin, it is suggested that the activation of platelets may be prerequisite to the occurrence of renal insufficiency induced by endotoxin. The results of this study thus show that PGE1 or aspirin may be applied in clinical use for renal insufficiency complicated by sepsis or endotoxemia.
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PMID:The possible involvement of platelet activation in endotoxin-induced renal insufficiency in a rabbit model. 166 36

Vibrio vulnificus, an opportunistic human pathogen causing wound infection and septicemia, produces a metalloprotease (VVP) which is suspected to be a virulent determinant. The interactions of VVP, as well as its derivative (PEG1-VVP) modified with polyethylene glycol, with a variety of human plasma proteins were investigated. We found that native VVP and its derivative were able to act directly on many biologically important human plasma proteins even in the presence of alpha-macroglobulin, the sole plasma inhibitor of native VVP. The activities of both classical and alternative pathways of the complement cascade system were drastically abolished by incubation with either VVP. Furthermore, these proteases rapidly digested the A alpha-chain of human fibrinogen into fragment(s) with no clotting ability. Therefore both VVPs are thought to function as a fibrinogenolytic enzyme, causing delay of the coagulation reaction. VVP and PEG1-VVP were also shown to destroy plasma proteinase inhibitors including alpha 1-proteinase inhibitor, a major inhibitor in human plasma. Because endogenous proteolytic enzymes and their inhibitors are indispensable in maintaining physiological homeostasis, these findings suggest that VVP (and PEG1-VVP) may cause an imbalance of human plasma proteinase-proteinase inhibitor systems, thus eliciting an immunocompromised state in the host and facilitating the development of a systemic V. vulnificus infection such as septicemia.
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PMID:Actions of Vibrio vulnificus metalloprotease on human plasma proteinase-proteinase inhibitor systems: a comparative study of native protease with its derivative modified by polyethylene glycol. 878 55