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)

Marked contractile failure of the heart is important in both sepsis and endotoxemia, and an understanding of its molecular basis is lacking. We investigated changes in rat myocardial proteins in endotoxemia. Rats were injected with lipopolysaccharide (LPS) and sacrificed 3, 6, 12 and 24 h later. Control rats were injected with a vehicle and sacrificed 6 h later.In the LPS-6 h and LPS-12 h groups, plasma nitrites (NO(x)(-)), were elevated while mean arterial blood pressure (MAP) was depressed as compared to the controls. In the LPS-24 h group, plasma (NO(x)(-)) was returning to the base level whereas MAP was still decreased in comparison to the control group. Six proteins showed changes between groups. All six proteins were decreased in abundance in the LPS-6 h group vs. control. Of the six proteins, three were normalized in the LPS-24 h group: albumin, heat shock protein 27 and triosephosphate isomerase. The three other did not normalize: glyceraldehyde 3-phosphate dehydrogenase, H+-transporting ATP synthase and dienoyl-CoA isomerase. A decrease in abundance of metabolic enzymes may be the result of mitochondrial damage and this decrease could play a protective role against the hypermetabolic state associated with the later stages of sepsis and endotoxemia.
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PMID:Proteomics analysis of changes in myocardial proteins during endotoxemia. 1936 82