Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The majority of intra-abdominal adhesions develop postoperatively or following peritonitis. We have previously shown that L-phosphatidylcholine reduces postoperative peritoneal adhesions in rats. In the present study, we examined whether adhesion formation after bacterial peritonitis is also reduced by L-phosphatidylcholine or by DL-alpha-phosphatidylcholine, which is degraded only 50% by phospholipase A2. Peritonitis was induced in the rat by caecal ligation and double puncture; cecotomy was performed 12, 15, or 18 h later. Adhesions were assessed blindly by a scoring system 7 days after cecotomy. When cecotomy was scheduled for 18 h after caecal ligation and puncture, the 7-day mortality was 90% (n = 20). When cecotomy was performed at 12 h, no mortality was seen; however, the adhesion score was low (2.3 +/- 0.7). When cecotomy was performed 15 h after caecal ligation and puncture, the mortality was 25% and the adhesion score was 4.3 +/- 0.9. This figure was reduced significantly by intraperitoneal instillation of L-phosphatidylcholine or DL-alpha-phosphatidylcholine for 3 subsequent days. However, the mortality increased by L-phosphatidylcholine (P < 0.01), whereas mortality after DL-alpha-phosphatidylcholine remained at 30%. We conclude that administration of both L-phosphatidylcholine and DL-alpha-phosphatidylcholine decrease adhesion formation after bacterial peritonitis.
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PMID:Phospholipase-resistant phosphatidylcholine reduces intra-abdominal adhesions induced by bacterial peritonitis. 851 62

Plasma concentration of lysophosphatidylcholine (LPC) was reported to decrease in patients with sepsis. However, the mechanisms of sepsis-induced decrease in plasma LPC levels are not currently well known. In mice subjected to cecal ligation and puncture (CLP), a model of polymicrobial peritoneal sepsis, we examined alterations in LPC-related metabolic parameters in plasma, i.e., the plasma concentration of LPC-related substances (i.e., phosphatidylcholine (PC) and lysophosphatidic acid (LPA)), and activities or levels in the plasma of some enzymes that can be involved in the regulation of plasma LPC concentration (i.e., secretory phospholipase A2 (sPLA2), lecithin:cholesterol acyltransferase (LCAT), acyl-CoA:lysophosphatidylcholine acyltransferase (LPCAT), and autotaxin (ATX)), as well as plasma albumin concentration. We found that levels of LPC and albumin and enzyme activities of LCAT, ATX, and sPLA2 were decreased, whereas levels of PC, LPA, and LPCAT1-3 were increased in the plasma of mice subjected to CLP. Bacterial peritonitis led to alterations in all the measured LPC-related metabolic parameters in the plasma, which could potentially contribute to sepsis-induced decrease in plasma LPC levels. These findings could lead to the novel biomarkers of sepsis.
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PMID:Alteration of Lysophosphatidylcholine-Related Metabolic Parameters in the Plasma of Mice with Experimental Sepsis. 2802 54