Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of laparotomy, intestinal resection, heparin and bacterial peritonitis on fibrinolysis of the peritoneum was evaluated in dogs. Heparin had no effect. Sterile laparotomy and intestinal resection severely, but incompletely, reduced fibrinolytic activity measured 24 hours after operation. Fibrinopurulent peritonitis induced by creation of a 10 centimeter long ischemic loop of the terminal part of the ileum abolished the fibrinolytic activity of the peritoneum almost completely. The data are consistent with findings that adhesion formation is inversely correlated with the fibrinolytic activity of the peritoneum. Untreated peritonitis abolished that activity by mechanisms as yet not elucidated. Heparin, which has been shown to reduce both adhesion-formation and the lethality of peritonitis, apparently does so by mechanisms independent of the intrinsic fibrinolytic system of the peritoneum.
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PMID:Fibrinolytic activity of the peritoneum during experimental peritonitis. 41 46

Sprague-Dawley rats with peritonitis treated with either a subcutaneous or intraperitoneal minidose of heparin show a significant increase in survival time when compared with controls. In the treatment groups, adhesions and abscesses were less severe and localized to the area of gangrenous bowel. Heparin also significantly reduced the incidence of recovery of viable bacteria from the blood and peritoneal cavity. These findings may be related to a decreased deposition of fibrinogen within the abdomen or to the early mobilization of fibrin.
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PMID:The effects of a minidose of heparin on peritonitis in rats. 43 73

To evaluate the effects of heparin on gram-negative septic shock, immature piglets were subjected to fecal Escherichia coli peritonitis. One group of animals received a continuous infusion of heparin 25 units/kg/hr, while the control animals were given an equivalent volume of lactated Ringer's solution. Heparin-treated animals (n = 5) had a mean survival time (+/- SEM) of 18.8 +/- 2.2 hr vs. 11.9 +/- 2.8 (P less than 0.05) in controls (n = 5). Animals receiving heparin tended to have improved hemodynamic profiles and less leukopenia than controls.
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PMID:Does heparin improve survival in experimental porcine gram-negative septic shock? 219 16

Ischemic tissue and intraperitoneal bacteria have been ascribed an etiologic role in the production of intra-abdominal adhesions. To further elucidate the role of these stimuli and to evaluate the potential protective effect of various agents, peritonitis was induced in 160 Sprague-Dawley rats. The experiment was stratified into those animals with peritonitis plus necrotic tissue, solid feces, both, or neither. The agents tested were a nonsteroidal anti-inflammatory (ibuprofen), free radical scavenger (SOD), and an anticoagulant (heparin). Death was less likely to occur in animals treated with heparin (3 of 40 vs. 12 of 40, p less than 0.01) or SOD (4 of 40 vs. 12 of 40, p less than 0.05). Ibuprofen did not increase survival in this model. Heparin protected against adhesions in animals with an ischemic ileum of limb and without solid feces. In animals with a nonischemic isolated segment of ileum and solid feces, adhesion formation was increased in both the ibuprofen and the heparin treatment groups (p less than 0.05).
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PMID:The role of feces, necrotic tissue, and various blocking agents in the prevention of adhesions. 338 37

Mesenteric vein thrombosis is generally difficult to diagnose and can be fatal. A case of extensive thrombosis of the mesenteric and portal veins was diagnosed early and successfully treated in a 26-year-old man with Down syndrome who was admitted to hospital because of abdominal pain, severe nausea and high fever. Ultrasonography revealed moderate ascites, and there was minimal flow in the portal vein (PV) on the Doppler examination. Computed tomography (CT) showed remarkable thickening of the walls of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, combined thrombolysis and anticoagulation therapy without surgical treatment was chosen. Urokinase was administered intravenously and later through a catheter in the superior mesenteric artery. Heparin and antibiotics were given concomitantly. The patient's symptoms and clinical data improved gradually. After 10 days, CT revealed that collateral veins had developed and the thrombi in the distal portions of the mesenteric veins had dissolved, although the main trunk of the PV had not recanalized. The only risk factor of thrombosis that was detected was decreased protein S activity.
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PMID:Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation. 1185 47

Heparin has been used clinically as an anticoagulant and antithrombotic agent for over 60 years. Here we show that the potent anti-inflammatory property of heparin results primarily from blockade of P-selectin and L-selectin. Unfractionated heparin and chemically modified analogs were tested as inhibitors of selectin binding to immobilized sialyl Lewis(X) and of cell adhesion to immobilized selectins or thrombin-activated endothelial cells. Compared with unfractionated heparin, the modified heparinoids had inhibitory activity in this general order: over-O-sulfated heparin > heparin > 2-O,3-O-desulfated > or = N-desulfated/N-acetylated heparin > or = carboxyl-reduced heparin > or= N-,2-O,3-O-desulfated heparin >> 6-O-desulfated heparin. The heparinoids also showed similar differences in their ability to inhibit thioglycollate-induced peritonitis and oxazolone-induced delayed-type hypersensitivity. Mice deficient in P- or L-selectins showed impaired inflammation, which could be further reduced by heparin. However, heparin had no additional effect in mice deficient in both P- and L-selectins. We conclude that (a) heparin's anti-inflammatory effects are mainly mediated by blocking P- and L-selectin-initiated cell adhesion; (b) the sulfate groups at C6 on the glucosamine residues play a critical role in selectin inhibition; and (c) some non-anticoagulant forms of heparin retain anti-inflammatory activity. Such analogs may prove useful as therapeutically effective inhibitors of inflammation.
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PMID:Heparin's anti-inflammatory effects require glucosamine 6-O-sulfation and are mediated by blockade of L- and P-selectins. 1209 96

Heparin is an excellent inhibitor of P- and L-selectin binding to the carbohydrate determinant, sialyl Lewis(x). As a consequence of its anti-selectin activity, heparin attenuates metastasis and inflammation. Here we show that fucosylated chondroitin sulfate (FucCS), a polysaccharide isolated from sea cucumber composed of a chondroitin sulfate backbone substituted at the 3-position of the beta-D-glucuronic acid residues with 2,4-disulfated alpha-L-fucopyranosyl branches, is a potent inhibitor of P- and L-selectin binding to immobilized sialyl Lewis(x) and LS180 carcinoma cell attachment to immobilized P- and L-selectins. Inhibition occurs in a concentration-dependent manner. Furthermore, FucCS was 4-8-fold more potent than heparin in the inhibition of the P- and L-selectin-sialyl Lewis(x) interactions. No inhibition of E-selectin was observed. FucCS also inhibited lung colonization by adenocarcinoma MC-38 cells in an experimental metastasis model in mice, as well as neutrophil recruitment in two models of inflammation (thioglycollate-induced peritonitis and lipopolysaccharide-induced lung inflammation). Inhibition occurred at a dose that produces no significant change in plasma activated partial thromboplastin time. Removal of the sulfated fucose branches on the FucCS abolished the inhibitory effect in vitro and in vivo. Overall, the results suggest that invertebrate FucCS may be a potential alternative to heparin for blocking metastasis and inflammatory reactions without the undesirable side effects of anticoagulant heparin.
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PMID:Selectin blocking activity of a fucosylated chondroitin sulfate glycosaminoglycan from sea cucumber. Effect on tumor metastasis and neutrophil recruitment. 1737 80

A 25-year-old man was admitted to our hospital because of abdominal pain, nausea and low-grade fever. An abdominal CT showed remarkable thickening of the wall of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, anticoagulation therapy was chosen. Heparin was administered intravenously and was used alternatively with warfarin later. The patient's symptoms and clinical data improved gradually. Concerning the etiological factors of the thrombosis, only protein S activity definitely decreased. Genetic analysis indicated a variant of protein S, protein S Tokushima.
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PMID:[A case of portal vein thrombosis associated with congenital protein S deficiency]. 1754 50

The results of comparative study of different heparin medications efficacy in patients with thrombohemorrhagic syndrome (THS) are presented. The study was conducted in 286 patients with THS as a result of peritonitis of various etiology (174 patients), massive hemorrhage, shock, microcirculation disorders (112 patients). Heparin therapy carried out in 249 patients (87.1%), 37 patients (12.9%) had no heparin therapy./ In "heparin" group 193 patients (77.5%) received low molecular weight heparin (LMWH), 56 patients (22.5%) took unfractionated heparin (UFH). LWMH demonstrated high efficiency with fewer hemorrhagic complications in comparison with UFH/.
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PMID:[Methods of heparin therapy in surgical patients with thrombohemorrhagic syndrome]. 2283 92

Inflammation and cancer are related pathologies acting synergistically to promote tumor progression. In both, hematogenous metastasis and inflammation, P-selectin participates in interactions involving tumor cells, platelets, leukocytes and endothelium. Heparin has been shown to inhibit P-selectin and as a consequence it blunts metastasis and inflammation. Some heparin analogs obtained from marine invertebrates are P-selectin inhibitors and do not induce bleeding effects. The present work focuses on the P-selectin blocking activity of a unique heparan sulfate (HS) from the bivalve mollusk Nodipecten nodosus. Initially, we showed that the mollusk HS inhibited LS180 colon carcinoma cell adhesion to immobilized P-selectin in a dose-dependent manner. In addition, we demonstrated that this glycan attenuates leukocyte rolling on activated endothelium and inflammatory cell recruitment in thioglycollate-induced peritonitis in mice. Biochemical analysis indicated that the invertebrate glycan also inhibits heparanase, a key player in cell invasion and metastasis. Experimental metastasis of Lewis lung carcinoma cells was drastically attenuated by the mollusk HS through a mechanism involving inhibition of platelet-tumor-cell complex formation in blood vessels. These data suggest that the mollusk HS is a potential alternative to heparin for inhibiting P-selectin-mediated events such as metastasis and inflammatory cell recruitment.
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PMID:Antitumor properties of a new non-anticoagulant heparin analog from the mollusk Nodipecten nodosus: Effect on P-selectin, heparanase, metastasis and cellular recruitment. 2536 17


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