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Low molecular weight heparin improves peritoneal ultrafiltration and blocks complement and coagulation.

Artikel i vetenskaplig tidskrift
Författare Farhan Bazargani
Ann Albrektsson
Noushin Yahyapour
Magnus Braide
Publicerad i Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis
Volym 25
Nummer/häfte 4
Sidor 394-404
ISSN 0896-8608
Publiceringsår 2005
Publicerad vid Institutionen för de kirurgiska disciplinerna, Avdelningen för biomaterialvetenskap
Institutionen för anatomi och cellbiologi
Sidor 394-404
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Anticoagulants, pharmacology, Blood Coagulation, drug effects, Capillary Permeability, drug effects, Complement System Proteins, drug effects, metabolism, Dialysis Solutions, toxicity, Disease Models, Animal, Heparin, Low-Molecular-Weight, pharmacology, Male, Neovascularization, Pathologic, metabolism, pathology, Peritoneal Dialysis, adverse effects, methods, Peritoneum, blood supply, drug effects, metabolism, Peritonitis, chemically induced, metabolism, pathology, Rats, Rats, Sprague-Dawley
Ämneskategorier Matematik

Sammanfattning

OBJECTIVES: Clinical studies have demonstrated that the intraperitoneal (IP) complement and coagulation systems are activated in peritoneal dialysis (PD) patients. In animal models, low molecular weight heparin (LMWH) was seen to inhibit peritoneal angiogenesis, and related compounds have increased ultrafiltration volumes after repeated administration to PD patients. The present study evaluated the effects of LMWH on ultrafiltration, coagulation, and complement activation during a single PD dwell. DESIGN: Rats were exposed to a single dose of 20 mL 2.5% glucose-based, filter-sterilized PD fluid, with or without supplementation with LMWH. The PD fluid was administered either as an IP injection or as an infusion through an indwelling catheter. The dwell fluid was analyzed 2 hours later concerning activation of the complement and coagulation cascades, chemotactic activity, neutrophil recruitment, ultrafiltration volume, and glucose and urea concentrations. RESULTS: Exposure to PD fluid induced activation of IP complement [formation of C3a (desArg) and increase of C5a-dependent chemotactic activity] and coagulation (formation of thrombin-antithrombin complex) and recruitment of neutrophils. In the case of IP injection, neutrophil recruitment and complement activation were inhibited by LMWH. In both models, LMWH inhibited thrombin formation, reduced complement-dependent chemotactic activity, and increased the IP fluid volume, indicating an improved ultrafiltration. CONCLUSIONS: The acute inflammatory reaction to PD fluid involves the complement and coagulation cascades. Addition of LMWH to the PD fluid improves ultrafiltration, inhibits formation of thrombin, and potentially blocks C5a activity. The present results motivate further investigations of the IP cascade systems in PD.

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