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

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.

Thrombin, kallikrein and complement C5b-9 adsorption on hydrophilic and hydrophobic titanium and glass after short time exposure to whole blood.

Hydrophilic and hydrophobic titanium and glass were exposed to capillary whole blood between 5s and 24h. The time-sequence for adsorption of thrombin, kallikrein and complement C5b-9, and their relationship with adherent platelets and polymorphonuclear granulocyte (PMN) activation were investigated. Adsorbed thrombin and kallikrein were measured by cleavage of specific chromogenic substances, S-2238 and S-2303, respectively.

Protection by glutathione of neutrophils against the toxic effects of peritoneal dialysis fluid.

The possibility of reducing the cytotoxic effect of heat-sterilized peritoneal dialysis (PD) fluid by addition of antioxidants/scavengers during incubation of titanium-adhering cells was investigated. Capillary blood from healthy donors was placed in drops on commercially available titanium pieces and incubated in a humidified chamber at 37 degrees C for 60min. After incubation the adherent polymorphonuclear leukocytes were immersed for 1-4h in PD-fluid, pH 7.

The respiratory burst response of surface-adhering leukocytes. A key to tissue engineering.

Biomaterials implanted into tissue will participate in the complex signalling between cells during wound healing. Recent studies have revealed that crucial cellular signalling pathways are regulated by the extra- and intracellular redox states and that reactive oxygen species function as intercellular signal molecules. Biomaterials have been shown to affect the respiratory burst response of surface-adhering leukocytes, thus interfering with major regulatory functions of cells also in surrounding tissues.

Surface-adhering Human Leucocytes: An In Vitro Model for Cytotoxicity Testing of Fluids.

A rapid screening method was developed for assessment of the toxic effects of fluid materials on the respiratory burst response of polymorphonuclear neutrophils (PMNLs). The method was used to detect adverse effects of peritoneal dialysis (PD) fluids. Intoxication of the respiratory burst response attenuates the bacterial killing capacity of PMNLs, and increases the sensitivity of patients to peritoneal infection.