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      Anti-C5a monoclonal antibodies and pulmonary polymorphonuclear leukocyte infiltration--endothelial dysfunction by venous gas embolism.

      European Journal of Applied Physiology

      Vasodilator Agents, pharmacology, Antibodies, Monoclonal, administration & dosage, immunology, Apoptosis, drug effects, Complement Activation, Animals, Complement C5a, analysis, Embolism, Air, pathology, Endothelium, Vascular, injuries, physiopathology, Female, Injections, Intravenous, Lung, Male, Neutrophil Infiltration, Neutrophils, Nitroprusside, Pulmonary Artery, Rabbits, Acetylcholine

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          Abstract

          Venous gas embolism (VGE) impairs endothelial function although there is no apparent mechanical damage to the endothelial layer. We investigated whether a monoclonal antibody against the complement anaphylatoxine C5a would affect endothelial dysfunction and pulmonary polymorphonuclear leukocyte infiltration caused by low-grade VGE. Six rabbits were pre-treated with the anti-C5a monoclonal antibody whereas a sham monoclonal antibody was administrated to six other animals 30 min before VGE. Six untreated rabbits subjected to an identical protocol except antibody treatment were used for control. The monoclonal anti-C5a antibody reduced PMN infiltration compared to the control group ( P<0.03). There were no major signs of apoptosis in endothelial cells inside the pulmonary artery in any of the examined animals. There was reduced PMN infiltration and improved endothelium-dependent relaxation in the sham-antibody group, these effects were however not significant. In conclusion, anti-C5a protects the endothelium against injury caused by small amounts of gas bubbles.

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          Journal
          10.1007/s00421-003-0804-8
          12682835

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