title: Endothelial injury during extracorporeal circulation. Role of the complement system.
abstract: This study attempted to elucidate in vitro, endothelial cell (EC) injury induced by complement activation in extracorporeal devices. The in vitro injury model using cultured bovine ECs showed the following: 1) a dose-dependent transmembrane injury, determined by monitoring intracellular calcium mobilization, occurred spontaneously upon addition of complement-activated serum. 2) The respiratory rate of adherent ECs, monitored by an oxygen electrode, was reduced with increases in activated complement serum levels, and increased further with time. 3) Whole cell activity, measured by the rate of cellular proliferation, was reduced with an increase in activated serum complement levels. 4) These cellular responses were almost completely absent in the presence of C3 antiserum, strongly indicating that activated C3 fragments are responsible for EC injury. Thus, complement activation during extracorporeal circulation may injure endothelium at the transmembranous, mitochondrial, and/or proliferative levels, depending upon contact time and concentration of activated complement.
authors: Department of Bioengineering, National Cardiovascular Center, Osaka, Japan.
authors: T
authors: T
authors: Matsuda
authors: Y
authors: Y
authors: Takemoto
authors: Y
authors: Y
authors: Watanabe
authors: T
authors: T
authors: Akutsu
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002417:Cattle; D002455:Cell Division / Q000502:physiology; D002478:Cells, Cultured; D003167:Complement Activation / Q000502:physiology*; D003176:Complement C3 / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology*; D004734:Energy Metabolism / Q000502:physiology; D008928:Mitochondria / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
chemical_list: D003176:Complement C3; D002118:Calcium