Biological Responses at Artificial Surfaces and Recent Progress in Extracorporeal Circulation
The activation of body defence mechanisms during extracorporeal circulation often causes local and systemic adverse effects on the body. The former is exemplified as thrombus formation at the blood-material interfaces, and the latter as peripheral circulation failure associated with microemboli and granulocyte aggregation, resulting in symptoms such as systemic hypertension and peripheral hypotension. Understanding the biological responses at the blood-material interface of extracorporeal devices, such as a hemodialysis, plasmapheresis and artificial oxygenator, is very important for upgrading the biocompatibility of a device under development. The body defence mechanisms associated with thrombus formation and immunological alterations include many biological systems, including the coagulation, complement and cellular systems. As schematically shown in Fig. 1, the multiple activations of these biological systems occur as blood comes in contact with a foreign surface. The characteristic feature of body defence mechanisms leading to thrombus formation is that, although they are independently activated at blood-material surfaces, there exists a positive feed-back mechanism in which an activated form also activates other biological systems. For instance, the activated form (Factor XIIa) of the coagulation system can activate the third component of the complement system, and the activated complement factor (C5a) is a potent aggregation activator of granulocytes. Besides participation in thrombus formation, immunological alterations are involved in humoral and cellular activation. Therefore, the understanding of molecular events at a blood-material interface is of particular importance for the logical surface design of blood-contacting material, particularly that used in extracorporeal devices.
KeywordsComplement System Coagulation System Extracorporeal Circulation Classical Pathway Butyl Methacrylate
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