Abstract
We investigated thein vitroeffect of different form s of acidosis (pH 7.0) on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 μ mol/ml blood) or lactic acid (5.5 μ mol/ml) to heparin blood(N=12)caused significant activation of C3a and C5a compared to control (bothp=0.002). Respiratory acidosis activated C3a(p=0.007)and C5a(p=0.003)compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These experiments show that acidosis itself and not lactate trigger for activation of complement components C3 and C5.
Highlights
Hypox ia and re perfusion c ause compleme nt activation in animal ex perime nts and in clinical studie s.1– 4 It c ould be show n, that after c ytological damage, contac t w ith cellular compone nts such as mitochondria, or ex c ess of hydrox yl radicals, w as re spons ible for the ac tivation of the compleme nt syste m.5,6 On the othe r hand, in vitro studies show ed a compleme nt ac tivation by ac idosis or hypox ia only.[7,8,9] In a pre vious study, w e found complement ac tivatio n induc ed by lactic ac id.[10]
There fore the re sults w e re compared to controls of the same handling method but w ithout pH change
The study show s that the acidosis itself is the trigger for ac tivation, be c ause all thre e forms of ac idosis le ad to a signific ant incre ase of anaphylatox in conc entrations
Summary
Hypox ia and re perfusion c ause compleme nt activation in animal ex perime nts and in clinical studie s.1– 4 It c ould be show n, that after c ytological damage, contac t w ith cellular compone nts such as mitochondria, or ex c ess of hydrox yl radicals, w as re spons ible for the ac tivation of the compleme nt syste m.5,6 On the othe r hand, in vitro studies show ed a compleme nt ac tivation by ac idosis or hypox ia only.[7,8,9] In a pre vious study, w e found complement ac tivatio n induc ed by lactic ac id.[10]. Hypox ia and re perfusion c ause compleme nt activation in animal ex perime nts and in clinical studie s.1– 4. It c ould be show n, that after c ytological damage, contac t w ith cellular compone nts such as mitochondria, or ex c ess of hydrox yl radicals, w as re spons ible for the ac tivation of the compleme nt syste m.5,6. The aim of the pre sent in v itro study w as to inve stigate: (1) w he the r lac tate itself or metabolic acidosis is re sponsible for activation, and (2) w hethe r re spiratory acidosis is able to ac tivate the complement syste m
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