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Báo cáo y học: "Circulating adenosine increases during human experimental endotoxemia but blockade of its receptor does not influence the immune response and subsequent organ injury"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Circulating adenosine increases during human experimental endotoxemia but blockade of its receptor does not influence the immune response and subsequent organ injury. | Ramakers et al. Critical Care 2011 15 R3 http ccforum.eom content 15 1 R3 KS CRITICAL CARE RESEARCH Open Access Circulating adenosine increases during human experimental endotoxemia but blockade of its receptor does not influence the immune response and subsequent organ injury 1.2 1.3 1 4 5 Bart P Ramakers 1 Niels P Riksen 1 Petra van den Broek Barbara Franke Wilbert HM Peters Johannes G van der Hoeven2 Paul Smits1 Peter Pickkers2 Abstract Introduction Preclinical studies have shown that the endogenous nucleoside adenosine prevents excessive tissue injury during systemic inflammation. We aimed to study whether endogenous adenosine also limits tissue injury in a human in vivo model of systemic inflammation. In addition we studied whether subjects with the common 34C T nonsense variant rs17602729 of adenosine monophosphate deaminase AMPD1 which predicts increased adenosine formation have less inflammation-induced injury. Methods In a randomized double-blinded design healthy male volunteers received 2 ng kg E. Coli LPS intravenously with n 10 or without n 10 pretreatment with the adenosine receptor antagonist caffeine 4 mg kg body weight . In addition lipopolysaccharide LPS was administered to 10 subjects heterozygous for the AMPD1 34C T variant. Results The increase in adenosine levels tended to be more pronounced in the subjects heterozygous for the AMPD1 34C T variant 71 22 P 0.04 compared to placebo- 59 29 P 0.012 and caffeine-treated 53 47 P 0.29 subjects but this difference between groups did not reach statistical significance. Also the LPS-induced increase in circulating cytokines was similar in the LPS-placebo LPS-caffeine and LPS-AMPD1-groups. Endotoxemia resulted in an increase in circulating plasma markers of endothelial activation intercellular adhesion molecule ICAM and vascular cell adhesion molecule VCAM and in subclinical renal injury measured by increased urinary excretion of tubular injury markers. The LPS-induced increase of these markers did not .