作者: Cher-Rin Chong , Saifei Liu , Giovanni Licari , Tamila Heresztyn , Yuliy Y. Chirkov
DOI: 10.1016/J.AMJMED.2014.11.007
关键词: Endocrinology 、 Oxidative stress 、 Endothelial progenitor cell 、 Inflammation 、 Medicine 、 Internal medicine 、 Sensitization 、 Platelet 、 Nitric oxide 、 Superoxide 、 Acute coronary syndrome
摘要: Abstract Background Hyperglycemia in patients with acute coronary syndromes is associated poor outcomes, and its rapid correction insulin infusion has been shown to restore platelet responsiveness nitric oxide suppress superoxide (O 2 − ) generation. Thioredoxin-interacting protein emerged recently as a pivotal modulator of hyperglycemia-induced inflammation, O production, impairment signaling, but it not known whether expression platelets can be downregulated rapidly. Methods In 12 hyperglycemic syndrome, we evaluated the putative role thioredoxin-interacting suppression response after reversal hyperglycemia infusion. Results Insulin for 13.0 ± 0.8 (standard error mean) hours decreased blood glucose level from 16.6 1.6 mmol/L 8.7 1.4 ( P = .002). This induced (1) sensitization antiaggregatory (from 6.5% 7.7% 39.7% 7.0%, Conclusions Correction syndrome rapidly reverses oxidative stress, restoring both endothelial progenitor cell function, this process largely or entirely independent protein.