作者: Heleen M Oudemans-van Straaten , Angelique ME Spoelstra-de Man , Monique C de Waard
DOI: 10.1186/S13054-014-0460-X
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摘要: This narrative review summarizes the role of vitamin C in mitigating oxidative injury-induced microcirculatory impairment and associated organ failure ischemia/reperfusion or sepsis. Preclinical studies show that high-dose can prevent restore flow by inhibiting activation nicotinamide adenine dinucleotide phosphate-oxidase inducible nitric oxide synthase, augmenting tetrahydrobiopterin, preventing uncoupling phosphorylation, decreasing formation superoxide peroxynitrite, directly scavenging superoxide. Vitamin additionally vascular responsiveness to vasoconstrictors, preserve endothelial barrier maintaining cyclic guanylate phosphatase occludin phosphorylation apoptosis. Finally, augment antibacterial defense. These protective effects against overwhelming stress due ischemia/reperfusion, sepsis burn seems mitigate injury dysfunction, promote recovery after cardiac revascularization critically ill patients, latter partially combination with other antioxidants. Of note, several questions remain be solved, including optimal dose, timing The obviously offers a synergistic effect reasonable during sustained critical illness. High-dose C, however, provides cheap, strong multifaceted antioxidant, especially robust for resuscitation circulation. given as early possible injurious event, before if feasible, most effective. could considered at start surgery, transplant major gastrointestinal surgery. Preoperative supplementation should consider on ischemic preconditioning. In future research focus use short-term intravenous drug, intervene oxidant cascade order optimize macrocirculation microcirculation limit cellular injury.