Anzeige
Erschienen in:
18.09.2020 | Editorial
Vitamin C and thiamine for sepsis: time to go back to fundamental principles
Erschienen in: Intensive Care Medicine | Ausgabe 11/2020
Einloggen, um Zugang zu erhaltenExcerpt
Vitamin C plays a vital role in human physiology. For decades, intriguing research has highlighted the possibility of acute effects of vitamin C deficiency in patients with sepsis [1]. Vitamin C is a mediator of endothelial function through its co-factor role with many enzymes (including one that catalyses the conversion of dopamine to noradrenaline). Vitamin C also works as an antioxidant by scavenging free radicals (Fig. 1). In animal models of sepsis, exogenous vitamin C increases perfused capillary density and arteriolar vasoconstrictor responsiveness, implying its possible role in treating vasoplegic status in sepsis [2].
Fig. 1
A diagram of vitamin C roles from in vitro or in vivo studies. Vitamin C is taken up into cells via SVCT2 and scavenge ROS and downregulate NOx. In adrenomedullary chromaffin cells, dopamine is translocated to chromaffin granules and is converted to noradrenaline. The conversion is catalysed by dopamine β-hydroxylase, where vitamin C works as a cofactor. SVCT2 sodium-vitamin C cotransporter 2, ROS reactive oxygen species, NOx NADPH oxidase. NF-kB nuclear factor-kappa B
× ![]()
…