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Under these conditions, NOS produces O2– instead of NO, with major potential pathophysiological consequences: the bioavailability of NO decreases by diminished NO production and efficient scavenging of NO by O2–, and the reaction between O2– and NO results in the formation of the strongly oxidizing and presumably deleterious product peroxynitrite (ONOO–).
The observation that NO decreases significantly between Pos. 1 and Pos. 2 even when no humidification system is present between those points might suggest that incomplete gas mixing inside the small internal volume of the respirator is responsible for that decline.
Thus, NO decreases below baseline values [ 22].
It is well-known that NO decreases blood pressure and promotes vascular actions of insulin.
We show in this study that NO decreases mitochondrial respiration and shift these cells towards maintaining high glycolytic rates in order to avoid a decrease in ATP production.
Due to a reduced activity of the endothelial NO synthase (eNOS) in liver endothelial cells NO decreases whereas hepatic stellate cells transform to contractile myofibroblasts [ 5, 7, 17- 21].
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