Does carbon dioxide suppress macrophage superoxide anion production independent of extracellular pH and mitochondrial activity?
Incubation in CO2 can directly suppress macrophage superoxide anion production. This effect is of short duration, fully reversible, and not correlated to changes in extracellular pH or mitochondrial activity. Air contamination does not affect macrophage superoxide anion release. We speculate that CO2 pneumoperitoneum could attenuate the intraoperative free radical production by directly inhibiting superoxide anion release of macrophages without long-lasting suppression of macrophages and their capacity to release superoxide anions postoperatively.
Hypervolemic hypernatremia is by far the most common cause of hypernatremia in patients in the intensive care unit. Even though the patients are in negative fluid balance at the time of the development of the hypernatremia, earlier saline administration has caused massive volume overload despite the ongoing losses. Post-AKI diuresis in the face of inability to maximally concentrate the urine because of renal failure often leads to mainly mild elevations in serum sodium concentration. The urine solute is mainly urea because of the often high serum urea concentrations with little electrolytes being present in the urine.