Ventilator Y-piece pressure compared with intratracheal airway pressure in healthy intubated children.

Objective: Compare airway pressure measurements at the ventilator Y-piece of the breathing circuit (P( Y )) to intratracheal pressure measured at the distal end (P( T )) of the endotracheal tube (ETT) during mechanical ventilation and spontaneous breathing of intubated children.

Methods: Thirty children (age range 29 days to 5 years) receiving general anesthesia were intubated with an ETT incorporating a lumen embedded in its sidewall that opened at the distal end to measure P( T ). Peak inflation pressure (PIP) was measured at P( Y ) and P( T ) during positive pressure ventilation.

Intravascular infusion of acid promotes intrapulmonary inducible nitric oxide synthase activity and impairs blood oxygenation in rats.

Objective: To test the hypothesis that intravascular acid infusion promotes intrapulmonary nitric oxide formation by promoting inducible nitric oxide synthase (iNOS) and inhibiting endothelial nitric oxide synthase (eNOS) expression in rats.

Design: Prospective, placebo controlled, randomized laboratory study.

Setting: University laboratory.

Dexamethasone suppresses iNOS yet induces GTPCH and CAT-2 mRNA expression in rat lungs.

The in vivo mechanisms by which glucocorticoids inhibit nitric oxide expression await detailed investigation. In cell culture experiments, glucocorticoids have been shown to inhibit inducible nitric oxide synthase (iNOS) formation and activity. Glucocorticoids can inhibit iNOS activity in cultured cells by blocking arginine transport and inhibiting tetrahydrobiopterin biosynthesis.

Resuscitation of hemorrhagic shock attenuates intrapulmonary nitric oxide formation.

Hemorrhagic shock has been shown to upregulate intrapulmonary inducible nitric oxide (NO) synthase (iNOS) expression. Increased intrapulmonary iNOS expression is reflected by increases in concentrations of NO in the airways. The purpose of this study was to examine the effects of resuscitation on this induction of intrapulmonary NO formation caused by hemorrhage.