• Critical care medicine · Jan 2010

    Comparative Study

    Distant effects of nitric oxide inhalation in endotoxemic pigs.

    • Manja C A Nilsson, Kristina Hambraeus-Jonzon, Kristina Hambraeus-Jonon, Marco Lattuada, Luni Chen, Ren Li, Kjell Alving, Peter Wiklund, Goran Hedenstierna, and Filip Fredén.
    • Department of Anesthesiology and Intensive Care, Uppsala University, Uppsala.
    • Crit. Care Med. 2010 Jan 1;38(1):242-8.

    ObjectiveInhalation of nitric oxide (INO) has distant effects. By a blood- borne factor, INO down-regulates endogenous nitric oxide production in healthy pig lungs, resulting in vasoconstriction in lung regions not directly reached by INO. The aim of this study was to investigate whether INO has distant effects in endotoxemic pig lungs. The hypothesis was that INO down-regulates endogenous NO production in lung regions not reached by INO.DesignProspective, randomized animal study.SettingUniversity hospital research laboratory.SubjectsTwenty-two pairs of domestic pigs.InterventionsCross-circulation was established in 22 pairs of anesthetized pigs. Nine pairs received endotoxin (control group) and 13 pairs received endotoxin, with one pig inhaling NO (80 ppm) and one pig receiving blood from that pig (NO-blood recipient group).Measurements And Main ResultsNO in exhaled air, NO synthase activity in lung tissue, endothelin-1 in the blood, ETA and ETB receptor immunoreactivity in lung tissue, vital parameters, and blood gases were measured. Endotoxin per se increased NO in exhaled air by 100% compared to baseline (control group). In the NO-blood recipient group, i.e., pigs receiving blood from the NO-inhaling pigs, NO in exhaled air increased by 300% (p = .03). The Ca-dependent NO synthase activity was higher in these pigs (p = .02), indicating increased endogenous NO production. The ET B receptor immunoreactivity was higher in the NO-blood recipient group (p = .004).ConclusionsAs opposed to findings in healthy pigs, INO in endotoxemic pigs causes an increase in endogenous NO production in lung regions not reached by INO. Increased NO production in nonventilated lung regions may cause vasodilatation, counteracting the INO-induced increase in blood flow to the ventilated lung regions.

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