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With systemic inflammation, hypoxia, and an increase in the respiratory, a significant increase in the systemic level of pro-inflammatory cytokines is observed. Recently we demonstrated that elevated IL-1β level in blood reduces the ventilatory response to hypoxia. The aim of the present study was to examine the hypothesis that the respiratory effect of IL-1β may be mediating the NO-dependent mechanisms.The experiments were performed on anaesthetized rats. We studied the effects of intravenous administration of cytokine during inhibition of iNO-synthase. In order to we used aminoguanidine bicarbonate - specific inhibitor of iNOS, which was injected in the tail vein for 30 minutes before the administration of cytokine. During the hypoxic rebreathing experiments, was found that the increase of IL-1β level in blood weakens the respiratory response to hypoxia. The ventilatory, tidal volume and mean inspiratory flow responses decreased by 29%, 31% and 53% respectively. INO-synthase inhibitor pretreatment eliminated these respiratory effects of IL-1β. Thus the data indicate that the ability of IL-1β to reduce the ventilatory hypoxic response is mediated by the NO-dependent pathway.

PARTICIPATION OF INOS IN THE EFFECT OF IL-1β ON LUNG VENTILATION AND HYPOXIC CHEMORECEPTION