The role of nitric oxide in the effects of the pro-inflammatory cytokine IL-1β on the hypercapnic ventilation response
DOI:
https://doi.org/10.33910/2687-1270-2020-1-2-101-107Keywords:
cytokines, interleukin-1, hypercapnia, respiratory chemoreflex, breathing, ventilation, NO-synthaseAbstract
The aim of the current study was to compare the respiratory effects of IL-1β before and after pre-treatment with L-NAME, a nonspecific NO-synthases inhibitor.
The experiments were performed on tracheotomised anaesthetised rats. The hypercapnic ventilatory response was measured by means of the rebreathing method using a hyperoxic-hypercapnic gas mixture (60 % O2, 7 % CO2) before and after the cerebroventricular administration of human recombinant IL-1β in the amount of 500 ng dissolved in 10 μl of saline. In order to determine the role of the NO-pathway in the ventilatory effects of IL-1β, L-NAME, a non-specific inhibitor of NO-synthase, was used.
As a result, the slope of the ventilatory response to carbon dioxide decreased almost twofold at 40 min. after the cerebroventricular administration of IL-1β. In contrast, the basal level of lung ventilation increased after the elevation of IL-1β in CSF. L-NAME pre-treatment reduced these respiratory effects of IL-1β. The data indicate that the inhibitor of NO-synthase significantly reduces the effect of the pro-inflammatory cytokine IL-1β.
The authors conclude that the ability of IL-1β to enhance basal ventilation and to reduce the ventilatory hypercapnic response may be mediated by NO-dependent mechanisms.
References
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Paxinos, G., Watson, C. (1982) The rat brain in stereotaxic coordinates. Sydney: Academic Press, VII, 12 p., 71 bl. pl. (In English)
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