The role of prostaglandins in the realization of respiratory effects of interleukin-1ss in case of hypercapnia.

Was shown that the cerebral level of interleukin-1β (IL-1β) increasing causes neuronal activation in the respiratory-dependent areas of the brainstem. Moreover, the direct action of IL-1β on the cerebral neuronal respiratory neurons in vitro does not change their activity. This suggests that the central respiratory effects of IL-1β are based on an indirect mechanism associated with the secondary messenger system activation. The role of such mediators can be performed by prostaglandins.The aim of the present study was to examine the hypothesis that the IL-1β respiratory effects basis is the action of prostaglandins.For this purpose intracerebroventricular injections of human recombinant IL- lβ were used in anaesthetized tracheostomized rats during the resting and hypercapnic stimulated breathing.The ventilatory hypercapnic response was measured by using rebreathing techniques before and after injection IL-1β. In order to determine the role of the cyclooxygenase (COX) pathway in the ventilatory effects of IL-lβ, intraperitoneal administration of diclofenac, a nonspecific COX inhibitor, was used.It was sown that when the resting breathing the injections of IL- lβ evoke the significant increase in minute ventilation and mean inspiratory flow. During the hypercapnic rebreathing experiments it was obtained that the increase of IL- lβ in liquor weakens the ventilatory, tidal volume and mean inspiratory flow responses to carbon dioxid...
Source: European Respiratory Journal - Category: Respiratory Medicine Authors: Tags: Mechanisms of Lung Injury and Repair Source Type: research