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Pro-inflammatory cytokine IL-1β, as inflammatory mediators participate in neuroimmune interactions in the central nervous system. It’s assumed that IL-1β affect the central and peripheral breathing control in acute hypoxia that occurs simultaneously with systemic inflammation. The purpose of this study was to evaluate the influence IL-1β on respiratory responses following progressive hypoxia and ability to survive after hypoxic apnea. We studied the influence of IL-1β (10 μg/kg) on respiration and the ability to survive acute hypoxic challenge in anesthetized Wistar rats. The response of tidal volume, breathing rate, minute lung ventilation, oxygen saturation, during acute hypoxia was examined using pneumotachography methods. Increasing hypoxia was created by rebreathing method. The results indicated that during progressive acute hypoxia animals given IL-1β were unable to sustain breathing efforts for as long as control rats. Following hypoxic apnea IL-1β decrease the ability to autoresuscitate compared with control groups. Thus IL-1β reduces the tolerance of animals to acute hypoxia and the ability to spontaneously autoresuscitate after apnea. We assume that that IL-1β inhibit inspiratory neurons and decrease the sensitivity of the carotid chemoreceptors to hypoxic stimulation.

THE EFFECT OF PRO-INFLAMMATORY CYTOKINE IL-1β ON THE CENTRAL AND PERIPHERAL RESPIRATORY CONTROL MECHANISMS ON THE BACKGROUND OF SEVERE HYPOXIA