Effect of intracerebroventricular injection of interleukin-1-beta on the ventilatory response to hyperoxic hypercapnia.

Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.
European journal of medical research (Impact Factor: 1.4). 11/2010; 15 Suppl 2:3-6.
Source: PubMed

ABSTRACT Oxidative stress developed at several disease states and strenuous resistive breathing lead to the elevation of plasma and cerebral levels of proinflammatory cytokines. We hypothesized that the elevation of the cytokine level in body fluids would modulate breathing pattern and the ventilatory response to stimulation of central chemoreceptors by hypercapnia. -
In experiments on anesthetized, tracheostomized, spontaneously breathing rats, the effects of intracerebroventricular injection of the human recombinant interleukin-1β (IL-1β) (0.5 μg/rat) on breathing were studied. -
During resting breathing IL-1β evoked a significant increase in minute ventilation and in mean inspiratory flow. Furthermore, injection of IL-1β into the cerebral-spinal fluid decreases the responses of ventilation, tidal volume, and of mean inspiratory flow to carbon dioxide. -
The elevation of a proinflammatory cytokine in cerebrospinal fluid intensifies ventilation by modulation of breathing pattern, but weakens the chemoreflex sensitivity to hypercapnia. The results suggest the participation of cytokines in the central control of breathing and in the mechanisms of central chemoreception.

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    ABSTRACT: This review summarizes and analyzes the results of the present experimental studies indicating immune system involvement in control of breathing. The hypothesis about the role of cytokines in the mechanisms of respiratory muscle fatigue and reduced ventilatory sensitivity to hypercapnia during respiration with the added resistive loading is justified. The possible ways of implementing of respiratory cytokine effects are discussed.
    Fiziologiia cheloveka 03/2012; 38(2):119-29. DOI:10.1134/S0362119712020028

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