CHANGE OF VENTILATORY RESPONSE TO HYPERCAPNIA IN LIPOPOLYSACCHARIDE INFLAMMATION MODEL
It is known that systemic inflammation influences respiratory function. Most lung disorders are associated with systemic inflammation, including chronic lung diseases, obstructive sleep apnea and others. At the same time very little is known about correlation between systemic inflammatory and ventilatory control. Hypercapnic and hypoxic chemoreception is a key element of a ventilatory control system. Objective. The purpose of this study was to investigate the effects of lipopolysaccharide inflammation model on the ventilatory response to hypercapnia. Materials and Methods. The experiment was conducted on 16 anesthetized tracheotomized spontaneously breathing hypercapnic hyperoxic gas mixture Wistar male rats. Lipopolysaccharide from Salmonella typhi was administrated in their femoral vein in the amount of 200 mg dissolved in 2 ml of saline. The hyper-capnic ventilatory response was measured using rebreathing techniques. The end-tidal partial pressure of carbon dioxide (PETCO2) was analyzed with quadruple mass spectrometer. All animal procedures were conducted in accordance with the ethical guidelines of the European Community Council Directives 86/609/EEC. Results. Under hypercapnic breathing stimulation a significant correlation between minute ventilation, tidal volume, mean inspiratory flow and increase in PETCO<sub>2</sub> was observed both before and after intravenous injections of lipopolysaccharide. However, the administration of lipopolysaccharide evoked changes in value of the hypercapnic responses. The level of the ventilatory response to carbon dioxide stimulation significantly decreased after lipopolysaccharide injection. Conclusions. The data obtained demonstrated that systemic inflammation had an inhibitory effect on the central chemoreceptor breath control.