The Effect of Acute Intermittent Hypercapnic Hypoxia Treatment on IL-6, TNF-α, and CRP Levels in Piglets

It is suggested that acute hypoxia causes a transient increase in IL-6 levels and has implications for the pathogenesis of increased cardiovascular disease in OSA, especially in childhood.

Abstract

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper-airway obstruction during sleep leading to significant hypercapnic hypoxic conditions. These conditions are associated with increased levels of proinflammatory cytokines (including interleukin [IL]-6, tumor necrosis factor [TNF]-alpha, and C-reactive protein [CRP]) and subsequent increased cardiovascular risk. It is unclear whether hypercapnic hypoxia itself causes inflammatory perturbations. DESIGN: We evaluated circulating IL-6, TNF- a and CRP in a piglet model of infant OSA, following exposure to acute intermittent hypercapnic hypoxia (IHH). Study groups comprised of treatment (n = 8) and control (n = 8) groups. Treatment was two 90-minute sessions of IHH with arterial blood sampled before and after each IHH session. MEASUREMENTS AND RESULTS: IL-6, TNF-alpha and CRP levels were measured before and after IHH treatment sessions. Results showed an increase in IL-6 following the first session of IHH that was neither sustained, nor repeated, during a subsequent exposure. Using mixed-modelling, TNF-alpha changed between time points and groups. There were no changes in CRP over the duration of the study. CONCLUSION: These results suggest that acute hypoxia causes a transient increase in IL-6 levels and has implications for the pathogenesis of increased cardiovascular disease in OSA, especially in childhood.