The effect of chronic intermittent hypoxia on atherosclerosis in rat offspring.

BACKGROUND

To determine whether rat offspring born under conditions of chronic intermittent hypoxia (CIH) would develop systemic inflammation and be susceptible to CIH-mediated injury on artery.

METHODS

CIH rat model was established. The expression levels of p38MAPK, NF-κB p65, CRP, TNFα, and IL-8 were measured. The arterial pathology of offspring whose mothers were exposed to CIH during pregnancy was evaluated.

RESULTS

The levels of p-P38MAPK and NF-κB p65 were significantly up-regulated following induction of intra-uterine CIH Induction of intra- and extra-uterine CIH had an interaction regarding the expression profiles of these markers (P < 0.01, P < 0.01, P < 0.01, P < 0.01, P = 0.020, respectively). Pathologic analysis of the arteries confirmed that intra-uterine CIH increased the tunica intima thickness (P < 0.01), but had no effect on the tunica media (P = 0.974). Furthermore, induction of intra- and extra-uterine CIH had a synergistic interaction on tunica intima thickness (P = 0.004).

CONCLUSIONS

Intra-uterine CIH caused tunica intima thickening and development of pre-atherosclerotic lesions in offspring via NF-κB p65 and p-p38 MAPK. Furthermore, the expression of NF-κB p65 and p-p38 MAPK and the extent of pre-atherosclerotic lesions were either exacerbated or alleviated in offspring when re-exposed to CIH later.