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Am J Physiol Lung Cell Mol Physiol 283: L628-L635, 2002. First published April 19, 2002; doi:10.1152/ajplung.00387.2001
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Vol. 283, Issue 3, L628-L635, September 2002

Combined effect of chronic hypoxia and in vitro exposure to gas pollutants on airway reactivity

Etienne Roux1, Michel Duvert2, and Roger Marthan1

1 Laboratoire de Physiologie Cellulaire Respiratoire, Institut National de la Santé et de la Recherche Médicale Equipe Mixte 9937; 2 Laboratoire de Cytologie, Institut National de la Santé et de la Recherche Médicale Equipe Mixte 9929 and Institut Fédératif de Recherche n°4, Université Victor Segalen Bordeaux 2, 33076 Bordeaux cedex, France

This study investigated the interaction between exposure to air pollutants and chronic hypoxia (CH). We used a hypobaric chamber (14 days at barometric pressure 380 mmHg) to produce CH in rats. Exposure to various doses of acrolein or ozone did not modify the mechanical response to cholinergic agonists. Exposure to 3 µM/min acrolein did not alter epithelium-free trachea responsiveness. In contrast, direct exposure of freshly isolated myocytes to 2 and 3 µM/min acrolein enhanced the amplitude of the first intracellular [Ca2+] rise in response to 0.1 µM ACh and the calcium oscillation frequency in response to 10 µM ACh. CH alone did not alter smooth muscle cross-sectional area (SMA) or epithelium-plus-submucosa thickness. CH decreased maximal contractile response (maximal force normalized to SMA) but increased sensitivity (pEC50) to cholinergic agonists. We conclude that unlike in normoxic rats, exposure to air pollutants does not induce airway hyperresponsiveness in CH rats, although it increased calcium signaling. These results cannot be explained by change in smooth muscle accessibility, but may be linked to the effect of CH on calcium-contraction coupling.

ozone; acrolein; smooth muscle; rat trachea; excitation-contraction coupling


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