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Articles in PresS, published online ahead of print April 19, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00387.2001
Submitted on October 2, 2001
Accepted on April 11, 2002
1 Laboratoire de Physiologie Cellulaire Respiratoire, Universite Bordeaux 2 & Inserm, Bordeaux, Gironde, France
* To whom correspondence should be addressed. E-mail: etienne.roux{at}u-bordeaux2.fr.
This study investigated the interaction between exposure to air pollutants and chronic hypoxia (CH). CH rats were obtained using a hypobaric chamber (14 days at barometric pressure 380 mmHg). Exposure to various doses of acrolein or ozone did not modify the mechanical response to cholinergic agonists. Exposure to 3µM.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 [Ca2+]i rise in response to 0.1 µM ACh, and the calcium oscillation frequency in response to 10µM ACh. CH alone did not alter smooth muscle cross-sectional area (SMA) or epithelium+submucosa thickness. CH decreased maximal contractile response (Fmax, 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, though 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.
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