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Articles in PresS, published online ahead of print June 21, 2002
J Appl Physiol, 10.1152/jap.00150.2002
Submitted on February 26, 2002
Accepted on June 17, 2002
1 Department of Physiology, University of Western Australia, Perth, Western Australia, Australia; Telethon Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth, Western Australia, Australia
2 Department of Physiology, University of Western Australia, Perth, Western Australia, Australia
* To whom correspondence should be addressed. E-mail: debrat{at}ichr.uwa.edu.au.
Increased smooth muscle contractility or reduced smooth muscle mechanical loads could account for the excessive airway narrowing and hyperresponsiveness seen in asthma. These mechanisms were investigated using an allergen-induced porcine model of airway hyperresponsiveness. Airway narrowing to electric field stimulation was measured in isolated bronchial segments, over a range of transmural pressures (0-20 cmH20). Contractile responses to acetylcholine were measured in bronchial segments and in isolated tracheal smooth muscle strips isolated from control and test (ovalbumin sensitised and challenged) pigs. Test airways narrowed less than controls (p<0.0001). Test pigs showed reduced contractility to acetylcholine both in isolated bronchi (p<0.01) and smooth muscle strips (p<0.01). Thus, isolated airways from pigs exhibiting airway hyperresponsiveness in vivo are hyporesponsive in vitro. The decreased narrowing in bronchi from hyperresponsive pigs may be related to decreased smooth muscle contractility. These data suggest that mechanisms external to the airway wall may be important to the hyperresponsive nature of sensitised lungs.
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