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1 Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan 100, Republic of China; and 2 Division of Pharmacology and Experimental Therapeutics, College of Pharmacy, University of Kentucky, Lexington, Kentucky 40536
Received 5 September 1995; accepted in final form 3 September 1996.
Lai, Y. L., and K.-R. Zhou. Eglin-c prevents
monocrotaline-induced ventilatory dysfunction. J. Appl. Physiol. 82(1): 324-328, 1997.
The present
study was carried out to investigate the relationship between elastase
and monocrotaline (MCT)-induced ventilatory dysfunction in rats. To
accomplish this, we used an elastase inhibitor eglin-c to suppress the
activity of endogenous elastase. Thirty-five young Sprague-Dawley rats
were randomly divided into six groups: control, MCT, eglin-c (1),
eglin-c (2), eglin-c (1)+MCT, and eglin-c (2)+MCT.
Rats in the control group received no treatment. Each MCT rat received
a single subcutaneous injection of MCT (60 mg/kg) 1 wk before the
functional test. Each eglin-c (1) rat was intratracheally
instilled with eglin-c (9 mg/rat) twice in 1 wk. Each eglin-c (2)
rat was intratracheally instilled with eglin-c (9 mg/rat) five times in
1 wk. Both eglin-c+MCT groups were treated with the combination of
eglin-c (1) or eglin-c (2) and MCT. In the MCT group, there
were significant decreases in dynamic respiratory compliance, maximal
expiratory flow rate at 50% total lung capacity, and the slopes of the
maximal expiratory flow-%total lung capacity curve and the maximal
expiratory flow-static recoil pressure curve. However, in the
eglin-c (1)+MCT and eglin-c (2)+MCT groups, all of the
above-mentioned MCT-induced changes were prevented. All ventilatory
values of the eglin-c (1) and eglin-c (2) groups were not
significantly different from those of the control group. These results
demonstrate that eglin-c treatment prevents MCT-induced ventilatory
dysfunction and suggest that endogenous elastase may play an important
role in MCT-induced inflammation-mediated ventilatory abnormality.
elastase inhibitor; tissue injury; inflammation; airway constriction; airway remodeling
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