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Am J Physiol Lung Cell Mol Physiol 262: L344-L350, 1992;
1040-0605/92 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 262, Issue 3 344-L350, Copyright © 1992 by American Physiological Society

ARTICLES

Isotonic relaxation of sensitized bronchial smooth muscle

H. Jiang and N. L. Stephens
Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

Although the mechanisms underlying asthma are not clear, we have demonstrated that in dogs antigen sensitization results in alterations of contractile properties, such as greater early maximum shortening velocity and capacity of bronchial smooth muscle. These changes could account for the hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining high airway resistance. This, a relatively less-studied area, requires study. In the current study, we therefore developed an index of isotonic relaxation, T1/2,CE (half-time for relaxation which is independent of muscle load and initial contractile element length) for evaluation of the relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle (SBSM) than that in controls studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by T1/2,CE showed no difference between sensitized and control muscles after 10 s of stimulation (8.38 +/- 0.92 s vs. 7.78 +/- 0.93, means +/- SE); however, it was prolonged significantly in SBSM stimulated only for 1 s (12.74 +/- 2.5 s, mean +/- SE) compared with the control (6.98 +/- 1.01). Unexpectedly, we found that during the late phase of isotonic relaxation, both groups showed spontaneous increase in zero load shortening velocity, which is an index of cross-bridge cycling rate.2


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