Hydrogen peroxide contracts human airways in vitro: role of the
epithelium.
Rabe, K. F., G. Dent, H. Magnussen.
Krankenhaus Grosshansdorf, Zentrum f[umlaut]ur Pneumologie und
Thoraxchirurgie, Landesversicherungsanstalt Freie und Hansestadt
Hamburg, D-22927 Grosshansdorf, Federal Republic of Germany
APStracts 2:0067L, 1995.
The effects of hydrogen peroxide (H2O2) on human airway smooth muscle
tone were determined in vitro. Treatment with H2O2 led to transient
concentration-related contractions in the organ bath, amounting to
118 +/- 14 mg (mean +/- s.e.m.; n = 12) at 1 mM H2O2, and to greater
and more prolonged contractions under superfusion conditions,
amounting to 451 +/- 71 mg (n = 17) at 1 mM H2O2. Epithelial removal
augmented the response to H2O2 in both systems. Addition of catalase
(500 U/ml) abolished the effects of H2O2. Pre-treatment of superfused
tissues with indomethacin (3 [mu]M) shifted the concentration-effect
curve to hydrogen peroxide rightwards and almost abolished the
response to 1 mM H2O2 in epithelium intact preparations (n = 16; p
< 0.05); the response in epithelium-denuded tissues was also
significantly inhibited (n = 16; p < 0.05). Pre-treatment of the
tissues with the TP prostanoid receptor antagonist GR 32191B (1
[mu]M) also inhibited the contractile effect of H2O2 in epithelium
intact and denuded tissues. In separate experiments H2O2 resulted in
concentration-related generation of prostaglandin (PG) D2 from
isolated airway preparations. The amount of PGD2 released was not
different in tissues with intact epithelium compared to those without
(n = 9; n.s.) We conclude that H2O2 exerts a contractile effect on
isolated human airways, which is augmented by epithelium removal and
is largely mediated by prostanoids. The source of PGD2 does not
appear to be the epithelium, which we suggest serves mainly as a
barrier against H2O2-mediated bronchoconstriction.
Received 16 September 1994; accepted in final form 17 April 1995.
APS Manuscript Number L275-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.