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Alterations of airway smooth muscle cell membrane by sensitization
Author(s) -
Souhrada M.,
Souhrada J. F.
Publication year - 1985
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950010408
Subject(s) - ovalbumin , sensitization , medicine , leukotriene d4 , guinea pig , in vitro , pharmacology , diphenhydramine , methysergide , immunology , endocrinology , antagonist , receptor , chemistry , antigen , biochemistry , histamine
The sensitization of guinea pigs with ovalbumin and Bacillus pertussis vaccine caused an increase ( P < 0.001) in the resting membrane potential (Em) of airway smooth muscle (ASM) cells, from −61.3 ± 0.5 mV (± SE) to −72.7 ± 0.6 mV (± SE). One, two, and three weeks after resensitization of sensitized animals with ovalbumin, Em further increased ( P < 0.001) to −76.2 ± 0.2 mV (± SE), −77.4 ± 0.3 mV, and −78.1 ± 0.5 mV, respectively. Similarly, both in vivo and in vitro passive sensitization caused an increase ( P < 0.001) in Em of ASM cells to −69.5 ± 0.3 mV and −68.5 ± 0.4 mV, respectively. ASM preparations isolated from rabbits showed a similar increase ( P < 0.001) in Em after passive in vitro sensitization with serum from ovalbumin‐sensitized rabbits. An increase in the contribution of the electrogenic Na + ‐pump was found to be responsible for the observed changes in Em following both active and passive sensitization. The presence of diphenhydramine (anti‐H 1 ), methysergide, indomethacin, 5,8,11,14‐eicosatetraenoic acid (ETYA), FPL 55712 (a leukotriene receptor blocker), phenoxybenzamine, and disodium cromoglycate (a stabilizing agent) during passive in vitro sensitization failed to prevent an increase in the Em of ASM cells. However, incubation of normal guinea pig and rabbit ASM preparations with heated serum (60°C for 2 hours) from ovalbumin‐sensitized guinea pigs or rabbits partially inhibited (in guinea pigs) or completely abolished (in rabbits) such an increase. From these data, it is concluded that the hyperpolarization of ASM cells, as observed after sensitization, seems to result from direct interaction of serum heatsensitive factors (presumably specific antibodies) and ASM cell membrane rather than from the interaction of ASM cells with specific mediator(s) of anaphylaxis. The results suggest that sensitization directly alters the ASM cell membrane.