Journal of Applied Physiology, Vol 54, Issue 3 720-729, Copyright © 1983 by American Physiological Society
Biochemical and physiological effects of compound 48/80 on canine trachea in vivo
A. R. Leff, J. K. Brown, M. Frey, B. Reed and W. M. Gold
We studied changes in tracheal histamine content and tracheal muscle
tension after degranulation of tracheal mast cells by compound 48/80 in 32
anesthetized dogs. In four dogs compound 48/80 caused an increase in
tracheal tension [13 +/- 5 (SD) g/cm], while femoral arterial blood
pressure decreased only 14 +/- 11%. Tracheal tissue histamine decreased 17
+/- 6% in five dogs receiving intra-arterial compound 48/80 (5 X 10(-3) to
10(-1) mg/kg). Chlorpheniramine, an H1-antagonist, selectively inhibited
tracheal contraction to compound 48/80 and histamine. Cimetidine, an
H2-antagonist, did not alter the response to intra-arterial histamine. In
11 dogs, the doses of both intra-arterial histamine and acetylcholine
required to produce a threshold increase in tracheal tension of 8 g/cm were
compared. Threshold doses for acetylcholine varied 10-fold, compared with
100-fold variation for histamine among these dogs. There was a significant
correlation between increased tracheal tension produced by compound 48/80
and histamine (r = 0.62). We conclude that compound 48/80 causes a variable
increase in tracheal tension in vivo because of marked variability in the
H1-receptor response of tracheal smooth muscle to histamine and because of
variability in the release of mediator from respiratory mast cells by
compound 48/80.
