Journal of Applied Physiology, Vol 71, Issue 1 50-59, Copyright © 1991 by American Physiological Society
Tracheal vascular and smooth muscle responses to air temperature and humidity in dogs
R. O. Salonen, S. E. Webber, M. E. Deffebach and J. G. Widdicombe
Department of Physiology, St. George's Hospital Medical School, London, United Kingdom.
Twenty-five dogs were anesthetized, paralyzed, and artificially ventilated.
Their cranial tracheal arteries were perfused bilaterally with blood at
constant flow, and the perfusion pressures (Patr) were measured. Tracheal
smooth muscle function was assessed by recording changes in external
diameter (delta Dtr). The perfused segment of the trachea was exposed to
air at a constant unidirectional airflow of 25 l/min. Group 1 (n = 6) was
exposed to cold dry air, ambient room air, and hot dry and hot humid air,
each for 10 min with exposures starting from zero flow. The tracheal
vascular responses to all four conditions were small vasodilations (delta
Patr from -2 to -6%) followed by recovery or small vasoconstrictions. In
group 2 (n = 19), exposures to cold dry and hot humid air were preceded and
followed by body-temperature fully humidified air. Cold dry air caused a
sustained vasodilation (delta Patr -9.0 +/- 1.1%), and hot humid air
usually caused a biphasic response: a vasoconstriction (delta Patr 4.4 +/-
1.0%) followed by a vasodilation (delta Patr -5.7 +/- 1.9%). The warm humid
air after cold dry air or hot humid air caused a further vasodilation,
which lasted a short time after cold dry air (delta Patr -3.7 +/- 0.4%) but
greater than 10 min after hot humid air (delta Patr -13.8 +/- 1.4%). In
both groups, all exposures that cooled the trachea (cold dry air, ambient
room air, and hot dry air) caused smooth muscle contraction, and hot humid
air that warmed the trachea caused relaxation.
