TRACHEAL VASCULAR AND SMOOTH-MUSCLE RESPONSES TO AIR-TEMPERATURE AND HUMIDITY IN DOGS

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 (Pa(tr)) were measured. Tracheal smooth muscle function was assessed by recording changes in external diameter (DELTA-D(tr)). 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-Pa(tr) 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-Pa(tr) -9.0 +/- 1.1%), and hot humid air usually caused a biphasic response: a vasoconstriction (DELTA-Pa(tr) 4.4 +/- 1.0%) followed by a vasodilation (DELTA-Pa(tr) -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-Pa(tr) -3.7 +/- 0.4%) but > 10 min after hot humid air (DELTA-Pa(tr) -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.