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Department of Biomedical Sciences, Creighton University School of Medicine, Omaha, Nebraska 68178; and Laboratory for Exercise and Environmental Medicine, Health, Leisure, and Human Performance Research Institute, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2
Received 8 October 1996; accepted in final form 17 December 1996.
Pisarri, Thomas E., and Gordon G. Giesbrecht. Reflex
tracheal smooth muscle contraction and bronchial vasodilation evoked by
airway cooling in dogs. J. Appl.
Physiol. 82(5): 1566-1572, 1997.
Cooling
intrathoracic airways by filling the pulmonary circulation with cold
blood alters pulmonary mechanoreceptor discharge. To determine whether
this initiates reflex changes that could contribute to airway
obstruction, we measured changes in tracheal smooth muscle tension and
bronchial arterial flow evoked by cooling. In nine
chloralose-anesthetized open-chest dogs, the right pulmonary artery was
cannulated and perfused; the left lung, ventilated separately, provided
gas exchange. With the right lung phasically ventilated, filling the
right pulmonary circulation with 5°C blood increased smooth muscle
tension in an innervated upper tracheal segment by 23 ± 6 (SE) g
from a baseline of 75 g. Contraction began within 10 s of injection and
was maximal at ~30s. The response was abolished by cervical vagotomy.
Bronchial arterial flow increased from 8 ± 1 to 13 ± 2 ml/min, with
little effect on arterial blood pressure. The time course was
similar to that of the tracheal response. This response was greatly
attenuated after cervical vagotomy. Blood at 20°C also increased
tracheal smooth muscle tension and bronchial flow, whereas 37°C
blood had little effect. The results suggest that alteration of
airway mechanoreceptor discharge by cooling can initiate reflexes that
contribute to airway obstruction.
cold air; exercise-induced asthma; bronchial artery; pulmonary mechanoreceptors; bronchoconstriction; lung innervation; vagus nerve; airway resistance
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