Project: Research project

Project Details


Although human airways are known to dilate during exercise, the
neural mechanisms causing this increase in airway caliber have
not yet been defined. The first goal of the proposed experiments,
therefore, is to characterize the bronchodilator responses arising
from the two neural mechanisms likely to function during
exercise. The two mechanisms are: a reflex arising from
contracting limb muscle, and central command arising from the
subthalamic locomotor region. The second goal of the proposed
experiments is to develop an understanding about the central
neural pathways and integrating mechanisms mediating exercise-
induced bronchodilation. The integrating mechanism is proposed
to occur in the caudal ventrolateral medulla. The final common
pathway to the airways is proposed to be the vagus nerve, whose
inhibition by the two mechanisms is likely to cause the
bronchodilation occurring during exercise. The proposed
experiments will be performed in unanesthetized decerebrate
dogs. Measurements of tracheal tension and total lung resistance
will be used to characterize the increases in airway caliber in
response to activation of central command and the reflex arising
from dynamically contracting skeletal muscle. Central command
will be activated by both electrical and chemical (i.e., d1-
homocysteic acid and picrotoxin) stimulation of the subthalamic
locomotor region. The reflex will be activated using "Kao type"
stimulation of the L7-S, ventral roots. The bronchodilator
responses to the two maneuvers will be measured before and after
electrical and chemical destruction of the caudal ventrolateral
medulla. The effects of the reflex and central command on the
discharge of cells with vagal preganglionic fibers projecting to the
lungs will be determined. The proposed experiments will be one
of the first to examine how the brain regulates airway caliber.
Effective start/end date1/1/901/1/90


  • National Heart, Lung, and Blood Institute

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