The general, long-tern objective of this proposal is to improve our understanding of the role of the expiratory muscles in the control of ventilation. The importance of the expiratory muscles on regulating expiratory airflow and the end expiratory lung volume is well known, but our understanding of their neural control is limited. We have learned from prior studies that lung inflation activities the abdominal and internal intercostal expiratory muscles through the influence of vagal afferent, but the role played by chemoreceptor in the control of these muscles is uncertain. Recent studies in a variety of species have shown that steady state hypoxia causes a diminution of abdominal and internal intercostal motor activity, particularly after vagotomy. In the present proposal, the vagotomized cat preparation will be utilized to explore the mechanisms underlying this effect. The studies are designed to answer three major questions: 1) Is the reduction in expiratory motor activity during hypoxia mediated by inhibitory inputs from the carotid body? This question will be evaluated by comparing changes in the efferent expiratory activity of abdominal and internal intercostal muscles and motor nerves induced by sustained electrical stimulation of a carotid sinus nerve, with that induced by steady state isocapnic hypoxia; 2) Does the inhibitory influence exert its effect ont he expiratory pre-motor neurons in the brain stem, or at the spinal core level? This question will be addressed by analyzing simultaneously the activity of abdominal muscle pre-motor neurons, and the efferent activity of motor nerves to the abdominal and internal intercostal muscles during steady state isocapnic hypoxia; 3) Are changes in the compound activity recorded in whole abdominal and internal intercostal nerves during hypoxia due to changes in motoneuron firing rate, recruitment pattern, or to a combination of both mechanisms? This question will be evaluated by analyzing changes in the activity of individual abdominal and internal intercostal muscle motoneurons during isocapnic hypoxia. The remaining experiment will examine how changes in the duration central expiratory period and its subdivisions influence the intensity of discharge in the motor nerves to the abdominal and internal intercostal muscles. Knowledge gained from the above studies will lead to a comprehensive understanding of the physiology of the expiratory muscles. The control of expiratory muscles by central nervous system is of obvious importance in obstructive lung disease, exercise, and other conditions where the pathway for expiratory airflow is impeded.
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