Date of Award

1-1-1979

Embargo Period

11-20-2024

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Physiology

College

College of Graduate Studies

First Advisor

Allan D. Horres

Second Advisor

Regina Frayser

Abstract

This study was undertaken to investigate the contribution of carbon dioxide to respiratory control made by the carotid bodies and vagus nerves. Small eupneically breathing dogs, anesthetized with IV ketamine HCL were subjected to inspired CO2 concentrations of 3% while recording simultaneously tidal volume, inspiratory and expiratory airflow rates, and single neuron activity in or near the ventral respiratory group. The burst activity of the ventral respiratory group neuron was considered to be representative of the final integrated motor output of the brain stem respiratory complex. This data provided information concerning: (1) the relationship between the central respiratory neuron in the ventral respiratory group and airflow, (2) the latency response to CO2, (3) the contribution of the carotid body to the hypercapnic response, (4) the vagal contribution to the hypercapnic response. Several specified measures of neuron activity were altered as airflow patterns changed. Subsequent analyses showed correlation between airflow parameters and neuron discharge patterns. Burst duration and inspiratory time were closely associated (r>0.90), burst duration decreasing in preparation to inspiratory time as respiratory rate increased. Peak inspiratory airflow showed good correlation (r>0.90) with the rate of rise to peak discharge frequency of the neuron. Mean discharge frequency increased during hypercapnia and correlated well (r>0.90) with mean airflow rate. Finally, integrated neuron burst activity was correlated with tidal volume (r>0.90). These data suggests: (a) the neural activity of the ventral respiratory group may represent the final integrated efferent activity of the brain stem respiratory complex's response to low levels of CO2 stimulus, and (b) the activity of individual ventral respiratory group neuron's may be used as a reliable index of this output. CO2 onset latency was significantly altered by either carotid body denervation or vagotomy. Neuron-airflow correlations were not affected. Carotid nerve section increased CO2 onset latency from a mean value of 11.1 ± 0.2 (SD) seconds to 22.6 + 3.1 (SD) seconds. Vagotomy decreased CO2 onset latency from 11.1 ± 0.2 (SD) seconds to 1.6 (SD) seconds. The CO2 latency results indicate that although carotid body denervation delays the onset of the CO2 response somewhat, tidal volume increases significantly within 30 seconds despite peripheral chemoreceptor denervation. The results obtained after vagotomy indicate that vagal afferent information has an inhibitory effect on the respiratory system's ability to respond to CO2. An isocapnic hyperpnea was obtained while breathing 3% co2. Carotid denervation did not abolish this result although the rate at which steady-state was obtained was slowed. The isocapnic hyperpnea results indicate that early in the response the carotid body contributions are highly significant but decreases in importance as ventilation is increased to the new steady-state. Total loss of vagal input altered the neuron burst pattern by decreasing the rate at which peak neuron discharge was attained, greatly increasing burst duration. Loss of phasic input only through tracheal occlusion also increased burst duration over control values, but not to the extent noted subsequent to vagotomy. Additionally, the neuron burst pattern was not affected by tracheal occlusion other than prolonging the offset phase. Vagal mechanisms influence both chemosensitivity as well as respiratory timing in a more complex manner than presently understood.

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