Peripheral neural modulation of endotoxin-induced hyperventilation.
OBJECTIVE
To delineate the role of the peripheral neural reflexes involved in modulating hyperventilation during endotoxemia.


METHODS
A prospective, randomized, controlled, multigroup study.


METHODS
Research animal laboratory.


METHODS
Adult Sprague-Dawley rats (n=43; 354+/-24 g) of either gender.


METHODS
Eight rats received a sham operation on their vagus, carotid sinus, and aortic nerves before the administration of a saline vehicle to serve as the time control. In the endotoxin group, 11 rats received a sham operation before endotoxin challenge. The remaining 24 rats received bilateral vagotomy (n=8), perivagal capsaicin treatment (n=8), or denervation of peripheral chemoreceptors (n=8) before endotoxin challenge. After the breathing pattern returned to a steady state, endotoxin (L-4130, serotype 0111, B4 lipopolysaccharide; 50 mg/kg) was injected into the vein. The rat's respiration was then monitored continuously for 5 hrs or until the animal died.


RESULTS
The respiratory rate and tidal volume did not change over the 5-hr observation period in the time control group. In the endotoxin group, the respiratory rate increased significantly from baseline (135.4%) 2 hrs after endotoxin challenge and increased persistently until the rats died. The tidal volume increased gradually to < or =132.8% of baseline 4 hrs after endotoxin challenge. Bilateral cervical vagotomy and perineural capsaicin treatment of the vagus nerves eliminated the tachypnea response to endotoxin injection. Denervation of the peripheral chemoreceptor accentuated the hyperventilation response to endotoxin, and resulted in the shortest survival time.


CONCLUSIONS
Both lung vagal C-fiber afferents and peripheral chemoreceptors are involved in modulating the hyperventilation response after endotoxin challenge in rat models. Stimulation of vagal C-fiber afferents increased the respiratory rate. Conversely, the role of peripheral chemoreceptors was to restrain the hyperventilatory response and these receptors may play a protective role during endotoxemia.
Tang
G J
GJ
Department of Anesthesiology and Surgical Critical Care, School of Medicine and Life Science, National Yang-Ming University, Taipei, Taiwan, Republic of China.
Kou
Y R
YR
Lin
Y S
YS
D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D019446:Endotoxemia / Q000139:chemically induced / Q000150:complications* / Q000503:physiopathology; D005260:Female; D006339:Heart Rate; D006985:Hyperventilation / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D010100:Oxygen / Q000097:blood; D017933:Peripheral Nervous System / Q000503:physiopathology* / Q000601:surgery; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley; D012119:Respiration; D013997:Time Factors
D002245:Carbon Dioxide; D010100:Oxygen