Peripheral neural modulation of endotoxin-induced hyperventilation

Gau Jun Tang, Yu Ru Kou, You Shuei Lin

研究成果: 雜誌貢獻文章

22 引文 (Scopus)

摘要

Objective: To delineate the role of the peripheral neural reflexes involved in modulating hyperventilation during endotoxemia. Design: A prospective, randomized, controlled, multigroup study. Setting: Research animal laboratory. Subjects: Adult Sprague-Dawley rats (n = 43; 354 ±24 g) of either gender. Interventions: 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. Measurements and Main 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 ≤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.

原文英語
頁(從 - 到)1558-1563
頁數6
期刊Critical Care Medicine
26
發行號9
DOIs
出版狀態已發佈 - 1998
對外發佈Yes

指紋

Hyperventilation
Endotoxins
Respiratory Rate
Unmyelinated Nerve Fibers
Endotoxemia
Vagotomy
Capsaicin
Tidal Volume
Denervation
Respiration
Tachypnea
Carotid Sinus
Vagus Nerve
Laboratory Animals
Sprague Dawley Rats
Reflex
Lipopolysaccharides
Veins
Observation
Lung

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

引用此文

Peripheral neural modulation of endotoxin-induced hyperventilation. / Tang, Gau Jun; Kou, Yu Ru; Lin, You Shuei.

於: Critical Care Medicine, 卷 26, 編號 9, 1998, p. 1558-1563.

研究成果: 雜誌貢獻文章

Tang, Gau Jun ; Kou, Yu Ru ; Lin, You Shuei. / Peripheral neural modulation of endotoxin-induced hyperventilation. 於: Critical Care Medicine. 1998 ; 卷 26, 編號 9. 頁 1558-1563.
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abstract = "Objective: To delineate the role of the peripheral neural reflexes involved in modulating hyperventilation during endotoxemia. Design: A prospective, randomized, controlled, multigroup study. Setting: Research animal laboratory. Subjects: Adult Sprague-Dawley rats (n = 43; 354 ±24 g) of either gender. Interventions: 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. Measurements and Main 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 ≤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.",
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