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Inhalation of isoflurane alters the pulmonary C‐fiber‐mediated respiratory responses in anesthetized rats
Author(s) -
Zhang Zhenxiong,
Zhuang Jianguo,
Zhang Cancan,
Xu Fadi
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1111.19
Subject(s) - isoflurane , tachypnea , anesthesia , respiratory system , respiratory rate , anesthetic , ventilation (architecture) , inhalation , chemistry , tidal volume , apnea , medicine , heart rate , mechanical engineering , blood pressure , engineering , tachycardia
This study is aimed to explore the effect of inhaling isoflurane, a commonly used volatile anesthetic, on pulmonary C‐fiber (PCF)‐mediated respiratory responses. We recorded ventilatory ( Study Series I ) and nodose ganglion neuronal responses ( Study Series II ) to right atrial bolus injection of phenylbiguanide (PBG, 20μg/kg), a selective PCF's stimulant, before and during 5% isoflurane exposure for 8 s in anesthetized spontaneously breathing and paralyzed rats, respectively. Isoflurane initially caused a remarkable increase in respiratory frequency (f) during the first 3–5 s exposure, and this response gradually disappeared during the following exposure without significant change in tidal volume. PBG evoked an apnea which was markedly reduced by isoflurane. Correspondingly, isoflurane also increased baseline firing rate of all C‐type neurons (n = 17) extracellularly recorded in the nodose ganglia by 136% and attenuated the PBG‐induced C‐type neuronal excitation by 52%. In sharp contrast, the firing rate of pump‐neurons (n = 5) and rapid adapting type neurons (n = 2) was not be affected by PBG injection, but decreased by isoflurane. Our result suggests that isoflurane can stimulate PCFs to produce tachypnea and depress PBG‐induced PCF's activity probably through different mechanisms.