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Respiratory responses to NaHS are mediated by central mechanisms
Author(s) -
Yu Jerry,
Li Huafeng,
He Yuwen,
Walker Jerome
Publication year - 2010
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.24.1_supplement.623.12
Subject(s) - tachypnea , hyperpnea , medicine , anesthesia , respiratory system , apnea , hypercapnia , sodium hydrosulfide , chemistry , tachycardia , hydrogen sulfide , sulfur , organic chemistry
Hydrogen sulfide, H2S, is a gasotransmitter that serves a variety of important physiological functions. On the other hand, it also produces fatal toxicity. Respiratory arrest is major cause of death; however, the underlying mechanism remains unclear. In the current study, we recorded phrenic nerve activity to monitor the central respiratory output in anesthetized, open chest, mechanically ventilated rabbits and examined the respiratory response to intravenous as well as lung parenchymal injection of sodium hydrogen sulfide, NaHS. Intravenous injection of NaHS caused immediate hyperpnea and tachypnea, which was followed by apnea. These respiratory responses were sustained after bilataral vagotomy, indicating they are the result of extra‐vagal mechanisms such as direct central effect through the circulation. This statement was further strengthened by the fact that intraparenchymal NaHS injection produces hyperpnea and tachynea but not apnea when the ipsilateral pulmonary artery was occluded. Apnea ensued after releasing the occlusion. We conclude that the respiratory responses to H2S exposure are mainly centrally mediated. Apnea as well as tachypnea and hyperpnea are caused by direct action of the CNS, although the vagal afferents may also contribute to the early hyperpnea and tachypnea responses. Supported by NIH (HL‐58727)