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Neuroreport. 2014 Apr 16;25(6):358-66. doi: 10.1097/WNR.0000000000000090.

Effects of H2S on the central regulation of respiration in adult rats.

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1
Departments of aPhysiology bHistology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan cDepartment of Histology and Embryology, Medical School, Henan University, Kaifeng, Henan dDepartment of Physiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia, People's Republic of China.

Abstract

Hydrogen sulfide (H2S) is a gasotransmitter synthesized from cysteine (Cys) by pyridoxal-5'-phosphate-dependent enzymes. We investigated the potential roles of H2S in the regulation of central rhythmic respiration in adult rats in vivo. Sodium hydrosulfide (NaHS: 2.5 mM, 10 mM, and 5 mM) as a source of exogenous H2S, Cys (2.5 mM, 10 mM and 5 mM) as a source of endogenous H2S, 2.5 mM Cys+10 mM hydroxylamine (NH2OH), and 10 mM NH2OH, respectively, were intracerebroventricularly injected into rats. The rhythmic discharge of the diaphragm, including burst duration (BD), burst interval (BI), burst frequency (BF), and integrated amplitude (IA), and arterial blood pressure (BP) were measured at different time points. The results were analyzed by analysis of variance. A total of 2.5 mM NaHS did not significantly affect changes in BD, BI, BF, IA, or BP (P>0.05), whereas 2.5 mM Cys significantly altered BD, BI, and BF (P<0.05); however, there was no change in IA and BP (P>0.05). A concentration of 5 mM Cys had effects similar to those of 5 mM NaHS; both induced biphasic respiratory responses and changed the BF (P<0.05). A concentration of 10 mM NH2OH irreversibly inhibited rhythmic discharge of the diaphragm except for IA. No change was seen in BI, BF, IA, or BP (P>0.05) except for BD was temporarily decreased (P<0.05) in the 2.5 mM Cys+10 mM NH2OH group. These results suggest that exogenous and endogenous H2S may participate in the regulation of respiratory activity in adult rats.

PMID:
24323123
DOI:
10.1097/WNR.0000000000000090
[Indexed for MEDLINE]
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