Tags

Type your tag names separated by a space and hit enter

Inhibitory effects of hyperoxia and methemoglobinemia on H(2)S induced ventilatory stimulation in the rat.
Respir Physiol Neurobiol 2012; 181(3):326-34RP

Abstract

The aim of this study was to clarify, using in vitro and in vivo approaches in the rat, the site of mediation of the inhibition of H(2)S induced arterial chemoreceptor stimulation, by hyperoxia and methemoglobinemia. We first determined the ventilatory dose-response curves during intravenous injections of H(2)S. A very high dose of NaHS, i.e. 0.4 μmol (concentration: 800 μM), was needed to stimulate breathing within 1s following i.v. injection. Above this level (and up to 2.4 μmol, with a concentration of 4800 μM), a dose-dependent effect of H(2)S injection was observed. NaHS injection into the thoracic aorta produced the same effect, suggesting that within one circulatory time, H(2)S pulmonary exchange does not dramatically reduce H(2)S concentrations in the arterial blood. The ventilatory response to H(2)S was abolished in the presence of MetHb (12.8%) and was significantly depressed in hyperoxia and, surprisingly, in 10% hypoxia. MetHb per se did not affect the ventilatory response to hypoxia or hyperoxia, but dramatically enhanced the oxidation of H(2)S in vitro, with very fast kinetics. These findings suggest that, the decrease/oxidation of exogenous H(2)S in the blood is the primary effect of MetHb in vivo. In contrast, the in vitro oxidative properties of blood for H(2)S were not affected by the level of [Formula: see text] between 23 and >760 mmHg. This suggests that the inhibition of the ventilatory response to H(2)S by hyperoxia during aortic or venous injection originates within the CB and not in the blood. The implications of these results on the role of endogenous H(2)S in the arterial chemoreflex are discussed.

Authors+Show Affiliations

Pennsylvania State University, College of Medicine, Division of Pulmonary and Critical Care Medicine, Penn State Hershey Medical Center, 500 University Dr., Hershey, PO Box 850, MC H047, PA 17033-0850, USA.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

22490362

Citation

Van de Louw, Andry, and Philippe Haouzi. "Inhibitory Effects of Hyperoxia and Methemoglobinemia On H(2)S Induced Ventilatory Stimulation in the Rat." Respiratory Physiology & Neurobiology, vol. 181, no. 3, 2012, pp. 326-34.
Van de Louw A, Haouzi P. Inhibitory effects of hyperoxia and methemoglobinemia on H(2)S induced ventilatory stimulation in the rat. Respir Physiol Neurobiol. 2012;181(3):326-34.
Van de Louw, A., & Haouzi, P. (2012). Inhibitory effects of hyperoxia and methemoglobinemia on H(2)S induced ventilatory stimulation in the rat. Respiratory Physiology & Neurobiology, 181(3), pp. 326-34. doi:10.1016/j.resp.2012.03.018.
Van de Louw A, Haouzi P. Inhibitory Effects of Hyperoxia and Methemoglobinemia On H(2)S Induced Ventilatory Stimulation in the Rat. Respir Physiol Neurobiol. 2012 May 31;181(3):326-34. PubMed PMID: 22490362.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibitory effects of hyperoxia and methemoglobinemia on H(2)S induced ventilatory stimulation in the rat. AU - Van de Louw,Andry, AU - Haouzi,Philippe, Y1 - 2012/04/02/ PY - 2011/12/08/received PY - 2012/03/26/revised PY - 2012/03/27/accepted PY - 2012/4/12/entrez PY - 2012/4/12/pubmed PY - 2012/12/10/medline SP - 326 EP - 34 JF - Respiratory physiology & neurobiology JO - Respir Physiol Neurobiol VL - 181 IS - 3 N2 - The aim of this study was to clarify, using in vitro and in vivo approaches in the rat, the site of mediation of the inhibition of H(2)S induced arterial chemoreceptor stimulation, by hyperoxia and methemoglobinemia. We first determined the ventilatory dose-response curves during intravenous injections of H(2)S. A very high dose of NaHS, i.e. 0.4 μmol (concentration: 800 μM), was needed to stimulate breathing within 1s following i.v. injection. Above this level (and up to 2.4 μmol, with a concentration of 4800 μM), a dose-dependent effect of H(2)S injection was observed. NaHS injection into the thoracic aorta produced the same effect, suggesting that within one circulatory time, H(2)S pulmonary exchange does not dramatically reduce H(2)S concentrations in the arterial blood. The ventilatory response to H(2)S was abolished in the presence of MetHb (12.8%) and was significantly depressed in hyperoxia and, surprisingly, in 10% hypoxia. MetHb per se did not affect the ventilatory response to hypoxia or hyperoxia, but dramatically enhanced the oxidation of H(2)S in vitro, with very fast kinetics. These findings suggest that, the decrease/oxidation of exogenous H(2)S in the blood is the primary effect of MetHb in vivo. In contrast, the in vitro oxidative properties of blood for H(2)S were not affected by the level of [Formula: see text] between 23 and >760 mmHg. This suggests that the inhibition of the ventilatory response to H(2)S by hyperoxia during aortic or venous injection originates within the CB and not in the blood. The implications of these results on the role of endogenous H(2)S in the arterial chemoreflex are discussed. SN - 1878-1519 UR - https://www.unboundmedicine.com/medline/citation/22490362/Inhibitory_effects_of_hyperoxia_and_methemoglobinemia_on_H_2_S_induced_ventilatory_stimulation_in_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1569-9048(12)00079-1 DB - PRIME DP - Unbound Medicine ER -