scholarly journals Ventilatory responses and carotid body function in adult rats perinatally exposed to hyperoxia

2003 ◽  
Vol 554 (1) ◽  
pp. 126-144 ◽  
Author(s):  
J. Prieto-Lloret ◽  
A. I. Caceres ◽  
A. Obeso ◽  
A. Rocher ◽  
R. Rigual ◽  
...  
2011 ◽  
Vol 226 (8) ◽  
pp. 1961-1969 ◽  
Author(s):  
M.C. Gonzalez-Martín ◽  
M.V. Vega-Agapito ◽  
S.V. Conde ◽  
J. Castañeda ◽  
R. Bustamante ◽  
...  

2015 ◽  
Vol 593 (11) ◽  
pp. 2459-2477 ◽  
Author(s):  
Jesus Prieto-Lloret ◽  
Maria Ramirez ◽  
Elena Olea ◽  
Javier Moral-Sanz ◽  
Angel Cogolludo ◽  
...  

1972 ◽  
Vol 175 (2) ◽  
pp. 268-273 ◽  
Author(s):  
Robert F. Hickey ◽  
William K. Ehrenfeld ◽  
F. Norman Hamilton ◽  
C. Philip Labson

1996 ◽  
Vol 80 (3) ◽  
pp. 892-898 ◽  
Author(s):  
C. Delacourt ◽  
E. Canet ◽  
M. A. Bureau

Apneas are very common and normal in newborns but may become life threatening if they are not terminated appropriately. The aim of this study in newborn lambs was to investigate the influence on apnea termination of postnatal maturation, peripheral chemoreceptor function, and hypoxia. Apneas were induced by passive hyperventilation at varying inspired O2 fraction levels. The apnea termination threshold PCO2 (PATTCO2) was defined as the arterial PCO2 value at the first breath after the apnea. Three groups of awake intubated lambs were studied: 1) intact lambs tested at both 1 and 15 days of life, 2) intact 1-day-old lambs with central tissue hypoxia induced by CO inhalation, and 3) 1-day-old lambs with carotid body denervation (CBD). In individual lambs and regardless of age and carotid body function, there was a PO2-PCO2 response curve that was a determinant for the termination of an apnea. PATTCO2 invariably increased when arterial PO2 increased, regardless of age. During hypoxia and normoxia, PATTCO2 was significantly lower in 15-day-old lambs compared with 1-day-old lambs. No difference was seen during hyperoxia. PATTCO2 values were shifted to higher levels after carotid body removal. Finally, hypoxia induced by either a low inspired O2 fraction or CO inhalation consistently failed to induce a depressive effect on the PATTCO2 even in CBD lambs. In conclusion, in awake newborn lambs, the PCO2 level for apnea termination changed with postnatal age, and carotid body function was essential in lowering PATTCO2, thus protecting the lambs against prolonged apnea. Furthermore, hypoxia consistently failed to depress the reinitiation of breathing after apnea, even in CBD lambs.


2013 ◽  
Vol 591 (14) ◽  
pp. 3565-3577 ◽  
Author(s):  
Tammie Bishop ◽  
Nick P. Talbot ◽  
Philip J. Turner ◽  
Lynn G. Nicholls ◽  
Alberto Pascual ◽  
...  

2007 ◽  
Vol 157 (1) ◽  
pp. 148-153 ◽  
Author(s):  
Nanduri R. Prabhakar ◽  
Yin-Jie Peng ◽  
Ganesh K. Kumar ◽  
Anita Pawar

2012 ◽  
Vol 303 (9) ◽  
pp. C916-C923 ◽  
Author(s):  
Vladislav V. Makarenko ◽  
Jayasri Nanduri ◽  
Gayatri Raghuraman ◽  
Aaron P. Fox ◽  
Moataz M. Gadalla ◽  
...  

H2S generated by the enzyme cystathionine-γ-lyase (CSE) has been implicated in O2 sensing by the carotid body. The objectives of the present study were to determine whether glomus cells, the primary site of hypoxic sensing in the carotid body, generate H2S in an O2-sensitive manner and whether endogenous H2S is required for O2 sensing by glomus cells. Experiments were performed on glomus cells harvested from anesthetized adult rats as well as age and sex-matched CSE+/+ and CSE−/− mice. Physiological levels of hypoxia (Po2 ∼30 mmHg) increased H2S levels in glomus cells, and dl-propargylglycine (PAG), a CSE inhibitor, prevented this response in a dose-dependent manner. Catecholamine (CA) secretion from glomus cells was monitored by carbon-fiber amperometry. Hypoxia increased CA secretion from rat and mouse glomus cells, and this response was markedly attenuated by PAG and in cells from CSE−/− mice. CA secretion evoked by 40 mM KCl, however, was unaffected by PAG or CSE deletion. Exogenous application of a H2S donor (50 μM NaHS) increased cytosolic Ca2+ concentration ([Ca2+]i) in glomus cells, with a time course and magnitude that are similar to that produced by hypoxia. [Ca2+]i responses to NaHS and hypoxia were markedly attenuated in the presence of Ca2+-free medium or cadmium chloride, a pan voltage-gated Ca2+ channel blocker, or nifedipine, an L-type Ca2+ channel inhibitor, suggesting that both hypoxia and H2S share common Ca2+-activating mechanisms. These results demonstrate that H2S generated by CSE is a physiologic mediator of the glomus cell's response to hypoxia.


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