Role of Cl--HCO3 - Exchanger and Anion Channel in the Cat Carotid Body Function

Author(s):  
Rodrigo Iturriaga ◽  
Sukhamay Lahiri
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.


2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Lalah Niane ◽  
Vincent Joseph ◽  
Aida Bairam

1986 ◽  
Vol 64 (2) ◽  
pp. 203-211 ◽  
Author(s):  
David W. Hudgel ◽  
Nancy A. Kressin ◽  
Ann M. Nielsen ◽  
Gerald E. Bisgard

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Ying‐Jie Peng ◽  
Jayasri Nanduri ◽  
Gayatri Raghuraman ◽  
Ning Wang ◽  
Ganesh K Kumar ◽  
...  

2013 ◽  
Vol 185 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Aida Bairam ◽  
Lalah M. Niane ◽  
Vincent Joseph
Keyword(s):  

2008 ◽  
Vol 81 (4) ◽  
pp. 678-685 ◽  
Author(s):  
Y. Ding ◽  
Y.-L. Li ◽  
M. C. Zimmerman ◽  
R. L. Davisson ◽  
H. D. Schultz

2016 ◽  
Vol 473 (2) ◽  
pp. 107-121 ◽  
Author(s):  
Jemma Gatliff ◽  
Michelangelo Campanella

The 18-kDa translocator protein (TSPO) localizes in the outer mitochondrial membrane (OMM) of cells and is readily up-regulated under various pathological conditions such as cancer, inflammation, mechanical lesions and neurological diseases. Able to bind with high affinity synthetic and endogenous ligands, its core biochemical function resides in the translocation of cholesterol into the mitochondria influencing the subsequent steps of (neuro-)steroid synthesis and systemic endocrine regulation. Over the years, however, TSPO has also been linked to core cellular processes such as apoptosis and autophagy. It interacts and forms complexes with other mitochondrial proteins such as the voltage-dependent anion channel (VDAC) via which signalling and regulatory transduction of these core cellular events may be influenced. Despite nearly 40 years of study, the precise functional role of TSPO beyond cholesterol trafficking remains elusive even though the recent breakthroughs on its high-resolution crystal structure and contribution to quality-control signalling of mitochondria. All this along with a captivating pharmacological profile provides novel opportunities to investigate and understand the significance of this highly conserved protein as well as contribute the development of specific therapeutics as presented and discussed in the present review.


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