HYPOXIA DEPLETES ASCORBATE IN THE CAT CAROTID-BODY

Citation
M. Pokorski et B. Gonet, HYPOXIA DEPLETES ASCORBATE IN THE CAT CAROTID-BODY, Respiration physiology, 107(3), 1997, pp. 213-218
Citations number
24
Categorie Soggetti
Respiratory System",Physiology
Journal title
ISSN journal
00345687
Volume
107
Issue
3
Year of publication
1997
Pages
213 - 218
Database
ISI
SICI code
0034-5687(1997)107:3<213:HDAITC>2.0.ZU;2-B
Abstract
Vitamin C or L-ascorbate is an effective endogenous reducing agent inf luencing the functions that are involved with the redox mechanism. Det ection of oxygen tension changes by the carotid body chemoreceptors is one such function. In this study we investigated the hypothesis that the level of ascorbate, if present, could change in the carotid body a s a result of ascorbate's interaction in the chemosensing process, whi ch would be reflected in the production of the ascorbyl radical. We ad dressed this issue by examining changes of the ascorbyl radical: using the in vitro electron spin resonance spectroscopy (ESR), in the carot id bodies dissected from pentobarbitone anesthetized cats exposed in v ivo to three eucapnic, breathing gas mixtures of different O-2 concent ration: normoxic, 21% O-2; hypoxic, 7% O-2; and hypoxic-reoxygenated, 7% O-2 followed by 100% O-2. Each group consisted of five cats, yieldi ng five pairs of carotid bodies for the ESR signal recording. We found that the intensity of ESR signals, measured as peak-to-peak amplitude , was diminished by 39 and 43% in the hypoxic and hypoxic-reoxygenated groups, respectively, compared with that in normoxia. The study shows that ascorbate was present in the normoxic carotid body and was deple ted by hypoxia. We conclude that ascorbate is part of free radical mec hanisms operative in the carotid body in hypoxia. (C) 1997 Elsevier Sc ience B.V.