Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat
- PMID: 1464840
- PMCID: PMC1175568
- DOI: 10.1113/jphysiol.1992.sp019239
Maturation of carotid chemoreceptor sensitivity to hypoxia: in vitro studies in the newborn rat
Abstract
1. A preparation was developed to record single-fibre chemoreceptor afferent activity from carotid bodies of newborn and adult rats in vitro. The response to severe hypoxia was studied as a function of developmental age in four age groups: 1-2, 4-7, 10-15 days and adult (25-30 days). 2. During superfusion with HEPES-saline at room PO2 and at 26 or 35 degrees C, afferent chemoreceptor activity could be recorded in all age groups. No significant difference was found among groups in baseline discharge frequency at 26 or 35 degrees C. 3. All chemoreceptors responded to anoxia (PO2 congruent to 0 Torr) with a rapid increase in discharge frequency. At 35 degrees C, peak discharge frequency of single chemoreceptor afferents was significantly greater in the adult (15.7 +/- 1.6 Hz, mean +/- S.E.M., n = 18) and 10-15 days (11.2 +/- 4.2, n = 8) compared to rats of 1-2 days (4.3 +/- 0.7, n = 14) and 4-7 days of age (3.9 +/- 1.0, n = 7). 4. At 2 min into the anoxia period, all chemoreceptor activities were reduced from their peak discharge levels. At 35 degrees C, this decrease was significantly greater in the adult compared to the newborn. 5. During the period of decreased activity during anoxia, the chemoreceptor discharge could not be increased by inter-stream injection of acetylcholine (100 micrograms) or dopamine (100 micrograms), although these drugs were effective in increasing discharge rate prior to hypoxia. 6. We conclude that: (1) postnatal maturation of chemoreceptor sensitivity to hypoxia is present in vitro, (2) maturation occurs between the first and second week after birth in the rat, and (3) the decrease in activity during prolonged anoxia is not greater in the newborn compared to the adult. Thus, maturational changes occur in the sensitivity of the glomus cell-nerve ending complex to hypoxia.
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