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- W763798190 abstract "Chronic sustained hypoxia (CSH) increases inflammatory cytokine gene expression in carotid bodies and medullary respiratory centers, and increases carotid body chemoreceptor and ventilatory responses to hypoxia in rats. Non-steroidal anti-inflammatory drugs (ibuprofen IBU) block these responses (Respir.Physiol.Neurobiol. (2011) 178: 362–369 & 381–386). We tested the hypothesis that IBU can reverse these responses after they are already established in CSH. We measured cytokine expression in medullary respiratory centers and ventilatory responses in adult male rats acclimatized to CSH (PiO2 = 70 Torr, 1 wk) before and after IBU (4 mg/kg intraperitoneal for 3 days) or sham (0.6 ml saline IP for, 3 days) treatments. We measured the effects of IBU vs. sham in normoxic animals too. Expression of mRNA for IL-1β, IL-6, and TNFα measured with RT-PCR in dorsal brainstem biopsies tended to be lower with IBU compared to sham: IBU = 68, 67 and 85% of sham levels for IL-1β, IL-6, and TNFα, respectively. However, ventilatory and metabolic responses to hypoxia measured with barometric pressure plethysmography and stop-flow respirometry were not significantly different between IBU and sham in CSH or normoxic rats (p>;0.1). Hence, inflammatory cytokines in the CNS and carotid bodies appear necessary for the induction but not the maintenance of an increased hypoxic ventilatory response with CSH. Supported by NIH RO1 HL-081823." @default.
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- W763798190 date "2013-04-01" @default.
- W763798190 modified "2023-09-23" @default.
- W763798190 title "Ibuprofen does not reverse time‐dependent increase in hypoxic ventilation in chronically hypoxic rats" @default.
- W763798190 doi "https://doi.org/10.1096/fasebj.27.1_supplement.721.5" @default.
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