Effects of hyperoxia on medullary ECF pH and respiration in chemodenervated cats.
The effects of transitions from air-breathing to hyperoxia (100% O2), and the reverse, on respiration (phrenic activity) and on medullary extracellular fluid (ECF) pH, or hydrogen ion concentration [H+], were studied in 8 anesthetized, paralyzed, vagotomized and glomectomized cats whose end-tidal PCO2 was kept constant. The transition from air to hyperoxia (7 cats) led to a small (1.23 nmol/L [H+], 0.010 pH unit) acidic shift of medullary ECF and a 24% increase of neural tidal and minute respiratory activity with no significant change of frequency. Opposite changes of approximately equal magnitude followed the transition from hyperoxia to air (8 cats). We show that the slopes of the respiratory responses to changing ECF [H+] in the present study are not different than the slopes with CO2-induced changes of ECF [H+] in 25 other cats. Our findings indicate that most, if not all, of the respiratory increase after hyperoxia is due to accumulation of CO2 and H+ in medullary ECF that act on the central chemoreceptors. We suggest that decreased medullary blood flow and the Haldane effect are the main mechanisms causing the rise of medullary PCO2 and stimulation of breathing.
D000818:Animals; D002245:Carbon Dioxide; D002415:Cats; D005110:Extracellular Space / Q000378:metabolism; D005703:Gallamine Triethiodide; D006863:Hydrogen-Ion Concentration; D008526:Medulla Oblongata / Q000378:metabolism*; D009431:Neural Conduction; D010100:Oxygen; D010313:Partial Pressure; D010791:Phrenic Nerve / Q000502:physiology; D011659:Pulmonary Gas Exchange; D012119:Respiration; D013563:Sympathectomy, Chemical / Q000379:methods
D002245:Carbon Dioxide; D005703:Gallamine Triethiodide; D010100:Oxygen