CONTRIBUTION OF IN-VIVO MICROVASCULAR PO2 IN THE CAT CAROTID-BODY CHEMOTRANSDUCTION

To understand the interplay between microcirculatory control and carot id body (CB) function, we simultaneously measured carotid body microva scular PO2 (CBM PO2) and chemosensory activity in the cat in vivo unde r several experimental conditions. Cats were anesthetized with pentoba rbital sodium, paralyzed, and artificially ventilated. CBs were expose d, and steady-state CBM PO2 was measured by the O2-dependent quenching of the phosphorescence of Pd-meso-tetra-(4-carboxyphenyl)porphine, wh ich was administered intravenously. A few fibers of the carotid sinus nerve were used to record chemosensory discharges. At arterial PO2 (Pa (O2)) of 103.4 +/- 4.1 Torr, CBM PO2 was 52.5 +/- 3.6 Torr (n = 9). Gr aded lowering of Pa(O2) from 160 to 50 Torr resulted in nearly proport ional decreases in CBM PO2, but at lower Pa(O2) the decrease in CBM PO 2 became more substantial. As Pa(O2) decreased, chemosensory discharge increased in parallel wit CBM PO2. Hypercapnia and hypocapnia did not significantly change the relationship between Pa(O2) and CBM PO2, alt hough the chemosensory discharge responded significantly. CBM PO2 and chemosensory discharge were not affected by hemorrhagic hypotension un til arterial blood pressure fell below approximately 50 Torr and then CBM PO2 decreased and chemosensory discharge increased. The lack of a significant effect of hemorrhagic hypotension indicated that O2 delive ry to CB was almost independent of the systemic blood pressure. Taken together, the observations suggest that CB microcirculation and PO2 ar e subject to control by intrinsic mechanisms and that CBM PO2 is compa tible with oxidative metabolism playing a role in O2 chemoreception du ring hypoxia.