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1. Carotid body blood flow (c.b.f.) and carotid arterialcarotid body venous oxygen (AV O2) difference were measured and carotid body oxygen consumption calculated in twenty-six cats anaesthetized with pentobarbitone sodium, paralysed with gallamine triethiodide and ventilated mechanically.
2. With the sinus nerves intact and with blood gas tensions and carotid sinus pressure within physiological limits, section of either the pre- or post-ganglionic cervical sympathetic nerve on the same side caused an average rise in c.b.f. of 9·2 µl./min, in AV O2 difference of 0·09 ml./100 ml. and in carotid body oxygen consumption of 0·075 µl./min.
3. When the pre- or post-ganglionic cervical sympathetic nerves were stimulated, c.b.f. and AV O2 difference fell. The fall in c.b.f. was enhanced at high Pa, CO2; the fall in AV O2 difference and in calculated oxygen consumption was enhanced at low mean arterial pressure (M.A.P.) or Pa, O2.
4. Following sympathectomy, a reduction of M.A.P. at constant Pa, O2 and Pa, CO2 caused a fall in c.b.f. and a commensurate rise in AV O2 difference so that carotid body oxygen consumption remained approximately constant.
5. When Pa, O2 was altered over the range 35 to > 400 mm Hg, or Pa, CO2 over the range 27-70 mm Hg at constant M.A.P., c.b.f. changed by amounts which were similar to those observed when the sympathetic nerves were intact and AV O2 difference changed in the opposite direction so that carotid body oxygen consumption similarly remained constant.
6. Comparison of these results with those observed when the sympathetic nerves were intact indicates that the sympathetic nerves exert a vasoconstrictor effect upon carotid body blood vessels over a wide range of blood gas tensions and arterial pressure and that they also tend to diminish the rate of carotid body oxygen consumption. The mechanisms which may be involved in this regulation are discussed.
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