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N. S. Cherniack^*, C. von Euler, I. Homma and F. F. Kao

Nobel Institute for Neurophysiology, Karolinska Institutet, S-104 01 Stockholm, Sweden

1. In cats under pentobarbitone anaesthesia the effects of focal temperature changes of the `chemoceptive' areas on the ventral surface of medulla, described by Loeschcke and his associates, were studied with respect to tidal volume, V_T, tidal variation in efferent phrenic activity, Phr_T, and respiratory rate. The cats were either paralysed and ventilated at various constant P_A,CO2 and P_a,O2 levels, or breathing spontaneously.

2. It was confirmed that focal bilateral cooling of the intermediate, `I_(S)', areas caused rapid depression of respiration even at constant artificial ventilation. In normocapnic and normoxic conditions apnoea usually ensued at brain surface temperatures of 20-22 °C.

3. The effects were graded along continuous temperature—response curves with enhancements of ventilation above and depression below normal body temperature.

4. The strongest effects on V_T and Phr_T were obtained from the I_(S) areas with no or only small effects on inspiratory or expiratory timing in the vagotomized animal. The Hering—Breuer inflation reflex and its effects on timing and amplitudes were not affected by cooling this area.

5. Focal cooling of the caudal or the rostral `chemoceptive' areas, `C_(L)' and `R_(M)' areas, caused smaller effects on V_T and Phr_T but produced significant effects on respiratory rate even after vagotomy.

6. The effects of focal cooling of these areas could be mimicked by topical application of procaine solution which has been shown not to penetrate deeper than 100 µm from the surface.

7. Moderate focal cooling of area I_(S) to temperatures above 28-30 °C caused a parallel shift in the CO₂—response (V_T, Phr_T) curves to the right with little change in slope. The P_CO2 thresholds for apnoea were correspondingly raised. These focal temperature effects could be compensated by changes in P_CO2 with, on the average, 2·7 torr/°C. Focal temperatures below 28 °C usually caused some decrease in slope of the CO₂—response curves in addition to further shifts.

8. Added hypoxic stimulus or electrical stimulation of the carotid sinus nerves caused an almost parallel increase of Phr_T at all P_CO2 levels and all focal temperatures suggesting an additive type of interaction between the input from the peripheral chemoreceptors and that from the central (CO₂, H⁺) sensing structures whether the latter was altered by changing P_CO2 or by focal temperature changes on the I_(S) areas.

9. In contrast to these effects of hypoxia and stimulation of the carotid sinus nerves the reflex increase of inspiratory activity caused by lung deflation or by electrical stimulation of the glossopharyngeal nerve distal to the carotid sinus nerves was CO₂ dependent. These reflex effects decreased with focal cooling of the I_(S) areas as with hypocapnia, suggesting a mainly multiplicative or `gain-changing' type of interaction with the central chemoceptive drive.

10. The close similarities in effect of focal cooling and of hypocapnia on the different respiratory parameters even during constant artificial ventilation indicate that focal temperature changes of the I_(S) areas intervene effectively with the normal ventilatory response to CO₂ without changing the chemical or physical environment of those neural structures in the brain stem which set respiratory pattern.

Present address: Department of Physiology, School of Medicine, The Tokyo Jikei University, Tokyo, Japan.

Present address: Department of Physiology, State University of New York, Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203, U.S.A.

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