Control of arterial PCO2 by somatic afferents in sheep.

The ventilatory response to electrically induced rhythmic muscle contractions (ERCs) was studied in six urethane-chloralose-anaesthetized sheep, while arterial oxygen and carbon dioxide pressure (P(a,O(2)) and P(a,CO2)) and perfusion pressure were maintained constant at the known chemoreception sites. With cephalic P(a,CO2) held constant, the response to inhaled CO2 was virtually abolished (0.03 +/- 0.04 l min(-1) Torr(-1)). During low-current ERC, which doubled the metabolic rate ( increased from 192 +/- 23 to 317 +/- 84 ml min(-1), P < 0.01), followed the change in closely (from 5.24 +/- 1.81 to -9.27 +/- 3.60 l min(-1), P < 0.01) in the absence of any chemical error signal occurring at carotid and central chemoreceptor level (Deltacephalic P(a,CO2)=-0.75 +/- 1 Torr). Systemic P(a,CO2) decreased by -2.47 +/- 1.9 Torr (P < 0.01). Both heart rate and systemic blood pressure increased significantly by 18.6 +/- 5.5 beats min(-1) and 7.0 +/- 9.3 mmHg, respectively. When the CO2 flow to the central circulation was reduced during ERC by blocking venous return ( decreased by 102 +/- 45 l min(-1), P < 0.01), ventilation was stimulated (from 11.99 +/- 4.11 to 13.01 +/- 4.63 l min(-1), P < 0.05). The opposite effect was observed when the arterial supply was blocked. Finally, raising the CO2 content and flow in the systemic blood did not significantly stimulate ventilation provided that the peripheral and central chemoreceptors were unaware of the changes in blood CO2/H+ composition. Our results support the existence of a system capable of controlling blood P(a,CO2) homeostasis when the metabolism increases independently of peripheral and central respiratory chemoreceptors. Information from the skeletal muscles related to the local vascular response provides the central nervous system with a respiratory stimulus proportional to the rate at which gases are exchanged in the muscles, thereby coupling ventilation to the metabolic rate.