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Control of arterial P CO2 by somatic afferents in sheep
Author(s) -
Haouzi Philippe,
Chenuel Bruno
Publication year - 2005
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2005.089649
Subject(s) - chemoreceptor , chemistry , chloralose , ventilation (architecture) , blood pressure , blood flow , perfusion , respiration , heart rate , anesthesia , arterial blood , medicine , endocrinology , anatomy , biochemistry , mechanical engineering , receptor , engineering
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 2and P a,CO 2) and perfusion pressure were maintained constant at the known chemoreception sites. With cephalic P a,CO 2held constant, the response to inhaled CO 2 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 (Δcephalic P a,CO 2=−0.75 ± 1 Torr). Systemic P a,CO 2decreased 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 CO 2 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 CO 2 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 CO 2 /H + composition. Our results support the existence of a system capable of controlling blood P a,CO 2homeostasis 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.