Correlation between ventilatory and cerebrovascular responses to inhalation of CO.
To study the determinants of carbon monoxide (CO) induced hyperpnea simultaneous measurements were made of carboxyhemoglobin level in arterial blood (HbCO), ventilation (VE), cerebral blood flow (CBF), O2 delivery to the brain (CBF X O2 content of arterial blood), O2 consumption of the brain (CMRO2), and O2 tension in cerebral venous blood (PVO2) during inhalation of 1% CO in 40% O2 by six unanesthetized goats. HbCO increased to 65% in 10 min; VE remained constant until a HbCO level of approximately 50% was reached and then increased abruptly; CBF increased progressively; O2 delivery to the brain and CMRO2 decreased somewhat with CO inhalation; these decreases reached statistical significance at a HbCO level of 30-40% whereupon the rate of decline with respect to HbCO level increased substantially; and PVO2 decreased progressively from an average of from 31 to 14.6 Torr and averaged 19.2 Torr when hyperpnea was manifest. When considered in the light of previous studies which indicate that CO-induced hyperpnea is not caused by stimulation of the carotid bodies, these data suggest that this phenomenon is related to brain hypoxia. Calculations of brain tissue O2 tension with the Krogh equation support this contention.
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000503:physiopathology*; D002249:Carbon Monoxide Poisoning / Q000503:physiopathology*; D002263:Carboxyhemoglobin / Q000378:metabolism; D002560:Cerebrovascular Circulation; D006041:Goats; D008168:Lung / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D012119:Respiration; D014680:Veins
D002263:Carboxyhemoglobin; D010100:Oxygen