Carbon monoxide and pulmonary circulation in an ovine model.
The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.
Theissen
J L
JL
Department of Anesthesiology, University of Texas Medical Branch, Galveston.
Loick
H M
HM
Traber
L D
LD
Herndon
D N
DN
Traber
D L
DL
D000818:Animals; D002249:Carbon Monoxide Poisoning / Q000503:physiopathology*; D002263:Carboxyhemoglobin / Q000378:metabolism; D002302:Cardiac Output / Q000502:physiology; D011651:Pulmonary Artery / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000502:physiology*; D011667:Pulmonary Veins / Q000503:physiopathology*; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D012756:Sheep; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology
D002263:Carboxyhemoglobin