Increases in arterial hydrogen ion concentration and carbon dioxide tension independently cause pulmonary vasoconstriction in intact dogs.
Should not alter human ventilatory management; leaves open independent roles of [H+] and CO2 in clinical pulmonary vasoconstriction.
The hydrogen ion concentration ([H+]) and the carbon dioxide tension [Formula: see text] of the arterial blood were varied independently of the other over a range of values while the respiration was controlled at resting levels. The independent effects of the two variables were examined in intact dogs anesthetized with 30 mg/kg sodium pentobarbital. Increases in [H+] and [Formula: see text] were significantly correlated (r = 0.859 and r = 0.646) with increases in the pulmonary vascular resistance (P.V.R.). The rise in P.V.R. in both cases was associated with rise in pulmonary perfusion pressure and no significant change in pulmonary blood flow. Decrease in [Formula: see text] had no effect on the measured parameters. We have demonstrated the independent pulmonary vasoconstrictor effects of increase in the [H+] and [Formula: see text]. The magnitude of the pulmonary vasoconstrictor response is dependent upon the degree of rise in [H+] and [Formula: see text]. [Formula: see text] does not play a role in maintaining resting pulmonary vasomotor tone.
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Malik et al. (1973) studied this question.
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