Pulmonary Capillary Flow Pulse and the Site of Pulmonary Vasoconstriction in the Dog

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Abstract
A nitrous oxide-plethysmographic method was used to measure simultaneously the instantaneous pulmonary capillary blood flow and the pressure gradient across the pulmonary vascular bed. The method entailed the use of lightly anesthetized, curarized dogs for the moment-to-moment measurement of nitrous oxide uptake and the corresponding pulmonary arterial and wedge pressures. After establishing the usual patterns of pulmonary capillary blood flow, the flow patterns were modified by atropine, norepinephrine, and acute hypoxia. Before the exhibition of these agents, pulmonary capillary flow was pulsatile, with peak rates of flow of approximately twice the mean. After atropine, the amplitude of the flow pulse decreased passively as stroke volume and the pulmonary arterial pulse pressure decreased. In contrast to atropine, acute hypoxia elicited precapillary vasoconstriction as manifested by an increase in pulmonary arterial pressure and an unchanged pulmonary arterial wedge pressure in conjunction with an unchanged, or diminished and blunted, pulmonary capillary flow pulse. The predominant effect of norepinephrine appeared to be exerted distal to the pulmonary capillary bed since pulmonary arterial and wedge pressures increased in parallel while the capillary flow pulse changed passively according to changes in stroke volume.