Abstract
The pulmonary vasculature is unique among the various regional circulations in that it must accommodate the entire cardiac output. Unfortunately, precisely the same factors that make this possible—the highly compliant vessels, their scant smooth musculature, the paucity of nervous control, and the consequent low intravascular pressures—also render the evaluation of pulmonary vasomotion difficult. The bed is so distensible that blood flow normally ceases at the end of diastole (MORKIN et al. [1965], KARATZAS and LEE [1969], and GABE et al. [1969]); nor is there a pressure gradient across the bed at that time. The use of mean pressure and mean flow for calculating resistance to pulmonary blood flow, in order to assess the effects of physiologic stimuli or pharmacologic agents, may lead, for these reasons, to conclusions which are quite inappropriate (HARVEY and ENSON [1969]).
Supported in part by grants HE-05741-09 and HE-02001-15 from the National Heart Institute, and by a grant-in-aid from the New York Heart Association.
Recipient of an investigatorship of the Health Research Council of the City of New York under contract 1–176.
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Enson, Y. (1974). The Effects of Carbon Dioxide and pH on the Regulation of the Pulmonary Circulation. In: Nahas, G., Schaefer, K.E. (eds) Carbon Dioxide and Metabolic Regulations. Topics In Environmental Physiology And Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-9831-1_19
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DOI: https://doi.org/10.1007/978-1-4612-9831-1_19
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