Critical closure of pulmonary vessels analyzed in terms of Starling resistor model.

Publisher Website
Google Scholar
Abstract
The limitations of the Starling resistor model were explored as applied to the pulmonary circulation under carefully controlled conditions in the excised dog lung. The effect on pulmonary arterial pressure (Ppa) was measured of changes in pulmonary venous pressure (Ppv) at constant blood flow ([image]) and alveolar pressure (Palv) and the effect on Ppa of changes in Palv at constant [image] and Ppv. During these runs, Ppa was measured under conditions of 0 [image], which was defined as Ppa[image]. Below a critical level of Ppv, which was defined as Ppv[image], changes in Ppv had no influence on Ppa. When the transpulmonary pressure (Ptp) was > 5 mm Hg, the pH of the blood normal, and alveolar CO2 not elevated, Ppa[image] = Ppv[image] = Palv when Ppa[image] was determined under conditions where Ppv < Ppv[image]. On the other hand, Ppa[image] = Ppv when Ppv was > Ppv[image]. When Ptp was < 5 mm Hg and Ppv < Ppv[image], both Ppa[image] and Ppv[image] were > Palv. If the pH of the blood was lowered or the PCO2 [CO2 pressure] of the alveolar gas increased, Ppa[image] at Ppv < Ppv[image] became > Palv even at high values of Ptp. Increased acidity or high CO2 may cause critical closing pressures both in alveolar and extra-alveolar vessels.