The vascular pressure-flow (P-Q) relationships in zone II (West et al.) were studied in isolated canine left lower lobes, in order to characterize the total resistance in the pulmonary vascular bed with respect to incremental or flow resistance and critical closure. At each of five levels of static lung inflation, the P-Q relationship was curvilinear at low flow and rectilinear at higher flows. The slope of the linear portion was not significantly different at alveolar pressures (PA) = 5, 7, or 9 cm H2O, but decreased significantly at PA = 11 and 15 cm H2O ((P less than 0.05), indicating an increase in flow resistance. The pulmonary artery pressure (Ppa) fell to the same value at zero flow regardless of inflation level [10.1 +/- 1.0 (SD) cm H2O at PA = 5 cm H2O to 10.9 +/- 2.7 (SD) at PA = 15 cm H2O]. The Ppa intercept (Ppai), extrapolated from the linear portion of the P-Q curve and representing the average closing pressure for the vascular bed, increased from 16.0 +/- 1.8 (SD) cm H2O at PA = 5.0 to 26.5 +/- 4.4 (SD) cm H2O at PA = 15 (P less than 0.05) in a direct one-to-one relationship with the increase in PA. Since this results in a constant transmural gradient at the alveolar vessel level, these vessels must be the major fraction which undergo critical closure. Operationally defined vascular compliance, determined from the slope of a simultaneously obtained pressure-volume (P-V) curve, decreased significantly from 1.51 +/- 0.62 (SD) ml/cm H2O at PA = 5.0 H2O to 0.87 +/- 0.27 ml/cm H2O at PA = 15 cm H2O (P less than 0.05).
We have tested the independent and combined effects of changes in mixed venous PO2 (PvO2) and blood flow (QT) on shunt fraction (Qs/QT) in isolated blood-perfused canine left lower lobes with edema. The lobes were ventilated with pure O2. Inflow (Pi) and outflow (Po) pressures always exceeded lobar alveolar pressure. PvO2 was varied by means of a clinical bubble oxygenator with appropriate mixtures of O2 and N2. QT was varied by changes in Pi and Po with care not to produce changes in lobar weight. Changes in QT did not influence Qs/QT. Increasing PvO2 from 40 +/- 6 to 88.4 +/- 40 Torr at constant QT significantly increased Qs/QT from 5.5 +/- 2.0 to 15.6 +/- 7.0%. Combined increases in QT and PvO2 from 66.4 +/- 2.7 to 135.6 +/- 21.5 ml/min and from 38.8 +/- 1.3 to 61.8 +/- 2.2 Torr, respectively, also produced a significant increase in Qs/QT from 7.33 +/- 2.27 to 15.43 +/- 4.45%. However, this combined change was explained exclusively by changes in PvO2. We therefore concluded that, under the conditions of our experiment, changes in PvO2 influence Qs/QT, and this may account for apparent dependence of Qs/QT on cardiac output in pulmonary edema.
The pressure-flow (P-Q) relationship of the pulmonary vasculature, in an isolated canine lobe perfused under classical zone II conditions, can be characterized by a rectilinear segment at high flow, a curvilinear segment at low flow, and a pulmonary arterial pressure (Ppa) that exceeds alveolar pressure at zero flow. This demonstrates the presence of critical closure in the pulmonary vascular bed. Effects of drugs on pulmonary vascular resistance (PVR) must take the normal P-Q relationship into account. We examined the effect of dopamine (D) and dobutamine (DB), alone and in combination with phentolamine (P), on the slope of the rectilinear segment of the P-Q curve (equivalent to vascular conductance), the extrapolated Ppa intercept (Ppai), and the Ppa at zero flow (Ppaz). Low-dose D (0.4-0.8 mg) and DB (1.0-5.0 mg) did not significantly alter any parameter from control. Higher-dose D (1.2-6.8 mg) and DB (13-38 mg) decreased vascular conductance 32.3 +/- 12.1 (SE) to 50.45 +/- 5.6% (P less than 0.05), and P alone increased conductance 12.0 +/- 2.6% (P less than 0.01) from control with no significant effect on Ppai or Ppaz. The change in conductance with D and DB alone was abolished when either drug was given in combination with P. Ppaz and Ppai decreased significantly from control with DB in combination with P when no significant effect on vascular conductance was noted. The results suggest that lung vessels determining changes in flow resistance are pharmacologically distinct from those subserving critical closure in the pulmonary vascular bed.
Static deflationary pressure-volume curves were obtained in 28 emphysema-free (18 male and 10 female) and 39 emphysematous excised human lungs inflated to a maximum transpulmonary pressure (Pl) of 30 cmH2O. In emphysema-free lungs, the lung volumes at Pl 30 cmH2O (V30) were significantly related to body length in males and were significantly larger than predicated total lung capacity in vivo. However, corrected for stature (V30/body length), there was no significant age correlation. In both males and females, highly significant correlations between the PL at 50--90% V30 and age were obtained. There were no significant differences in these regressions between males and females. The emphysematous lungs were divided into three groups with increasing emphysema grades. Progressive decreases in the PL at 50--90% V30 and increases in the V30 were seen in the groups with increasing degrees of emphysema. Significant changes occurred in these measurements even in group 2 with mild emphysema, suggesting that the lesions of emphysema are not directly responsible for these changes.
Human case reports and controlled animal experiments lead to different conclusions about vasopressors in TICS. Most animal studies indicate that vasopressors impair hemodynamic function and increase mortality. In contrast, human case reports suggest that vasopressors are often ineffective but not necessarily harmful.
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