The pressurevolume relationship of the normal pleural capillary bed

In isolated lung preparations (1, 2) and in nor-mal subjects (3, 4), acute pulmonary vascular congestion increases breath-holding diffusing ca-pacity for carbon monoxide (DLco) by increasing the instantaneous volume of blood available for CO absorption (Vc). Conversely, in normal men, procedures that decrease pulmonary vascular pres-sure decrease DLco (4, 5); yet, the pulmonary capillary bed of the lung chronically subjected to increased intravascular pressure is less able to de-crease its volume in response to procedures de-signed to decrease pulmonary vascular pressure (6). Although this may be the consequence of structural changes in the lung, this observation suggests that the curve relating DLCO to pulmonary vascular pressure may reach a plateau, beyond which changes in pulmonary vascular pressure produce no further changes on DLCO. Such a re-lationship does not imply a solution to the question whether increased intravascular pressure recruits a limited number of capillaries or dilates capil-laries within a limited range. In either case, a plateau of the DLco-vascular pressure curve would be anticipated. This study was undertaken to examine the be-havior of the normal pulmonary capillary bed acutely subjected to increased intravascular pres-sure with two specific aims in mind: 1) to describe, in normal man, the effects on DLCO of graded in-creases in, intravascular pressure and to determine * Submitted for publication November 30, 1964; ac