The lungs and intrathoracic cardiovascular structures compete for space within the thorax, interacting through their adjacent surfaces via the pleural space. Theoretical analysis and in vitro model studies (detailed here) established that when a vessel indents the lung surface, the increase in intravascular pressure with positive pressure lung inflation can be greater than the change in the pleural surface pressure measured outside of the interaction area. We define this phenomenon as intravessel pressure augmentation. We determined the average intravessel pressure gain as the slope of the linear regression of the pressure in a vascular structure or balloon indenting the lung on the pleural surface pressure measured by a flat disk-shaped device (disk). The analysis showed that the disk pressure overestimates the pleural pressure. Therefore, the derived pressure gain underestimated the pressure augmentation. In five dogs, the disk and a 2-ml balloon were placed in the lateral pleural space, and a segment of IVC was ligated at both ends and filled with saline. The dogs were ventilated with fixed tidal volumes, while the positive end-expiratory pressure was changed. The pressures were compared at the end of expiration. For the IVC segment, the pressure gains under four different tidal volumes were significantly greater than one 95% confidence interval of mean value (CIM) = 1.57 +/- 0.16, P less than 10(-4), and for the small balloon, this was the case for three of four tidal volumes (95% CIM for all four volumes 1.13 +/- 0.04, P less than 10(-4)). We conclude that the surface interaction of the lungs with adjacent cardiovascular structures causes appreciable pressure augmentation in those structures during ventilation with the positive end-expiratory pressure.