Effect of positive end-expiratory pressure on leukocyte transit in rabbit lungs.

Abstract

Previous experiments in humans and animals have shown that neutrophils (PMN) are delayed in the lung by the inhalation of cigarette smoke. Others have shown that cigarette smoking raises airway resistance, and it follows that this will increase the expiratory time constant of the airways. When the expiratory time constant of the airways exceeds that of the chest wall, alveolar pressure will rise and compress alveolar capillaries. To determine the effect of alveolar compression on PMN retention, we measured the arteriovenous (A-V) difference for leukocytes across the lung and determined the retention of 51Cr-labeled PMN in the lungs of anesthetized ventilated rabbits. The results show that the application of positive end-expiratory airway pressure (PEEP) produced an immediate difference for PMN across the lung, which disappeared in approximately 3 min when PEEP was continuously applied. This effect was attributed to alveolar compression rather than reduced cardiac output, because a similar A-V difference for PMN was observed in separate experiments in which cardiac output was maintained by vascular expansion during PEEP. The results also show that, when PEEP was continuously applied for approximately 30 min, it failed to increase the percent retention of either inactivated (PEEP = 14 +/- 2% vs. non-PEEP 16 +/- 3%) or activated (PEEP = 62 +/- 7% vs. non-PEEP 63 +/- 6%) 51Cr-PMN. We conclude that the application of PEEP traps PMN in compressed alveolar capillaries, creating an immediate A-V difference that disappears as blood flow is redistributed to vessels that are not compressed by PEEP.(ABSTRACT TRUNCATED AT 250 WORDS)