Pulmonary microvascular fluid flux in a large animal model of sepsis: evidence for increased pulmonary endothelial permeability accompanying surgically induced peritonitis in sheep.

To characterize some of the remote effects of systemic sepsis on the lung, we evaluated changes in pulmonary microvascular fluid flux before and during sepsis secondary to a peritoneal focus of inflammation in sheep. We induced peritonitis by cecal ligation, perforation, and devascularization. During a subsequent 72-hour study period, both the mean blood pressure and the pulmonary capillary wedge pressure were unchanged, while the cardiac index increased slightly. The PaO2 fell by 48 hours (98 +/- 8 to 84 +/- 10 mm Hg; p less than 0.05) (mean +/- SD) and subsequently remained low throughout the experiment. Simultaneously, pulmonary lymph flow increased by 24 hours (11.5 +/- 4.9 to 26.7 +/- 13 ml/hr; p less than 0.05) and remained elevated throughout the experiment while [L/P] total protein ratios remained unchanged at 24 hours (baseline: 0.59 +/- 0.15 at 24 hours: 0.65 +/- 0.16). Morphologic examination of the lung showed that this model of peritonitis was characterized by neutrophil emigration into the pulmonary interstitium by 24 hours and interstitial edema by 48 hours. Therefore this model of bacterial peritonitis in sheep demonstrates that one of the remote effects of surgically induced systemic sepsis is an increase in permeability of the pulmonary microvascular membrane.