Lung fluid and protein flux during postoperative sepsis.

Pulmonary microvascular injury during sepsis after injury appears to be amplified with plasma fibronectin deficiency, but the degree of injury relative to the extent of sepsis has not been defined. We evaluated pulmonary vascular permeability in sheep as influenced by various levels of postoperative Pseudomonas sepsis during a period of plasma fibronectin deficiency. The hemodynamic response to Pseudomonas was very similar regardless of the intensity of septic challenge and characterized by systemic arterial hypotension, decreased cardiac output, and pulmonary arterial hypertension. In contrast, increased pulmonary microvascular permeability was observed with increments in the bacterial challenge. Thus, lung protein clearance (LPC) or so called pulmonary transvascular protein clearance (TPC) used as an index of lung vascular permeability was 9.1 +/- 1.9 ml/hr, 15.1 +/- 1.7 ml/hr, and 19.3 +/- 3.0 ml/hr 2 hr after low (3 X 10(9) i.v.; 1 X 10(10) i.p.), medium (3 X 10(9) i.v.; 3 X 10(10) i.p.), and high (5 X 10(9) i.v.; 5 X 10(10) i.p.) dose Pseudomonas challenges, respectively. Thus, the extent of the altered pulmonary microvascular integrity in sheep during sepsis after surgery in the presence of fibronectin deficiency is dependent on the degree of bacterial sepsis. In addition, infusion of cryoprecipitate was an effective means of reversing the plasma fibronectin deficiency. Accordingly, this may be used as a model to investigate the mechanism of altered lung fluid balance during postoperative septic shock and the effect of fibronectin on this response.