Activation of complement and neutrophils increases vascular permeability during air embolism.

Pulmonary air embolism occurs in diving and aviation during acute pressure reductions and in clinical complications. Undoubtedly physical obstructions play a role, but bubbles in blood can produce a number of indirect effects leading to tissue injury. In the present study, we investigated the involvement of the complement system and polymorphonuclear leukocytes (PMN) in altering segmental vascular resistance, lung weight gain, and filtration coefficient (Kf), by using isolated and perfused rat lungs. After establishing ventilation with air and 5% CO2, the lung was removed en bloc and suspended in a humidified chamber at 37 degrees C. Lung weight and arterial and venous pressures were monitored continuously. The buffered salt perfusate contains 4% Ficoll for osmotic balance. We used four series of perfusates containing 20% of: a) normal plasma; b) decomplemented plasma (from donor rats pretreated with a cobra venom factor); c) normal plasma and PMN at 2 x 10(6).ml-1; and d) decomplemented plasma and PMN at 2 x 10(6).ml-1. Pulmonary air embolism, air bubbles introduced through the pulmonary artery, increased pulmonary arterial resistance and pulmonary arterial blood pressure. The lung weight and lung water content were greater than those in the control groups. Air embolism increased vascular permeability, which was shown by an elevated Kf after air infusion. After air embolism, Kf was 0.63 +/- 0.05 g.min-1.cm H2O-1.100 g-1 in lungs perfused with both PMN and plasma, which was significantly greater than those in lungs perfused with either plasma (0.49 +/- 0.04), decomplemented plasma (0.44 +/- 0.03), or PMN and decomplemented plasma (0.47 +/- 0.03). These results demonstrated that air embolism increases vascular permeability of the lung by pulmonary hypertension, activation of the complement, and activation of PMN.