Increased plasma oncotic pressure inhibits pulmonary fluid transport when pulmonary pressures are elevated.

Hydrostatic and oncotic pressures are the primary determinants of fluid movement across the pulmonary vascular membrane. The precise role of oncotic pressure in regulating transvascular fluid exchange especially when hydrostatic pressure is high is not known. Awake, adult sheep were instrumented for pressure monitoring and the collection of pulmonary lymph. A left atrial (LA) balloon catheter was utilized to control LA pressure. Statistically significant increases in lymph protein flux were seen with infusion of saline and elevated pulmonary microvascular pressure (Pmv) over elevated Pmv alone (15.3 +/- 1.23 versus 11.2 +/- 1.09 mg/min) concomitant with a decrease in plasma colloid oncotic pressure (COP) (14.9 +/- 0.5 versus 16.9 +/- 0.5 mm/Hg). The protein flux seen with elevated Pmv and saline infusion was blunted when plasma was infused (13.8 +/- 1.58 mg/min) and the plasma COP augmented (18.1 +/- 0.05 mg Hg) but was not statistically different. We conclude that under conditions of stable membrane permeability and elevated Pmv, the plasma COP appears to be an important mechanism for protection against pulmonary edema.