Sustained venous occlusion plethysmography: Effects on protein osmotic pressure, intravascular volume, and capillary filtration

Abstract

In six acutely anesthetized, mechanically ventilated mongrel dogs, we evaluated sequential changes (over 30 minutes) of sustained forelimb venous occlusion (occlusion pressures 30 to 65 mm Hg) on strain gauge dimension, radionuclide blood pool emissions, and venous, subcutaneous, and intramuscular pressures (Wick technique). Forelimb intravascular volume (assessed by decay-corrected radionuclide counts/unit time) changed by a mean of only −1.2 ± 2.8% (±SEM) and thus was ignored in the calculation of filtration rate. Forelimb (distal to the occlusion site) hematocrit changed insignificantly (45.3 ± 1.4% at the control point to 48.2 ± 1.1% at 30 minutes), colloid osmotic pressure rose slightly (19.4 ± 1.4 mm Hg to 22.7 ± 1.6 mm Hg, p < 0.01), and serum osmolality remained unchanged. During sustained occlusion, venous pressure remained constant, subcutaneous pressure rose (−0.7 ± 1.2 mm Hg control vs 0.5 ± 1.4 mm Hg at 30 minutes, p < 0.05), and intramuscular pressure also rose (−0.4 ± 1.1 mm Hg to 2.6 ± 1.6 mm Hg, p < 0.01). Driving pressure, defined by venous pressure - oncotic pressure less the average of intramuscular and subcutaneous pressure declined slightly over the 30 minutes of the study (27.8 ± 5.5 mm Hg to 23.3 ± 1.3 mm Hg, p < 0.05). The relationship between either the initial driving pressure or the initial difference between venous and protein osmotic pressure correlated ( r = 0.83 for both) well with strain gauge estimates of capillary fluid flux (evaluated by the change in forelimb strain gauge dimension over time and given as cc/100 cc forelimb volume/min). There was a poorer correlation when intravascular venous pressure alone was used ( r = 0.69). We conclude that protein osmotic pressure and venous occlusion pressure directly alter capillary filtration rate as determined by strain gauge dimension changes. While predictable changes in the tissue pressure and intravascular osmotic pressure occur, the major driving force constitutents (occlusion pressure and initial protein osmotic pressure) change only slightly over 30 minutes of occlusion. Little change in intravascular volume was found, so that strain gauge dimension change (once venous engorgement has occurred) did not reflect subsequent changes in intravascular volume.