R. E. Drake

Outflow pressure reduces lymph flow rate from various tissues

We previously reported that the very act of cannulating a lung lymph vessel could alter the unique flow characteristics that existed within the lymphatic before cannulation. We postulated that this phenomenon could hold true for lymphatics draining any organ within the body. Since it is frequently important to know the relationship between the transmicrovascular fluid flux and true lymph flow rate, it would be critical that a cannulated lymphatic vessel have the same flow characteristics as those uncannulated vessels draining the same organ. In order to test our hypothesis we cannulated lymph vessels draining the heart, liver, small intestine, kidney, and skeletal muscle. By altering the lymphatic outflow pressure (normally related to systemic venous pressure) and by using lymphatic cannulas of various resistance, we were able to demonstrate that lymph flow varied linearly with lymphatic outflow pressure in every organ. By increasing transmicrovascular fluid flux and lymph flow rate in each organ we were also able to demonstrate that effective resistance of the lymphatic vessels and the effective pressure driving lymph flow varied as a function of the physical characteristics of the organ under investigation. Characteristic effective resistances of the heart, liver, skeletal muscle, kidney, and small intestine lymphatics decreased by 83, 40, 61, 36, and 50%, respectively. Along with these changes in effective resistance, the effective lymph driving pressure in the same organs varied by 49, 0, 257, 0, and 63%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Cardiac Output on Extravascular Lung Water Estimates Made with the Edwards® Lung Water Computer

The Edwards lung water computer system uses the thermal-dye indicator technique to estimate the lung extravascular fluid volume (EVLW). The authors tested the effect of changes in cardiac output (CO) on EVLW estimates made with the lung water computer in six dogs anesthetized with halothane. Baseline CO was 2.5 +/- 1.3 l/min (mean +/- SD); CO subsequently was increased either by 220% or decreased by 70% by either giving 0.5 mg/kg of isoproterenol or increasing the inspired halothane (1-4%), respectively. There was a significant correlation between the estimated EVLW and CO in each animal (P less than 0.05) such that a 50% decrease in CO from baseline caused an approximately 40% increase in estimated EVLW. Postmortem examination showed that the lungs were not edematous, even though the lung water computer data indicated that severe pulmonary edema had developed at reduced COs. At increased COs, estimated EVLW decreased. The authors conclude that the Edwards lung water computer overestimates lung water, possibly because the thermal indicator diffuses into nonpulmonary as well as pulmonary tissue. The overestimate is greatest at low cardiac outputs.

A model of the lung interstitial-lymphatic system

Our model of the pulmonary interstitial-lymphatic system is based on the assumption that the lung interstitial space can be divided into two compartments. The first compartment (C1) contains the terminal lymph vessels. Increases in the fluid pressure within this compartment, along with increased pressure generated by lymph vessel pumping, cause the lymph flow rate to increase. The lymph vessels run through the second compartment (C2) which we believe represents the perivascular spaces. Increases in the fluid volume of C2 cause the lymph vessels to dilate and this causes lymph vessel resistance to decrease. Normally the lymph flow rate equals the microvascular filtration rate so that lung fluid volume is constant. According to our model, increases in filtration rate cause fluid to collect in C1 and C2. The resulting increase in fluid pressure in C1, increased lymph vessel pumping, and the decrease in lymph vessel resistance in C2 cause lymph flow to increase. Eventually, the lymph flow rises to equal the filtration rate and lung fluid volume becomes constant again. The results of simulations with our model indicate that decreases in lymph vessel resistance are essential for lymph flow to increase substantially as edema develops.

Dog lymph flow in increased capillary permeability states

The lung lymph flow rate (QL) is increased in edema caused by an increase in lung microvascular permeability. This increase in QL could be caused by either a decrease in the effective resistance of the lymph vessels (RL), or by an increase in the effective lymph driving pressure (PL), or by a change in both RL and PL. We estimated PL and RL from the linear relationship between QL and the pressure at the outflow end (PO) of five cannulated dog lung lymph vessels (RL = - delta Po/delta QL and PL = the PO at which QL = 0). We increased lung microvascular permeability by giving the dogs 100 mg/kg of alloxan and found that QL increased from 24.5 +/- 8.9 microliters/min to 112 +/- 41 microliters/min (mean +/- SD). RL decreased from 0.35 +/- 0.12 to 0.11 +/- 0.04 cm H2O min/microliters and PL increased from 8.5 +/- 1.5 to 15.9 +/- 2.7 cm H2O. We then increased the capillary pressures from 18.3 +/- 3.8 to 41.3 +/- 7.3 cm H2O and QL increased to 169.9 +/- 47.8 microliters/min. PL increased by an additional 6.3 cm H2O but RL decreased by only an additional 0.02 cm H2O min/microliters. These results show that the QL vs PO relationship is changed in edema secondary to an increase in microvascular permeability, and that this change can be represented as changes in RL and PL. In terms of these parameters, QL increased in edema as a result of a decrease in RL and an increase in PL.