Key result
Elevated lymphatic outflow pressure increases myocardial interstitial hydrostatic pressure by ~13 mmHg, reducing microvascular filtration.
Why the study?
The regulation of myocardial microvascular filtration rate by changes in interstitial fluid pressure and lymph flow was not well understood.
Answers are grounded in this paper and cite their sources.
Myocardial interstitial pressure may modulate microvascular filtration; extends lymphatic control of Starling forces in vivo but leaves clinical translation open.
We hypothesized that myocardial microvascular filtration rate (Jv) could be manipulated by varying end-diastolic myocardial interstitial hydrostatic (P(int)) pressure. Dogs under general anesthesia were instrumented with intramyocardial capsules to measure P(int) and with prenodal myocardial lymphatic trunk cannulas and superior vena caval balloon-tipped catheters to manipulate myocardial lymph flow. Because, for a given surface area, the lymph-to-plasma protein concentration ration (CL/CP) varies inversely with JV, CL/CP was utilized as an index of changes in JV. When lymphatic outflow pressure (P0) was elevated to abolish lymph flow and force myocardial interstitial fluid volume to expand, P(int) rose significantly from 15.0 +/- 0.8 to 27.6 +/- 1.0 mmHg and CL/CP increased significantly from 0.75 +/- 0.04 to 0.85 +/- 0.04, indicating a decrease in JV. When P0 was lowered and lymph flow resumed, P(int) and CL/CP decreased significantly to 15.3 +/- 0.9 mmHg and 0.75 +/- 0.04, respectively, indicating an increase in JV. We conclude that myocardial microvascular filtration rate may be modulated by changes in P(int) resulting from alterations in myocardial interstitial fluid volume secondary to variations in lymph flow from the heart.
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Stewart et al. (1996) studied this question. Elevation of lymphatic outflow pressure (P0) vs. Baseline (normal or lowered lymphatic outflow pressure) was evaluated on Myocardial interstitial hydrostatic pressure (P(int)) in mmHg. Elevating lymphatic outflow pressure significantly increased myocardial interstitial hydrostatic pressure from 15.0 to 27.6 mmHg and CL/CP ratio, decreasing microvascular filtration.
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