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Microvascular, interstitial, and lymphatic interactions in normal heart.

G A Laine, H J Granger

The American Journal of Physiology

|October 1, 1985

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This study quantifies fluid exchange forces in the heart, revealing that increased interstitial hydrostatic pressure is key to preventing myocardial edema during venous pressure elevation. Lymph flow significantly rises with pressure.

Area of Science:

Cardiovascular Physiology
Myocardial Fluid Dynamics
Edema Formation Mechanisms

Background:

Control of transmicrovascular fluid exchange in the heart is vital for preventing myocardial edema.
Understanding the forces and flows governing cardiac fluid balance is crucial.

Purpose of the Study:

To quantify absolute values of forces and flows governing fluid balance in the normal heart.
To determine the interrelationships between these variables under control and elevated venous pressure conditions.

Main Methods:

Measured arterial pressure (Pa), coronary sinus pressure (Pcs), interstitial fluid pressure (Pint), plasma protein concentration (Cp), and oncotic pressures (tau cap, tau int).
Recorded interstitial protein concentration (CL) and left ventricular lymph flow rate (Jv).

Related Experiment Videos

Evaluated parameters under control conditions and during graded elevations in venous pressure.

Main Results:

Control values: Pa (125 mmHg), Pcs (7.3 mmHg), Pint (14.9 mmHg), CL/Cp (0.82), Jv (7.0 ml/h).
Elevating Pcs eightfold increased Pint to 50 mmHg and Jv sixfold.
A filtration-independent CL/Cp value for total plasma protein was unobtainable; a washdown value for beta-lipoprotein was 0.04.

Conclusions:

The heart's system relies on a substantial increase in interstitial hydrostatic pressure to limit edema.
A large surface area of myocardial exchange vessels and less sensitive lymphatics contribute to this mechanism.
This highlights the importance of hydrostatic pressure regulation in preventing cardiac edema.