For further clarification, we provide Rossing’s findings on the matter:
1. the intravascular masses of albumin and immunoglobulin depend on the amount of synthesis
and the amount of fractionated catabolism;
2. the ratios of intravascular masses to the total masses depend on the amount of
transcapillary escape and on the amount of extravascular return;
3. the amount of transcapillary escapes are inversely related to the molecular weights of the
proteins; the amount of transcapillary escape increases with the filtration pressure in the
vessels, i.e. with the loss at micro vessel level, as seen in diabetes mellitus;
4. the amount of extravascular return reflects the lymphatic protein transport and is inverse to
the extravascular transit time. It is of the same magnitude for albumin, lg.G, and perhaps a
bit less for lg.M;
5. the extravascular transit time includes a wide series of transit times: short (liver, kidneys,
lungs), long (skin, muscles, with maximum deposit of extravascular proteins);
6. in most cases of hypoproteinemia, the amount of intravascular/extravascular plasmatic
protein distribution changes in favor of the intravascular space;
7. the extravascular pathological build-up of plasmatic protein occurs in a few diseases, and
when the transcapillary escape increases without a corresponding increase in the amount of
lymphatic return. This can be seen in cirrhosis with ascites, in untreated myxedema and in
some types of cancer, particularly those with hepatopathy and ascites. If anything, the
extravascular build-up of plasmatic protein will occur in the tumoral and post-operative tissue
in the wounds.
The main function of the lymphatic system is therefore to allow its penetration by the previously
mentioned molecules, prevent escape, and encourage progression.
By way of the capillary filtration, protein molecules and water are plentiful in blood circulation,
thus causing a build-up of liquids osmotically linked to the protein in the interstitial tissue.
The liquid leads to an imbibition of the tissue, stretching the endothelial cells of the initial
lymphatics and further opening the lymphatic interendothelial junctions.
Other movements intervene in keeping the junctions “open”:
• muscular movement;
• rhythmic contractions of the arterial vessels;
• the negative intrathoracic pressure;
• the cells and any other elementary corpuscles that are pushed through the open
junctions in the initial lymphatics.
During their transit, these corpuscles act like dilators, keeping the passage free through the
junction of the initial capillary lumen. In the most active areas of the body, the products of
cellular metabolism increase blood flow and the capillary permeability, so liquid contained in the
interstitial tissue increases further, and its pressure keeps the input routes accessible to the
lymphatic capillaries.
An increase in local tissue pressure follows this initial stage, caused by muscular contraction
that compresses the initial lymphatics, and therefore pushing the lymph to close the intercellular
junctions. In this phase, a certain quantity of water spreads out from the lymphatics and the
lymph itself becomes more concentrated than the interstitial liquid.
The higher compression releases the system from fibrils attached to the lymphatic endothelium.
The lymphatics that have been compressed like this will obviously be smaller with lower
diameters, being adhesive endothelial cells and therefore overlapping with the junctions
hermetically closed.
At this point, the third phase begins: a further compression on the initial lymphatics pushes the
lymph through the first valve, the sudden lowering of pressure means that the lymphatics
expand again, and the intercellular junctions open up again.
This mechanism is called the “CASLEY-SMITH lymphatic pushing pump”. Intercellular lymphatic
junctions have been defined as “aspiration valves” while the first lymphatic valve is known as
the “escape valve”.