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Redistribution of lectin receptor sites in the mam-lymphatics of human extremities in primary and secondary lymphedema in comparison with normal lymphatics has been investigated using conjugates to peroxidase of LCA, PNA, RCA, SBA, WGA and LAA. Chronic lymphedema caused no essential differences in lectin binding to tissue structures of intima and adventitia: endotheliocytes were strong reactive both with LCA, PNA, WGA and LAA; all lectins used bound fibrillary structures in subendothelial layer and adventitia. On the opposite, tunica media of main lymphatics in primary lymph stasis displayed accumulation of LCA-, PNA-, SBA- and LAA-binding deposits round smooth myocytes. When PNA used, the appearance of a specific "wide loop shaped reticulum" within lymphatics media in lymph stasis was observed. We consider, that lectin receptor sites accumulation phenomenon reflects some changes in smooth myocytes metabolism, possibly caused by dystrophia of these cell population with consequent incomplete glycosylation of synthesized glycopolymers.

The possibility of isolating the lymphatic system from the circulatory system by draining the thoracic lymphatic duct and infusion of different agents (Evans blue, kanamycin, staphylococcus, sodium thiopental and potassium chloride) to the peripheral lymphatic vessels was examined in 22 fresh cadavers and 65 mongrel dogs. The release of the agents to the blood vessels did not occur if the volumetric consumption of intralymphatic infusion did not exceed 0.3 ml/min per peripheral vessel. Both the outflow and toxicity of the lymph from the thoracic duct increased while conducting the perfusion of the lymphatic system by autolymph.