Fibrin foam

Bering, E.A. (1944) C4iemical, clinical and immunological studies on tire products of human plasma fractionation. XX. The development of fibrin foam as a hemostatic agent and for use in conjunction tvith human thrombin./ Clin. Iinvsl.. 23, 586-589. 

For some purposes the principal fractions can be employed as such. For instance. Fraction I is a suitable starting material for the preparation of fibrin foam and film and Fraction V, after a single reprecipitation, as already described, can be dissolved in a solution containing a suitable stabilizing agent, such as the sodium salt of aceiyl-tryptophan at 0.04 M, to give a concentrated solution of high stability which has found extended clinical use. However for many purposes further subfractionation of the principal fractions is essential, in order to obtain separately the many important components they contain. 

This is a dry sponge of human fibrin prepared by elotting a foam of human fibrinogen solution with human thrombin. It is then freeze-dried, cut into shapes and sterilized by dry heat at 130°C for 3 hours. Before use, it is saturated with thrombin solution. Blood coagulation occurs in contact with the thrombin in the interstices of the foam. 

The accumulation of apo(a) in the aorta wall and in saphenous vein bypass grafts in relation to Lp(a) levels was recently demonstrated (C14, R3). Subsequently, the preferential deposition of extracellular apo(a) in atherosclerotic lesions of aortic and coronary artery tissue, in conjunction with the intracellular localization of apo(a) in macrophage-derived foam cells, has been the focus of a number of studies (N6, P7, S34, S35, W17). These careful studies also demonstrated the avid binding of Lp(a) to extracellular matrix components and the colocalization of fibrin and apo(a) in atheromatous lesions (N8, W16). 

To explain the relationship between Lp(a) concentrations and risk of atherosclerosis, several hypothesis could be brought forward first, Lp(a) affects the metabolism of cholesterol and LDL secondly, Lp(a) plays a role in foam-cell and plaque formation thirdly, Lp(a) interacts with the activation of plasminogen to plasmin, the key step in the fibrinolytic system (L10, M27). Such activation can occur in two different localizations, i.e., on fibrin and its proteolytic residues, and on the surface of endothelial and monocytic cells. 

We have recently presented ascorbate deficiency as the primary cause of human CVD. We proposed that the most frequent pathome-chanism leading to the development of atherosclerotic plaques is the deposition of Lp(a) and fibrinogen/fibrin in the ascorbate-deficient vascular wall. - In the course of this work we discovered that virtually every patho-mechanism for human CVD known today can be induced by ascorbate deficiency. Beside the deposition of Lp(a) this includes such seemingly unrelated processes as foam cell formation and decreased reverse-cholesterol... 

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