The physiological significance of the endoendothelial fibrin lining (EEFL) as the critical interface in the 'vessel-blood organ' and the importance of in vivo 'fibrinogenin formation' in health and disease.
The author's theory of the endoendothelial fibrin lining (EEFL), first advanced in 1953 and developed by him ever since, localizes the homeostasis between steady fibrin formation and deposition, or 'fibrination', and continuous fibrinolysis in the more or less immobile portion of the plasmatic zone next to the vessel wall. In 1971, the author advanced, in relation to the EEFL, the theory of fibrinogen gel clotting without thrombin action or 'fibrinogenin' formation in vivo. Considerable direct and indirect experimental evidence, secured by the author and by several other investigators, advanced markedly the knowledge of the normal physiology and the pathophysiology of various disease processes involving the vessel wall and blood circulation. The information presented is an extension to that given in the author's recent overview (Clin. Hemorheology 1, 9-72, 1981). It deals both with new data by several investigators including those by the author, as well as with older data from the literature. The author maintained already in 1960 that the blood together with the blood vessels, in which it circulates, constitute 'an entity'. In 1981 he postulated this entity to be a very special organ, named conveniently 'vessel-blood organ', which is ubiquitous and penetrates all other organs and adjacent tissues. The EEFL of the vessel-blood organ is considered by the author as the crucial critical interface between the blood and the vessel wall. It is the primary barrier, followed by the endothelium (comprising the endothelial cells and the interendothelial cement substance which contains or is identical with 'cement fibrin') and the basement membrane for the exchanges between the blood, the vessel wall and its surrounding tissues and spaces. The EEFL acts as anticoagulant, is antithrombogenic, maintains vascular patency and aids cardiac action by decreasing significantly the apparent viscosity of blood, referred to in the literature as the 'Copley-Scott Blair phenomenon'. A new concept of leukocyte emigration traversing the capillary wall is presented, affecting focal fibrinolysis of the EEFL and of fibrin contained in the interendothelial cement substance and in the basement membrane. The physical property of capillary (or vascular) permeability is related to the existence of the EEFL, since, as found by Copley et al, both fibrinopeptides, liberated in the transition of fibrinogen to fibrin, and plasminopeptides, freed in the conversion of plasminogen to plasmin, enhance capillary permeability. Capillary fragility, which is antagonistic to capillary permeability, is in great part due to fibrinolytic action on fibrin as a constituent of the basement membrane.(ABSTRACT TRUNCATED AT 400 WORDS)
D001485:Basement Membrane / Q000378:metabolism; D001808:Blood Vessels / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D002196:Capillaries / Q000033:anatomy & histology; D002199:Capillary Permeability; D004727:Endothelium / Q000502:physiology; D005337:Fibrin / Q000378:metabolism / Q000502:physiology*; D005340:Fibrinogen / Q000096:biosynthesis*; D005342:Fibrinolysis; D005782:Gels; D006706:Homeostasis; D010539:Permeability; D013499:Surface Properties; D013927:Thrombosis / Q000503:physiopathology; D014652:Vascular Diseases / Q000503:physiopathology*
D005782:Gels; D005337:Fibrin; D005340:Fibrinogen; D002118:Calcium