ATHEROSCLEROSIS

ATHEROSCLEROSIS IN ASPECT OF RECONCILIATION
Author: dr.med. professor Kilessa V. V.

Therapy and family medicine chair. Faculty of post degree education. Crimean state medical university by Georgiyevsky S.I., Ukraine, Simferopol city.

ABSTRACT
This review presents the working hypothesis that roots of atherosclerosis are in the phylogenetic aspect. Excessive loadings on a vascular aorta mesenchyma and coronary arteries force it to come back to the remote philohystogenetic past after exhaustion of phylogenetic newer potentials with initiation of angioblastic hematosis type.
Reconciliation intensively discussed in embryology and histology can't be limited with antenatal period of development only, it stretches for all ontogenesis. The material aspect of problem is an inhibition of tissue reconciliation in ontogenesis. The material aspect of problem is an inhibition of tissue reconciliation in ontogenesis.

Keywords: atherosclerosis, reconciliation, vascular mesenchyma.

Originally, formation of the theory is a consequence of the phenomena which couldn't be explained with the settled views. New formulated theory still has no material realization, or will be never realized, because of various circumstances. But, in any case, the theory is capable to create system of new coordinates.
Anichkov N. N. and Halatov S. S. theoretical position "there is no atherosclerosis without cholesterol", formulated in 1913-1915 today realizes in the form of effective hypolipodemic therapy with Hydroxymethylglutaryl-CoA reductase inhibitors. The "infiltrative and inflammatory" theory of R.Virchow (1856) and "encrusted-thrombus gene" theory of K.Von.Rokitansky (1852) realize in system treatment with acetylsalicylic acid, anticoagulants and dezagree-gants. But it is necessary to admit fact, that atherogenesis is extremely difficult process, and any theory reflected and will reflect nevertheless any private aspect of аtherogenesis. And today remain inexplicable some important aspects:
1. Stereotype of dislipidimia process regardless of character;
2. Process locality;
3. In the conditions of a permanent system hypercholesterolemia, dislipidemia and hypertrigliceridemia, atherosclerosis, nevertheless is local pathology; it never developing in small arteries, arteriolas, veins, venules, capillaries, lymphatic vessels;
4. Atherosclerosis development in the conditions of a normal lipidic exchange;
5. Under- endothelial localization of cell-containing atherosclerotic lumps;
6. Existence of atherosclerotic formations of various maturity degree;
7. Locality of antheronecrosis, atherotrombosis and atherocalcinosis;
8. Lack of atherosclerotic lumps in a.pulmonales in the conditions of bad lipidic exchange with system character in normal level of arterial pressure in it, but atherosclerosis development in a pulmonary artery in pulmonary hypertension and not changed lipidic exchange;
9. Existence of foamy cells in lipidic cell-containing atherosclerotic formations is absolutely not typical;
10. Atherocalcinosis;
11. Development of atherosclerosis after aorta-coronary shunting in shunts and continuation of atherosclerosis progression after stent’s implanting;
12. Wavy course of pathology.
According to the opinion of I.V.Davydovsky I.V. who wrote in 1966 - «Atherosclerosis represents the natural and specific phenomenon connected with age. The quantitative and qualitative aspects of this phenomenon are the time of its approach, but intensity of process can't be individually regulated". Earlier in 1961 Davydovsky I.V. specified – «Roots of atherosclerosis consign to the remote phylogenetic past on the one hand. Atherosclerosis is observed in birds and mammals, being as a rule, asymptomatic. On the other hand, the same roots are closely connected with ontogenesis, with age and, in general, with life expectancy. All of this considerably destroys purely medical nosological aspect in relation to atherosclerosis". Being guided by Davydovsky's logic, it is necessary to consider that problems of atherogenesis should be solved, as far as possible not only in the plane of phenomenon, but in aspects of philogenesis, uniting people, mammals and birds. Gekkel-Müller's biogenetic law says: "Ontogenesis is fast and short repetition of philogenesis". But, what if to look at Gekkel-Müller's biogenetic law «completely"? Differently, what is the biological base for the post antenatal period of life? A.A.Zavarzin's theory – "The theory of overlapping and evolutionary dynamics of cell" is the continuation of the biogenetic Gekkel-Müller’s low. According to this theory:
1. Identical functions in all fauna make identical structures;
2. All types of fauna have histological structures developing according to the same plan, sufficiently, irrespective of animal position in system and his organization as. Thus, histological structures can be located in the parallel ranks in all phylogenetic ranks with identical members;
3. In complication process of histological structure the number of elements increases, but their structure becomes simpler.
What "parallels" are in atherosclerosis?
It is known that atherosclerosis develops in an aorta and coronary arteries.
The dynamics of occurrence and atherosclerosis development in population in various temporary intervals: According to Vikhert A.M. and Drbkova I.P (1985) lipidic spots and strips in chest and belly departments of aorta are in children till 10 years old in 92,2% of cases, from 10 till 16 years – in 100% of cases. In the age of 25 years old, the area of aorta lesion reaches 30-50% from its surface. According to A.M.Vikhert (1985) atherosclerotic lesion are found in 65% (men) and 62% (female) in coronary arteries in the age of 10-19 years. On the third decade of life only 11-12% men and women have no atherosclerotic changes. And 46% (men) and 33% (female) have fibrous lesion, and in 35-45 years old atherosclerotic lesion are found and in brain arteries. On the fourth decade of only 4% of men and 7% of women have no atherosclerotic changes, but 3-4, 5% have atherocalcinosis. On the fifth decade of life there are no atherosclerotic lesions in 1% of men and 4% of women only. On the sixth decade of life there are no affected coronary arteries.
Athecalcinosis in coronary arteries begins after 30 years in men and after 40 years in women. Atherocalcinosis is an exclusive consequence of atheronecrosis and atherothrombosis. Atherocalcinosis is a morphological unit and has nothing common with other independent nosological unit – mediocalcinosis of Mönckenberg J.G. – diffusion calcinosis of middle coat vessel, damaging large arteries of pelvis, the bottom extremities, belly aorta, elbow and humeral arteries, but not damaging coronary, brain, axillary and popliteal arteries (Vikhert A.M. and co-authors 1970).
Proceeding from Vikhert A.M. statistical large-scale epidemiological researches, it follows that aorta and coronary arteries atherosclerosis represents not a casual disease, but certain regularity of all-biological property. So what concrete all-biological lines, besides the blood vessel are inherent in aorta and coronary arteries in human, mammal, birds, reptiles and fishes? The answer is – angioblastiс hematosis in human, mammals, birds, reptiles and fishes in aorta development, which is source of cell's hemopoesis.
In early stages of histogenesis the quantity of cellular elements isn’t many; their traffic is provided by liquid circulation in intercellular cracks and channels – "before" vessel microcirculation. Some channels limited by mesenchyma cells contain cells of an erithroid row in a look of "blood islands".
Functioning of "blood islands" in yolk sac begins from 19 days in human. Till the 22th day of the embryonic period the haematogenic cells get into mesoderm tissue of developing hearts, aortas, and arteries – it is angioblastic type of hematosis. Neogenic erythrocytes and leukocytes are moved not directly in vessels, but get on interweft substance on the periphery and go in circulation (Malyshevskaya V.A. 1971; Fruntash N. M., 1982; Bobrik I.I. and co-authors, 1991). On the 6th week of the embryonic period, the activity of hematosis in yolk sac decreases, but completely angioblastic hematosis type stops only in IVth month of the pre-natal period, replaced with hepatic hematosis type and then with myeloid hematosis which completely functions till the birth (Kassirsky I.A., Alekseev G. A., 1970).
The similar hystogenotic aorta development plan with one-stage existence of angioblastic hematosis type is in mammals, birds, reptiles and fishes only with a difference of hystogenesis terms. However, the angioblastic hematosis type ( besides hematosis is in a kidney, spleen, an intestine wall) is in bony fishes throughout all life, without being replaced with any other type, and isn't transformed to marrowy type – the bone skeleton in fishes has nothing common with homopoesis (Shchelkunov S. I., 1977). "Blood islands" are located on a circle of vessels at various distances from each other. This sort acts on cuts of a bringing branchiate artery and its coronary arteries. The centers of hematosis have the various size and outlines, they are scattered in a disorder. Many of them are so thick that their cellular structure isn't looked through. From a vascular lumen the hematosis centers are blocked by endothelium. Its structure differs from the endothelium sites lying between the haematogenic centers. Features of endothelium are cells of smaller and endothelium is friable with holes, but cells withdrawal from blood islands in circulation happens not directly in vessels lumen, but on the periphery getting on intercellular substance, going to microcirculation. There are no granular leukocytes in the hematosis of fishes (Shchelkunov S. I., 1977). Changes of an endothelial lining over atherosclerotic lesion in human are described in detail by Walski M. (2002) according to scanning electronic microscopy. Endothelial cells are cubic, covered with numerous microfibers, with cup on a calls surface with violation of endothelia surface. Platelets and leukocytes are fixed on a surface of such cells. Cubic endothelium was earlier observed by Taylor K.E. et al. (1989) in monkeys with the experimental atherosclerosis induced by a diet with fats. Cubic endothelium was also observed by Ross R. (1993) in human. These changes of endothelial cells form Taylor K.E. et al. (1989) and Ross R. (1993) connected with accumulation under it of foamy cells. Walski M. et al. (2002) consider that cubic endothelia represents a certain phenotype an endothelia.
It was described the relapse of angioblastic hematosis type in reptiles (snakes) in spring (Zavarzin A.A., 1953). Possible shifts of hemopoesis types in the post embryonic period of life in birds aren't described in literature; it is known that in the embryonic period the angioblastic hematosis is replaced by myeloid type, passing hepatic hematosis type (Kassirsky I.A., Alekseev G. I., 1970).
The dynamic of homopoesis in the post-natal period in human described concerning of a myeloid hematosis zone shift in various years of life. Hemopoesis in a diaphysis of tubular bones stops till the sexual puberty, the intensity of hemopoesis in epiphysis of tubular bones sharply decreases till 20-30, the intensity hemopoesis in edges decreases for 80% till 70, in a breast for 40%, in a backbone for 20%. Stereotypic easing and the termination of hematosis is a consequence of transformation of red marrow in yellow. The reason for this process isn't known (Vorobyov A.I., 1998). The human has a transformation of yellow marrow in the red in leucosis (Kassirsky I.A. Alekseev G. I. 1970). The transformation of yellow marrow in the red in dogs observed Parkhon K.I. and Kahane M.C. (1928) under the influence of bloodletting and haemolytic anemia (Kahane M. S., Melnik B. E. (1982)) .

Vascular mesenchyma in the post-natal period.

Vascular mesenchyma in the post-natal period is presented by Langassovs layer intims of an aorta and lasts without interrupting through a layer of adventitial capillary cells to veins and always settles down on a course of capillaries and post-capillary veins which are a source endothelium and connecting tissues (Zavarzin A.A., 1953) ; Shchelkunov S. I. 1977). Whether the vascular mesenchyma in the post-natal period is active? It is enough to tell that lipidic atherosclerotic lesions "sprout" by the new capillaries combined with v.vasorum and natural replacement of endothelial cells happens throughout all life.

Cellular elements of lipidic atherosclerotic lesions in tissues.

The most characteristic features of cellular elements colonies.
1 . Developing cellular elements are presented by colonies (from 50 cages and more in proliferation sites).
2 . High spontaneous and induced by some anti-genes "daily" speed of cells elements formation and the same high speed of a total cells disappearance.
3 . Lack of observed mitoses in colonies.
4 . Anti-genes of microorganisms and ultra-violet radiation Stimulating have effect of cellular elements formation.
It is rather difficult to consider phylogenetic aspects of atherosclerosis, as well as other diseases. The literary actual material is separate, executed in various temporary intervals, it relied on certain technical capabilities and existing ideological stereotypes. We have only basic researches concerning angioblastic hematosis type by A.A.Maksimov at the beginning of XXth century.
It is enough to tell that in angioblastic hematosis type, micro phagocytes instead of macro phagocytes are more phylogenetic structures with ferriferous cells.
But in any case it is possible to make a working hypothesis that roots of such natural and specific phenomenon are in the phylogenetic aspect. Excessive loadings on a vascular aorta mesenchyma and coronary arteries force it to come back to the remote philohystogenetic past after exhaustion of phylogenetic newer potentials with initiation of angioblastic hematosis type. Organism development – movement on a phylohystogenetic ladder up, aging – movement down. Movement goes like a "breakthroughs". Various phylohistogenetic steps of the same kind are among themselves in unity and contradiction.
The fight of phylogenetic more ancient genes with phylogenetic newer is realized through immunity.
Evolution and Involution is inherent in each tissue. And it is projected not only on mature tissue, but also on its cambial component. Apparently, human hereditary structures have not only "today", but also all historical course of histological evolution and involution of types. It would be better to consider tissue involution and evolution from phylogenetic positions.
Reconciliation intensively discussed in embryology and histology (Severtsov A.N. 1949) can't be limited with antenatal period of development only, it stretches for all ontogenesis. The material aspect of problem is an inhibition of tissue reconciliation in ontogenesis.