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Our studies allowed us to establish that simulating coarctation of aorta in laboratory animals results in tone reduction of vessels carrying blood to the liver and from it and a subsequent development of their intima atrophy. In spite of that fact the number of vessels containing intimal musculature, muscularelastic sphincters and polypoid pulvini in the arterial bed flow increases and in the major outflowing veins, on the contrary, thinning of their muscular tori takes place. Appearance and functioning in the hepatic vessels of adaptive formations contributes to keeping up homeostasis at the microcirculatory level. With cardiac decompensation decreasing because of venous plethora, hypotonia and atrophy of the intima of the vessels responsible for the blood inflow to the liver and the outflow from it progress. Besides, the number of arteries and the rate of development of arteries with adaptive smooth muscle formations in the arteries, as well as in hepatic veins with muscular tori decreases dramatically. The reason of compensatory reaction failure is a long-term hypoxia leading to vessel and their adaptive formation sclerosis. The consequence of the exhaustion of the above-mentioned mechanisms is development of perisinusoidal fibrosis and depression of the transcapillary metabolism.

Structural Changes of the Liver Vessels in Compensated and Decompensated Coarctation of Aorta in Experimental Studies