REMODELING PECULIARITIES OF ATRIAL ARTERY IN CONDITIONS OF POSTRESECTION PORTAL HYPERTENSION

Abstract

It is known that structural and functional changes in the heart can be caused by various changes in hemodynamics, which include post resection portal hypertension. It should be noted that the structure of the atrial arteries in postresection portal hypertension has not been studied enough. The purpose of the study is to investigate the peculiarities of atrial artery remodeling in the conditions of post resection portal hypertension. Material and methods. The arteries of the atria of 34 male rats, which were divided into 2 groups, were studied by a complex of morphological methods. The group 1 consisted of 15 experimental intact animals; group 2 included 19 rats with post resection portal hypertension, which was simulated by removal of the left and right lateral lobes of the liver. Euthanasia of rats was performed by bloodletting under conditions of thiopental anesthesia one month after the start of the experiment. The outer and inner diameters of the atrial arteries of medium and small calibers, the thickness of the media and adventitial membrane, Wagenworth and Kernogan indices, the height of endothelial cells, the diameters of their nuclei, nuclear-cytoplasmic ratios in the studied endothelial cells, and relative volumes of damaged endotheliocytes were measured. Quantitative indicators were processed statistically. Results. It was established that in the conditions of post resection portal hypertension the arteries of small caliber of the atria changed more markedly. The outer diameter of these vessels of the left atrium increased by 4.2 %, the right - by 3.3 % (p <0.05), the thickness of the media and the adventitial membrane increased by 12.58 % and 45.7 % and respectively 11.8 % and 33.7 % (p <0.001, their lumen decreased by 13.5 % and 10.7 %, respectively) (p <0.001). The Wagenworth index of small caliber arteries increased markedly, and the Kernogan index decreased. Nuclear-cytoplasmic ratios in endotheliocytes of small arteries of the left atrium were changed by 7.6 %, and in the right - by 6.1 % (p<0.01), the relative volumes of damaged endotheliocytes respectively increased by 7.6 and 5, 2 times (p <0.001). Damage to a significant number of endothelial cells led to their dysfunction, blockade of NO synthase, decreased NO synthesis, activation of its degradation, which exacerbated spasm, narrowing of vessels and significantly impaired blood supply to the body and complicated by hypoxia.Histologically at post resection portal hypertension, there were pronounced vascular disorders, plethora, dilation of mainly venous vessels, perivasal edema and stroma edema, foci of dystrophic, necrobiotic, apoptotically altered endotheliocytes, stromal structures and cardiomyocytes. There was also swelling of endothelial cells, their dystrophy, necrobiosis, desquamation and proliferation. Conclusion. Post resection portal hypertension leads to severe remodeling of mainly small atrial arteries, which is characterized by thickening of their wall, narrowing of the lumen, changes in the Kernogan and Vaughanworth indices, endothelial cell damage, endothelial dysfunction, decreasing of organ blood supply, hypoxia, trophic disorders, dystrophic and necrobiolic changes of tissues and cells, infiltration, sclerosis.