Morphological changes of the myocardium and liver at the background of tetrachlormetane hepatitis and cardiotoxic adrenaline action and their correction with mexidol
Introduction. Under conditions of aggravating anthropogenic toxic effect on the human constitution, combined cardio-vascular pathology and toxic liver damage are common in the medical practice. The liver damage influences both the pathogenesis of cardio-vascular diseases and the efficacy and specifics of the treatment. Therefore, extensive research of the comorbid pathology and the search of effective corrective agents are reasonable.
Objective: To determine the structural dynamics of myocardial damage induced by administration of high doses of adrenaline, against hepatitis tetrahlormetanovoho and effectiveness of the correction of these changes meksydolom.
Materials and methods. Experiments were performed on 36 non-linear white male rats weighing 170-200 g, which were kept on a standard diet vivarium Ternopil State Medical University Horbachevsky.
Toxic liver damage caused intraperitoneally introduced a 50% oil solution of carbon tetrachloride in doses of 1.0 ml / kg. Acute myocardial damage adrenalin fueled by a single intramuscular injection of 0.18% solution of adrenaline hydrotartrate ( "Darnitsa", Ukraine) at a dose of 0.5 mg/kg.
To correct drug is used from the group of antioxidants and antihypoxants - Meksydol (Russian Federation). The drug was administered vnutrishnoocherevyno 50 mg/kg three times - once with the introduction of adrenaline, after 24 and 48 hours after injection of adrenalin hydrotartrate.
Euthanasia was performed using thiopental sodium at 3, 24 and 48 hours from the start of injection of adrenalin on the background of 7 days of acute toxic hepatitis. The animals were divided into 3 groups: 1 - intact animals 2 - infected animals 3 - affected the animals used to correct Meksydol.
For histological studies were liver and heart test animals on day 7 of hepatitis after 3, 24 and 48 hours after administration of epinephrine and after correction Meksydolom in those terms. Samples of fixed in 10% formalin solution, dehidratuvaly in alcohols of increasing concentration and embedded in paraffin-tseloyidyn by conventional methods. Sections were stained with hematoxylin and eosin.
All experiments were performed in compliance with the general rules and regulations of the European Convention for the Protection of vertebrate animals used for experimental and other scientific purposes (Strasbourg, 1986), the General ethical animal experimentation (Kyiv, 2001).
Results. The data analysis found toxic hepatitis developing on the 7th day after intraperitoneal tetrachlormetane introduction to experimental animals. It is morphologically characterized by dystrophy and necrosis of most particle hepatocytes and grows from the centre to the peripheral area thus causing discomplexation of the plates. Concurrently, fibroplastic processes are in progress, leading to sinusoid capillarization and certain ischemia.
Impaired microcirculation as well as growing dystrophic and necrotic changes in the hepatocytes within 3, 24 and 48 hours are the major liver changes at the background of tetrachlormetane hepatitis following the introduction of cardiotoxic adrenaline dose. 48 hours after the introduction of cardiotoxic adrenaline dose at the background of tetrachlormetane hepatitis, progressively disturbed circulation in the liver particles occurs.
Myocardium damage with high adrenaline doses at the background of tetrachlormetane hepatitis primarily involved the damage to the microcirculation stream as well as perivascular and interstitial swelling alongside with necrotic and necribiotic cardiomyocytes’ changes, found 3 hours after adrenaline introduction. The changes were found to grow up to the 48th experimental hour.
Light optic study of the liver at the background of tetrachlormetane hepatitis after the introduction of cardiotoxic adrenaline dose, within 3, 24 and 48 hours following mexidol treatment revealed microcirculation disturbance as well as the liver plates discomplexation and marked histiolymphocytic infiltration of portal tracts.
However, it was not before 48 hours within adrenaline introduction that the mosaic structure of hepatocyte damage due to mexidol effect revealed itself in the liver particle of experimental animals. Myocardium microscopy following adrenaline introduction at the background of tetrachlormetane hepatitis and mexidol treatment within 3, 24 and 48 hours revealed insignificant mexidol effect on the myocardium structure on the 3d and 24th experimental hour. It was not before the 48th experimental hour that the decreasing of necrotizing cardiac hystiocytes and their microfocal form were found.
Conclusions. 1. Tetrahlormetanovyy hepatitis is characterized by structural and functional restructuring of the liver, which shows combined solid fat and hydropic degeneration, necrosis, accompanied by a decrease in functional activity of hepatocytes. Alterativnoe changes hepatocytes ischemia intensified the development and proliferation of lymph histiocytic infiltrate in periportal tracts. 2. Cardiotoxic dose of adrenaline increases metabolic disorders in the liver, increasing degenerative changes of hepatocytes and necrobiotic inhibited and reparation processes. 3. Morphological study of ventricular myocardium of experimental animals after administration of a toxic dose of adrenaline on the background tetrahlormetanovoho hepatitis showed violations of the microcirculation changes of cardiomyocytes and necrobiotic that 48 hours increased. Meksydolu positive influence on morphofunctional state of the liver and myocardium is manifested only after 48 hours from the start of the experiment.