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HEART FAILLURE  STRUCTURAL BASIS  IN EXPERIMENTAL ATHEROSCLEROSIS

Kakauridze N., Kipshidze N., Tsagareli Z., Gogiashvili L.
National Center of Therapy, Institute of Experimental Morphology

The most important point of the problem is  that  atherosclerosis proceed  saliencies and reveals  in the developing clinical  stage.

               Whereas, the pose of diagnosis of atherosclerosis is impossible in preclinical stage by absents of adequate morphological (Gold standard) means in vivo, the experimental model of atherosclerosis play an

importante role for pathogenesis and treatment studies of disease actually.

               The aim of the work is to study morphological, ultrastructural basis of heart failure from an early period of atherogenesis (14 days) to its late period (6 months) in experimental atherosclerosis (80 rabbits with initial weight within 2.5-3 kg), felled into two groups: I group-control animals, II group of experimental atherosclerosis(by Anichkov method: 0.3 g /kg cholesterol). In dynamics blood was sampled from an otic vein of each animal for biochemical analyses and total cholesterol  was assessed by Ilka method, while for apo- B-lipoproteins (b-Lp), Burstein method was used. For establishing the degree of atherosclerotic damage (by Avtandilov’s planimetric method) aortas specimens  were dyed with Sudan in toto.  The specimens were fixed in 2.5% glutaraldehyde and osmic acid on S coleedin buffer PH 7.4-7.5. Semithin section and ultrathin section were obtained with ultratome Reichert OMU 3. For histological and histochemical studies semithin section were dyed with Uranil acetate and led citrate and were studied under electron microscope Tesla-500 III.

               The first  earliest reaction is edema of mitochondria(Mc) and disruption of their outer membrane. An increase in volume  of these organs leads to cryst expansion and extension of their energy producing surface while destruction of membranes leads to release of phospholipids later transformed in unesterified fatty acids representing an additional energy substrate. The blockade of this mechanism  results in a considerable contractility and marked aggregation of pathologic process. More over energy deficiency also causes another typical reaction in heart-decrease the refractor period(the possible mechanism of Arrhythmia), whose manifestation depends on heart muscle damage and the stage of the process. Provided Mc  hypertrophy fails to meet an increased energy want of myocardium energy, depletion of heart starts so called vicious circle. At this stage the amount of mitochondria and cristae id reduced. Progression of energy deficiency is followed by exclusion of a part of myofibrils from the contractile action ( mechanism of heart failure) and hypertrophy of the rest accompanied by hyperfunction of energy producing. Concurrently myocardium hemodinamic function decreases. Since early stage of atherosclerosis can develop an  alternative form of myocardium insufficiency which is due to metabolic and ischemic damage of myocardium manifested in various types of microcirculation damage, contractura and myolysis.

               The second significant reaction occurring in the heart during an increased activity of the function is lysosome arise, which come in contact with mitochondria, destructing them at the contact sites. The amount of lyzosome is in significant correlation with intensity of mitochondria division . More over during the decomposition of mitochondria genetic information kept in them passes to cytoplasm, resulting in a possible formation of new mitochondria on the basis of other intercellular elements. These reactions act together to restore bioenergy of heart myocites. Thus, the vicious circle initiated at ultrastructural level represents the reason of simultaneously developed vicious circle at the organ level.

               The represented material confirms that during experimental atherosclerosis the structural basis of heart failure appears from early period of atherosclerosisal as a whole result in the profound changes in myocardyocite structure and function and development of diffused small focal cardiosclerosis.