Functional, morphological and damage marker troponin I (TnI) changes to New Zealand rabbit's myocardium in experimental infarction

The aim of the present study – to evaluate the complications during induced experimental myocardial infarction in New Zealand laboratory rabbits, as well as changes in myocardial function, morphology, damage marker troponin I (TnI) and the effect of implanted stem cells into the MI affected area. Goals of the study: 1. to experimentally induce myocardial infarction in laboratory rabbits and determine the most common complications; 2. to determine the level of biochemical myocardial damage marker troponin (TnI) in rabbits before and after MI, as well as evaluate its information value in determining myocardial damage; 3. to determine echocardiography parameters of non anesthetised and anesthetised rabbits with a combination of ketamine–xylazine; 4. to evaluate echocardiographic changes of anesthetised rabbits before and after experimentally induced MI, as well as after the implantation of myogenic cells; 5. to evaluate electrocardiographic changes before and after experimentally induced MI; 6. to evaluate the morphological changes in induced experimental myocardial infarction; 7. to assess myocardial morphological changes by implanting myogenic stem cells cultivated from the same individuals quadriceps muscle in the MI affected area; 8. to assess myocardial morphological changes by implanting modified myogenic stem cells with Cx43 connexins in the MI affected area. During this research a high-technology development project - \"Development of regeneration models of heart structures using stem and specialized cells and biological tissues\" was carried out. In this research MI was experimentally induced in New Zealand white rabbits by the tying off a rabbit heart's left coronary artery at the middle segment; the main postoperative complications and the morphological features of myocardial infarction were discussed. For the first time in Lithuania troponin (TNI) test was applied to confirm experimentally induced MI in New Zealand white rabbits. The data show that the level change in biochemical blood parameters of troponin I is useful for the diagnosis of myocardial injury confirmation. It was determined that Cx43 stem cells modified by connexins implanted into the damaged MI area had a positive effect on the regeneration of the damaged heart muscle. For the first time in Lithuania heart echocardiography was applied to experimental rabbits as a basic research tool in instrumental cardiac diagnosis. We determined the reference values of a rabbit’s heart parameters by the standard M-mode and Doppler echocardiography. This work showed that applied anaesthetic combination of ketamine (30 mg/kg) – xylazine (4 mg/kg) is correct and can be applied to anesthetize rabbits when performing instrumental studies. That way, the animal is placed quite well and cardiovascular system is minimally affected by anaesthetic when a rabbit is anesthetized this way. Morphological studies confirmed that the development of morphological changes in experimentally induced MI, from an early to formed MI, in its pathological morphological expression is similar to that found in humans during the same pathology case. Conclusions: 1. New Zealand laboratory rabbits are suitable models for the induction of experimental myocardial infarction and its treatment using stem cells. It was determined that the main post-operative MI complications in laboratory animals, used as experimental models for stem cell trials, were acute respiratory distress syndrome and cardiac tamponade. 2. Troponin I level determination method is suitable for approval of experimentally induced myocardial infarction (MI) in rabbits. TnI blood amount after experimentally induced MI reached 2.1-13.3 ng/ml (before MI-0-0.1). 3. Anaesthetic combination of ketamine (30 mg/kg) - xylazine (4 mg/kg) can be applied to anesthetize rabbits. The animal can be observed quite well and cardiovascular system is minimally affected by anaesthetic when a rabbit is anesthetized this way; the experiment can be safely performed and clinical echocardiographic parameters are determined. 4. Heart contractility rate (HCR) of anesthetised rabbits, the amplitude of mitral annulus (M mode) and the amplitude of the tricuspid valve (M mode) were lower than those of not anesthetised rabbits: HCR=175.66±30.16 (t/min.) vs HCR=234.57±38.16 (t/min.) respectively, right ventricle (5.52±0.79 mm) and left atrium (8.4±1.08 mm) were smaller 6.74±0.52 mm and 9.33±0.66 mm respectively, p