Ultrastructure of the sinus and atrioventricular nodes in experimental myocardial infarct

The ultrastructure of sinus and atrioventricular nodes was studied in white rats with experimental myocardial infarction. 24 hours after the induction of the disease mitochondrial enlargement characterized by the increase in their area, decrease in the number of cristae and the decline in the rate of mitochondrial energy effectiveness was detected. Different degrees of nuclear chromatin aggregation and membrane permeability for colloidal lanthanum were observed. Characteristic types of conduction cellular lesions were revealed in experimental myocardial infarction.     

Effect of the hexapeptide dalargin on ornithine decarboxylase activity in the duodenal mucosa of rats in experimental duodenal ulcer

The effect of an opioid antiulcerogenic hexapeptide dalargin on ornithine decarboxylase activity of duodenal mucosa has been studied in rats with experimental duodenal ulcers induced by cysteamine. The intraperitoneal injection of 12.5 micrograms/kg of dalargin inhibited ulcerogenesis and activated the enzyme. The effect of the peptide was antagonized by an opiate antagonist naloxone. 5000 micrograms/kg of dalargin failed to inhibit the ulcer formation or to activate ornithine decarboxylase. Since ornithine decarboxylase activation is a marker of intensified cell proliferation and tissue regeneration, our results suggest that the antiulcerogenic effect of dalargin is due to the enhancement of duodenal mucosa regeneration.     

The adenylic system in the brain structures of rats with experimental myocardial infarct

In rats experimental myocardial infarction, whether it was reproduced after a preliminary stress or in its absence, a reduction was found of ATP content initially appearing in the neocortex at the second day of the experiment. The deficit of providing of the energy in brain structures in a traditional variant of infarction reproduction increased still greater, and in the case of preliminary stressing the ATP content was reduced. Parallelly a characteristic change took place in the concentration of products of the fermentative ATP hydrolysis in the brain structures.     

The mechanism of the action of dalargin in experimental myocardial ischemia]

In acute experiments on cats it has been shown that dalargin possess antiarrhythmic affect in myocardial ischemia. Antiarrythmic effect of dalagrig may be connected both with reflex and with direct action of dalargin on neurons structure, which     

Ultrastructure and metabolism of cardiomyocytes under experimental stress

Morphogenesis of adaptational, disadaptational, and alterative changes affected structure and function of all live-supporting systems (contractile elements, macroergic phosphate synthesis, intracellular regeneration, and electrolyte exchange control) was studied in cardiomyocytes under experimental chronic stress using ultrastructural and cytochemical methods.     

Comparative cytophotometric analysis of the nucleic acid content in the cardiomyocytes of normal rats and following experimental infarct

The cytophotometrical investigation of gallocyanine-chrome alum stained cardiac muscle cells allows to ascertain that a mean content of the nucleic acids calculated for a single nucleus is essentially higher in the left ventricle myocytes in comparison with the left auricle cells of healthy adult rats. These values in 1-, 2- and 3-nuclear cells of the ventricle are, respectively, 21.3, 19.3, and 18.0, and 14.1, 13.7, 13.5 of arbitrary units (a. u.) in the auricle cells. A difference in cytoplasmic RNA contents of the same cells is more significant, these values are 65.7, 116.4, and 158.9 a. u. in ventricle myocytes, and 33.4, 60.8 and 95.2 a. u. in auricle cells. The nucleic acids content in the nuclei and RNA content in the cytoplasm increase with the development of proliferation in myocytes after experimental myocardial infarction. A relative increase in the nucleic acids content in the nuclei of the same cell types reaches 50, 24, and 10% 11 days after infarction and 56, 38, and 45% 31 days after infarction. A relative increase in cytoplasmic RNA of the same cells reaches, respectively, 52, 17, and 25%, and 70, 57, and 53% 11 and 31 days after infarction. These findings evidence on the greatest synthetic activity of the single-nuclear auricle muscle cells in the process of heart restoration after infarction.     

Electromechanical analysis of infarct border zone in chronic myocardial infarction

To test the hypothesis that alterations in electrical activation sequence contribute to depressed systolic function in the infarct border zone, we examined the anatomic correlation of abnormal electromechanics and infarct geometry in the canine post-myocardial infarction (MI) heart, using a high-resolution MR-based cardiac electromechanical mapping technique. Three to eight weeks after an MI was created in six dogs, a 247-electrode epicardial sock was placed over the ventricular epicardium under thoracotomy. MI location and geometry were evaluated with delayed hyperenhancement MRI. Three-dimensional systolic strains in epicardial and endocardial layers were measured in five short-axis slices with motion-tracking MRI (displacement encoding with stimulated echoes). Epicardial electrical activation was determined from sock recordings immediately before and after the MR scans. The electrodes and MR images were spatially registered to create a total of 160 nodes per heart that contained mechanical, transmural infarct extent, and electrical data. The average depth of the infarct was 55% (SD 11), and the infarct covered 28% (SD 6) of the left ventricular mass. Significantly delayed activation (>mean + 2SD) was observed within the infarct zone. The strain map showed abnormal mechanics, including abnormal stretch and loss of the transmural gradient of radial, circumferential, and longitudinal strains, in the region extending far beyond the infarct zone. We conclude that the border zone is characterized by abnormal mechanics directly coupled with normal electrical depolarization. This indicates that impaired function in the border zone is not contributed by electrical factors but results from mechanical interaction between ischemic and normal myocardium.     

Protein-synthesizing function of the liver of rabbits in experimental myocardial infarct

The content of serum albumin in rabbit blood was found to be lowered within the first day after reproduction of experimental myocardial infarction. The rate and the level of translation of endogenous mRNA were studied in cell-free systems from normal rabbit liver and 6-12-24 h after experimental myocardial infarction. The decrease of the total protein synthesis in the crude cell-free system from the liver of experimental animals was shown to depend on the lack of energy supply rather than on the reduced activity of the protein-synthesizing apparatus. The relative drop of protein synthesis in the cell-free system with saturating concentration of ATP, GTP and creatine phosphate is likely to be connected with a decrease in the proportion of membrane-bound polysomes.     

The differential indicator method of determining the areas of ischemia and necrosis in experimental myocardial infarct in rats

Valid method for estimation of relationship between ischemic and infarct sizes was elaborated. The method is based on separate determination of Evans blue and formazan in injured and intact areas of myocardium for later calculation of myocardial ischemic and necrotic zones. The procedure ensures high level of accuracy and reproducibility of experimental data because of intrinsic control.     

Functioning of the monooxygenase system of the liver in experimental myocardial infarct

The experiments on rats have shown that coronary artery ligation reduces the content of microsomal cytochromes P-450 and b5 and causes amidopyrine-N-demethylation and aniline-p-hydroxylation disturbances that persist throughout a 3-week period of myocardial infarction. The investigation of spontaneous lipid peroxidation of microsomal membranes in myocardial infarction has shown that concentration of malonic dialdehyde in microsomal fraction significantly increased by the 7th day after coronary artery ligation, as compared to sham-operated rats.     

Isoflurane post-conditioning influences myocardial infarct healing in rats

Isoflurane post-conditioning causes an early increase in cardiac progenitor cells; however, during the chronic phase of infarct healing, the number was smaller compared to control, which suggests a positive effect on infarct scar maturity. Myofibroblasts participate in early phase infarct contraction, but their number is small in a mature scar. We investigated whether isoflurane post-conditioning stimulates differentiation of progenitor cells to myofibroblasts and to verify our hypothesis that isoflurane post-conditioning improves maturation of a myocardial scar. Ischemia was induced for 30 min in female rats. From the last 5 min of ischemia until 10 min into reperfusion, the isoflurane group received 1.5% isoflurane, while the control group received only an air-oxygen mixture. Infarct area was analyzed using immunohistochemistry. During the subacute phase of infarct healing, the number of myofibroblasts was greater in isoflurane-treated animals than in the control group. During the chronic phase of infarct healing, post-conditioned animals exhibited fewer myofibroblasts compared to control animals, even those derived from progenitor cells, i.e., α-smooth actin-nestin positive cells. In addition, isoflurane post-conditioning resulted in higher percentage of mature blood vessels compared to control animals. The myocardium of the isoflurane treated animals exhibited more myofibroblasts in granulation tissue compared to control animals. The smaller number of myofibroblasts together with the greater number of mature blood vessels during the chronic phase of healing demonstrated faster healing of the infarct area of isoflurane-treated animals compared to control animals.     

Effects of dalargin on hemodynamics of anesthesized rats during truncal vagotomy

I/v dalargin injection (20-25 g/kg) to narcotized rats in case of total myoplegia effectively protect hemodynamic changes under nociceptive stimulation. Bilateral truncal vagotomy partially decrease the protective effect of dalargin. Protective effect of the medicine results in activation of central and peripheral opioid receptors.     

Lipid peroxidation in experimental myocardial infarct: the action of hyperbaric oxygenation

Rats with experimental myocardial infarction demonstrated decrease in the activity of superoxide dismutase and catalase and increase in the content of lipid peroxidation (LPO) products and Schiff bases both in and outside the area of necrosis. The combined ischemic damage and hyperbaric oxygenation resulted in the over additive effect of accumulation of LPO products in and outside the area of infarction. The data suggest that it is desirable to use antioxidants during hyperbaric oxygenation.