Ivanchenko M. V.

Ultrastructure of Mitochondria in Rat Contractile Atrial Cardiomyocytes during Hypoxic Injury of Cardiogeny


About the author:

Ivanchenko M. V.

Heading:

MORPHOLOGY

Type of article:

Scentific article

Annotation:

According to world literature there are 40­70 % new­borns with injury of the cardiovascular system due to abnormally low levels of oxygen in utero. Changes of myocardial energy metabolism are leading to a rapid decline in its contractile function. This is supported by the following anatomical and physiological characteristics of the new­born. Changes of cardiomyocytes mitochondrial apparatus can be marked as the main factors which are the basis of various forms of cardiovascular disease, but the dynamics of morphogenetic rearrangements heart mitochondria are poorly under the influence of chronic hypoxia. Objective. аnalysis of the formation and reactions of the mitochondria network in rat atrial muscle cells during prenatal and postnatal ontogeny under the influence of chronic hypoxia. Methods. White rats were used as a material. Intrauterine hypoxia was modelled by intraperitoneal injection of sodium nitrite from 10th to 21st day of pregnancy. Embryonic hearts on the 14th, 16th, 18th and 20th days of prenatal ontogeny new­born rats on the 3rd, 7th, 14th, 30th day of postnatal ontogeny and adult animals were investigated by the transmission electron microscopy. Volume density and numerical density of mitochondria were estimated. The Paired Student’s t­test was applied. Results. Formation mitochondrial network of atrial and auricles on the stages of prenatal cardiogeny under con­ ditions of hypoxia was observed. It was shown significant decrease of the volume density of mitochondria and slow­ ing the formation heterogeneity of mitochondria in the sarcoplasm contractile cardiomyocytes on the 18th day in right atrium and right auricle and 20th day in left atrium and left auricle. At prenatal stages of cardiogeny by influence hypoxia mitochondria were not form of intermitochondria contacts in the atria. Reactions were characterized by mitochondrial swelling and degradation of organelles. The processes of al­ teration of mitochondrial apparatus were different at the parts of the atria and decreases in the sequence: right auricle – right atrium – left atrium – left auricle. Reducing the volume density of mitochondria in the sarcoplasm of the contractile cardiomyocytes under conditions of hypoxic injury may be associated with a group of factors. First, intrauterine hypoxia is lead to a slowdown in the perinatal shift from lactate and glucose to free fatty acids as pri­ mary fuel sources and the result was reduction of growth and mitochondrial oxidative phosphorylation, which can be enhanced by high dependence on glycolysis as an energy source in hypoxic myocardium. Second, prenatal hy­ poxia generates a significant delay in incorporating mechanisms involved in mitochondrial growth and imbalances in plastic processes leading to these reactions. During the first week of postnatal atrial cardiogeny was observed progression of the pathological process, ac­ companied by a further reduction in the rate of mitochondrial growth and formation heterogeneity of mitochondrial swelling and destruction mitochondria at intermyofibrillar and subsarcolemmal localization. The above characteris­ tics were reduced to left atrium – left auricle – right atrium – right auricle. From the 7th day to the 14th there were adaptation mechanisms by increasing the number of new mitochondria and accumulation of “low­energy” in all areas of the cells. There was the growth of the associations as whole orga­ nelles in the cell compared to the norm in all parts of the atria. Analysis of mitochondrial apparatus in adult atrial contractile cardiomyocytes did not reveal any significant dif­ ferences between the experimental group and control.

Tags:

rats, atrium, myocardium, cardiogeny, mitochondria, hypoxia

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Publication of the article:

«Bulletin of problems biology and medicine» Issue 3 part 2 (111), 2014 year, 294-300 pages, index UDK 611. 127:611. 018:611. 013