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The features of mitochondria of cardiomyocytes from rats with chronic heart failure

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Abstract

Electron-microscopy study of rat myocardium 2 weeks after a heart attack revealed significant alterations in the ultrastructure of cardiomyocytes than for the control. The location of myofibrils was less regular than for normal cells. The population of interfibrillar mitochondria decreased. Mitochondrial cristae were located less densely and formed cellated structures. Swollen mitochondria were observed in the periinfarction and intact areas, indicating the development of ischemia in the myocardium as a whole. Six months after the occlusion of coronary vessels alterations in the location of myofibrils and mitochondria were mainly observed in the peri-infarction area. Mitochondria also formed cellated structures. A 30% decrease in the density of the arrangement of the inner membranes of mitochondria on an area unit was found in the periinfarction zone. The ratio between the relative volumes of mitochondria and myofibrils in the cardiomyocytes of the peri-infarction area was increased by 20%. The area of mitochondria in the intact zone of the left ventricle was 30% greater than for the control. A study of isolated living cardiomyocytes revealed that the mitochondrial- membrane potential in the rats subjected to myocardial infarction half a year ago previously was significantly lower than for the mitochondrial-membrane potential in the control rats. Thus, cardiomyocytes that were similar to healthy cardiomyocytes in their morphology exhibited lower total mitochondrial-membrane potential, indicating their decreased energy state.

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Abbreviations

MI:

myocardial infarction

LV:

left ventricle

CHF:

chronic heart failure

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Correspondence to G. A. Sakuta.

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Original Russian Text © A.V. Stepanov, E.V. Baidyuk, G.A. Sakuta, 2016, published in Tsitologiya, 2016, Vol. 58, No. 11, pp. 883–890.

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Stepanov, A.V., Baidyuk, E.V. & Sakuta, G.A. The features of mitochondria of cardiomyocytes from rats with chronic heart failure. Cell Tiss. Biol. 11, 458–465 (2017). https://doi.org/10.1134/S1990519X17060086

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  • DOI: https://doi.org/10.1134/S1990519X17060086

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