Cardiomyocyte autophagia and morphological alterations

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In experiments on rabbits we evaluated the intensity of cardiomyocyte autophagia by the level beclin-1 protein and morphology of the left ventricular myocardium on days 1, 3, and 5 after the onset of focal ischemia caused by ligation of the descending branch of the left coronary artery. The morphological alterations in the left ventricular myocardium were accompanied by intensification of cardiomyocyte autophagia, which attained maximum on postligation day.

The experiments were carried out on male Chinchilla rabbits weighing 3.0-3.5 kg. The animals were main- tained, operated, and examined in strict adherence to Order No. 75 of USSR Ministry of Health 5 (August 12, 1977) and European Convention for the Protec- tion of Vertebrate Animals Used for Experimental and Other Scientific Purposes (Strasbourg, 1986). The rab- bits (n=16) were randomized into 4 equal groups: one control (intact) and 3 experimental groups that com- prised rabbits with modeled acute focal ischemia of the left ventricle (LV) examined on postsurgery days 1, 3, and 5. Focal ischemia was produced in narcotized rabbits by ligation of the descending branch of the left coronary artery between its middle one-third and lower one-third subdivisions.

Taking into account growing character of structural alterations in the myocardium provoked by isch- emia, one can hypothesize that gradual down-regu- lation of cardiomyocyte autophagia relatively to the

peak value observed on postischemic day 1 results from a decrease of energy used by the cells for the adaptive and accommodation processes. This study corroborates the view that autophagia is a mechanism protecting the cardiomyocytes against the death and preventing expansion of the necrotic area during myo- cardial infarction .

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