Korean J Anat.
2002 Aug;35(4):325-333.
Morphological Observations on the Changes of Membrane Permeability by Immobilization Stress in the Rat Atrial Myocyte
- Affiliations
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- 1Department of Anatomy and Institute for Medical Science, Chonbuk National University Medical School, Jeonju, Korea. alms@chonbuk.ac.kr
Abstract
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This study was performed to investigate the effect of immobilization stress on the ultrastructural changes and membrane permeability in rat atrial myocyte using immunohistochemical and lanthanum tracer techniques. Male Sprague-Dawley rats, body weight 160~200 g, were used for all immobilization stress group. Rats were immobilized in small round plastic tube for 6, 12 or 24 hours, except for the control group. Alterations of myocardial myoglobin and alpha-actinin as well as membrane permeability after immobilization stress were examined by immunohistochemistry, and lanthanum permeability of the rat atrial myocyte were observed by electron microscopy. In the control group, there was no loss of myoglobin or alpha-actinin from the atrial myocytes. After 6 and 12 hours immobilization stress, the loss of myoglobin and alpha-actinin could be identified the atrial myocytes. In the 24 hour immobilization groups, the content of the myoglobin and alpha-actinin recovered partially. Lanthanum was deposited only in the intercellular space of the atrial myocardium in the control group. In the 6 hour immobilization group, the atrial myocytes showed severe ultrastructural changes during immobilization stress. Lanthanum deposited in the sarcoplasm, myofibrils, adjacent of mitochondria, and mitochondrial matrix. In the 12 or 24 hour immobilization groups, the morphological alteration of atrial myocytes appeared weekly. In the 12 hour group, lanthanum deposited in myofibrils, adjacent of mitochondria and in the mitochondrial matrix. In the 24 hour group, lanthanum deposited mainly in intercellular space of atrial myocardium, and rarely in the sarcoplasm of myocytes. These results suggest that the immobilization stress may induce the alteration of cardiac cell membrane permeability and the ultrastructures of atrial myocardium.