SEM TEM INVESTIGATION OF RAT CARDIAC SUBCELLULAR ALTERATIONS INDUCED BY CHANGING DURATION OF NOISE STRESS/

Citation
P. Soldani et al., SEM TEM INVESTIGATION OF RAT CARDIAC SUBCELLULAR ALTERATIONS INDUCED BY CHANGING DURATION OF NOISE STRESS/, The Anatomical record, 248(4), 1997, pp. 521-532
Citations number
45
Categorie Soggetti
Anatomy & Morphology
Journal title
ISSN journal
0003276X
Volume
248
Issue
4
Year of publication
1997
Pages
521 - 532
Database
ISI
SICI code
0003-276X(1997)248:4<521:STIORC>2.0.ZU;2-S
Abstract
Background: Many studies have shown that loud noise is an environmenta l stressor, Noise exposure causes changes at different levels in livin g beings; the cardiovascular system, considered to be the most affecte d apparatus, has received much attention in both animals and humans, T he present study investigated the effect of changing duration of noise stimulation on rat myocardium to determine whether the responses coul d be related to time. Methods: The study was performed on young albino male rats, Three groups of animals were exposed to white noise (100 d BA) for 1, 6, and 12 hr, respectively, and samples of right atrium and ventricle were processed for ultrastructural examination, The subcell ular organization of cardiomyocytes was examined by transmission and s canning electron microscopy, the latter being carried out with the mod ified osmium maceration method. Results: After 1 hr of noise exposure, atrial and ventricular cardiomyocytes did not present significant alt erations, After 6 hr, changes were observed in atrial tissue at the mi tochondrial level, whereas the ventricular structure appeared unaffect ed. After 12 hr of treatment, in addition to the mitochondrial alterat ions, changes in atrial and ventricular myocardium, consisting of area s of enlargement in intercalated disc membranes and decreased density in sarcoplasm, were detected. Conclusions: The methods we applied for the visualization of cellular organelles allowed us to demonstrate tha t atrial tissue is primarily involved in stress response, especially a t the mitochondrial level; a more prolonged time of exposure seems to be necessary for ventricular involvement. (C) 1997 Wiley-Liss, Inc.