Histological Modifications Aging Aorta in Male Albino Rat
- *Corresponding Author:
- Eman A. Abdelrahim
Professor of Histology
Sohag Faculty of Medicine
Sohag University Egypt
Tel: 20-97 3481101
E-mail: [email protected]
Received Date: February 15, 2016; Accepted Date: April 15, 2016; Published Date: April 25, 2016
Citation: Abu-Dief EE, Abdelrahim EA, Abdelrahim KM (2016) Histological Modifications Aging Aorta in Male Albino Rat. J Cytol Histol 7: 408. doi: 10.4172/2157-7099.1000408
Copyright: © 2016 Abu-Dief EE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Aging represents a major risk for vascular diseases. Diseases of the aorta causes serious back effects on the heart. This study aims to detect the histological changes of the aged aorta and to understand their underlying mechanisms to help in development of the prophylactic and treatment measures. Ten adult and ten aged male albino rats were used. Specimens from their thoracic aorta were prepared and stained with Hematoxylin and Eosin, Orcein for elastic laminae, and anti-actin antibody. Morphometric measurements for the thickness of the tunica intima and elastic laminae of the tunica media were performed. Aged aorta showed thickening of the tunica intima, thinning and fragmentation of elastic laminae, proliferation of medial smooth muscle with reduction of their actin myofibrils, and fibrosed tunica adventitia. Atherosclerosis was also detected with epithelioid changes in the medial smooth muscle and focal thickening of the intima. It is concluded that, aging is a risk factor for aortic atherosclerosis. Intimal thickening and proliferation of medial smooth muscle are the earliest signs. Thinning and fragmentation of elastic laminae, decreased contractile myofibrils of the aortic smooth muscle, and fibrosis of the tunica adventitia lead to aortic stiffness which interferes with its active function and shares in the age-related arterial remodeling.