Morphological Study on the Arterial Intimal Hyperplasia and the Inhibitory Action of Dexamethasone.
10.11637/kjpa.2004.17.2.139
- Author:
Soo Won KIM
1
;
Sun KIM
;
Seung Ro HAN
;
Soo Il KIM
;
Geun Ja CHO
;
Won Sik KIM
Author Information
1. Department of Anatomy, College of Medicine, Chungnam National University, Korea. wonsikk@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
Arterial intimal hyperplasia;
Dexamethasone;
Apoptosis
- MeSH:
Animals;
Apoptosis;
Dexamethasone*;
Extracellular Matrix;
Hyperplasia*;
Myocytes, Smooth Muscle;
Myofibroblasts;
Rats;
Sodium;
Tunica Intima;
Tunica Media;
Vacuoles
- From:Korean Journal of Physical Anthropology
2004;17(2):139-152
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This study is performed to reveal the changes of the arterial wall, especially, tunica intima and tunica media, after endothelial denudation and the effects of dexamethasone sodium on intimal hyperplasia morphologically in the rat. After arterial denudation by modified air drying technique, dexamethasone 1, 200 mg/kg/day was administered intramuscularly daily from the day of operation for 14 days. At 5 DAT (days after treatment) and 14 DAT, tunica intima was greatly thickened in control groups compared with normal group, but not in the dexamethasone-treated groups. Light microscopically, greatly increased cells and intercellular matrix in the tunica intima are observed in control group, but not in the dexamethasone-treated group. In the TEM observation, the cells considered as myofibroblasts and extracellular matrix were greatly increased in both tunica intima and tunica media just below the internal elastic lamina in the control group. Myofibroblasts and extracellular matrix migrated through the apertures of internal elastic lamina into the endothelial layer. Characteristic false internal elastic lamina also found. In dexamethasone-treated group, myofibroblasts and extracellular matrix decreased significantly, and apoptotic electron-dense cells, fragmented nucleus and autophagic vacuoles are observed. Through the apertures of internal elastic lamina, comma-shaped fragmented nuclei migrated into the tunica intima. These results suggest that dexamethasone inhibits the myofibroblast-transformation and proliferation of smooth muscle cells, migration of myofibroblasts and matrix synthetic activity, and induces the apoptosis of smooth muscle cells under the internal elastic lamina.
