Evaluation of Hot Spring Effects on FeCl3-Induced Arterial Injury in Rats

• Main Authors: Yi-Fen Tsai, 蔡宜芬
• Other Authors: 郭家驊
• Format: Others
• Language: zh-TW
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/10278594061043211720

碩士 === 台北巿立體育學院 === 運動科學研究所 === 95 === Regular exercise increases organ/tissue antioxidant activity to prevent and/or ameliorate cardiovascular diseases, and to protect cardiovascular system integrity. Although endogenous defense mechanisms are temporarily and frequently enhanced to increase organ tolerance in response to intense exercise, ischemia, hypoxia, oxidative stress and endotoxin, an appropriate and alternative method for some patients without exercise performance to increase protective potential is necessary. In this study, we developed a progressive 42°C thermal stimulation during 15 min and evaluated the effects of progressive thermal stimulation on systemic hemodynamics and cardiovascular protection after FeCl3-induced arterial injury. In the first part of study, we divided Female Wistar rats into three groups to identify the hemodynamic effects of 42°C whole body thermal stimulation, progressive 42°C thermal stimulation and control rats in this study. We found that in spite of similar anus temperature, the progressive 42°C thermal stimulation ameliorated whole body thermal stimulation-enhanced hypertension and tachycardia. In the second part of study, we used one time or three times of progressive 42°C thermal stimulation in one day to evaluate its protective potential against FeCl3-induced femoral and carotid arterial injury (evaluated by time to occlusion, TTO) after 24 or 72 hours. Our results showed that FeCl3 induced femoral and carotid arterial injury in the endothelial area by producing reactive oxygen species, 3-nitrotyrosine and 4-hydroxynoneal accumulation, and intercellular adhesion molecule I consequently leading to arterial occlusion. TTO level（mean±SE）of femoral and carotid arterial in control（399±56 sec, 1313±107 sec）, 1-24 hr（868±94 sec, 1836±99 sec）, 1-72 hr（727±57 sec, 2109±200 sec）, 3-24 hr（1015±203 sec, 2701±453 sec）, 3-72 hr（1086±208 sec, 2693±382 sec）. One time or 3 times of progressive 42°C thermal stimulation/day significantly elongated TTO level (P<0.05) and decreased endothelial reactive oxygen species production, 3-nitrotyrosine and 4-hydroxynoneal accumulation, and intercellular adhesion molecule I expression. In addition, 3 times of progressive 42°C thermal stimulation exerted a more efficient protection than one time of progressive 42°C thermal stimulation by the upregulation of heat shock proteins (Hsp60 and Hsp70), antiapoptotic proteins (Bcl-2 and Bcl-xL), and antioxidant Magnesium superoxide dismutase in the cardiovascular tissues, liver and kidney. This study suggests that a modified progressive 42°C thermal stimulation provides an efficiently protective potential against oxidative stress induced cardiovascular diseases.