Chronic noise exposure in the spontaneously hypertensive rat

自发性高血压大鼠的慢性噪声暴露

阅读:1

Abstract

INTRODUCTION: Epidemiological studies have suggested an association between the relative risk for developing cardiovascular disease (CVD) and long-term exposure to elevated levels of transportation noise. The contention is that this association is largely owing to an increase in stress-related biomarkers that are thought to be associated with CVD. Animal models have demonstrated that acute noise exposure is capable of triggering a stress response; however, similar studies using chronic noise models are less common. MATERIALS AND METHODS: The current study assessed the effects of intermittent daily exposure to broadband 80 kHz bandwidth noise of 87.3 dBA for a period of 21 consecutive days in spontaneously hypertensive rats. RESULTS: Twenty-one days of exposure to noise significantly reduced body weight relative to the sham and unhandled control groups; however, noise had no statistically significant impact on plasma adrenocorticotropic hormone (or adrenal gland weights). Noise was associated with a significant, albeit modest, increase in both corticosterone and aldosterone concentrations following the 21 days of exposure. Interleukin 1 and interleukin 6 levels were unchanged in the noise group, whereas both tumour necrosis factor alpha and C-reactive protein were significantly reduced in noise exposed rats. Tail blood sampling for corticosterone throughout the exposure period showed no appreciable difference between the noise and sham exposed animals, largely due to the sizeable variation for each group as well as the observed fluctuations over time. DISCUSSION: The current pilot study provides only modest support that chronic noise may promote stress-related biological and/or developmental effects. More research is required to verify the current findings and resolve some of the unexpected observations.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。