Heart Failure Research Laboratory, R2020, Canadian Centre for Agri-Food Research in Health and Medicine and Department of Physiology, University of Manitoba, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
J Nutr. 2010 May;140(5):962-8. doi: 10.3945/jn.109.115006. Epub 2010 Mar 24.
Cardiac hypertrophy is a compensatory enlargement of the heart due to either volume overload (VO) and/or pressure overload (PO) that develops into heart failure if left untreated. The polyphenol resveratrol has been reported to regress PO-induced cardiac hypertrophy in rats. Our aim in this study was to assess the effectiveness of resveratrol on VO-induced cardiac hypertrophy. Sprague Dawley rats were subjected to aortocaval shunt and abdominal aortic banding surgeries to create VO and PO, respectively; sham-operated rats served as controls. To arrest the development of cardiac hypertrophy, daily resveratrol treatment (2.5 mg/kg body weight) was started 2 d postsurgery for 26 d and assessed by echocardiography at 2, 14, and 28 d postsurgery. Similarly, to regress cardiac hypertrophy resveratrol treatment was started after structural and functional abnormalities developed (14 d postsurgery) for 14 d and assessed by echocardiography at 14 and 28 d postsurgery. VO surgeries induced eccentric hypertrophy characterized by increased left ventricle internal dimensions (LVID) without wall thickening. Conversely, PO induced concentric hypertrophy with increased wall thickness without change in LVID. Lipid peroxidation, a marker for oxidative stress, was significantly elevated in both PO and VO rats. Resveratrol treatment arrested the development and regressed abnormalities in cardiac structure and function in PO but not VO rats. Treatment with resveratrol also significantly reduced oxidative stress in cardiac tissue of PO and VO rats. The results on cardiac structure and function demonstrate a potential for resveratrol in the treatment of cardiac hypertrophy due to PO but not VO.
心肌肥厚是由于容量超负荷(VO)和/或压力超负荷(PO)导致的心脏代偿性增大,如果不加以治疗,会发展为心力衰竭。有报道称,多酚白藜芦醇可使大鼠的 PO 诱导性心肌肥厚消退。本研究旨在评估白藜芦醇对 VO 诱导性心肌肥厚的作用。Sprague Dawley 大鼠接受腔静脉-腹主动脉分流术和腹主动脉缩窄术,分别造成 VO 和 PO;假手术大鼠作为对照。为了阻止心肌肥厚的发展,白藜芦醇治疗(2.5mg/kg 体重)于术后 2 天开始,持续 26 天,并于术后 2、14 和 28 天通过超声心动图进行评估。同样,在结构和功能异常发生后(术后 14 天)开始逆转心肌肥厚的白藜芦醇治疗,持续 14 天,并于术后 14 和 28 天通过超声心动图进行评估。VO 手术引起非对称性肥厚,表现为左心室内部尺寸(LVID)增加而壁无增厚。相反,PO 引起对称性肥厚,表现为壁增厚而 LVID 无变化。脂质过氧化,氧化应激的标志物,在 PO 和 VO 大鼠中均显著升高。白藜芦醇治疗可阻止 PO 但不能阻止 VO 大鼠的心脏结构和功能异常发展和逆转。白藜芦醇治疗还显著降低了 PO 和 VO 大鼠心脏组织中的氧化应激。这些心脏结构和功能的结果表明,白藜芦醇有可能用于治疗 PO 引起的心肌肥厚,但不能用于治疗 VO 引起的心肌肥厚。