Melatonin improved rat cardiac mitochondria and survival rate in septic heart injury. Issue 1 (17th January 2013)

• Record Type: Journal Article
• Authors: Zhang, Hongmin; Liu, Dawei; Wang, Xiaoting; Chen, Xiukai; Long, Yun; Chai, Wenzhao; Zhou, Xiang; Rui, Xi; Zhang, Qing; Wang, Hao; Yang, Quanhui
• Is Part Of: Journal of pineal research. Volume 55:Issue 1(2013)
• Page Start: 1
• Page End: 6
• Publication Date: 2013-01-17
• Subjects: melatonin -- mitochondrial function -- mitochondrial resuscitation -- myocardial depression; Pineal gland -- Periodicals; Pineal Gland -- Periodicals; Épiphyse (Glande); Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 612.492
• DOI: 10.1111/jpi.12033
• Languages: English
• ISSNs: 0742-3098

Abstract

Abstract: The pathogenesis of septic myocardial depression is complicated. Mitochondrial dysfunction has been suggested to be one of the main reasons for the reduced cardiac function. As melatonin is an antioxidant with the potential to scavenge radicals in mitochondria, we therefore employed a sepsis model, that is, cecal ligation and double puncture (CLP) in rats, to study the melatonin effects on: (i), myocardial mitochondrial function; (ii), heart systolic function; and (iii), prognosis of septic rats. We demonstrate that melatonin treatment (30 mg/kg, 3, 6, 12, 18, 24 hr after CLP) (i) improved myocardial cytochrome c oxidase (CcOX) activity and blood lactate level, (ii) attenuated heart dysfunction with a higher left ventricular ejection fraction (EF), and (iii) promoted 48‐h survival of the rats compared to CLP animals with no melatonin treatment. In conclusion, our results show that rat myocardial mitochondrial CcOX activity was depressed during severe sepsis accompanied by myocardial depression characterized by the decline of EF. In septic rats, melatonin increased the CcOX activity, improved heart systolic function, and lowered mortality rate. The clinical use of melatonin in septic myocardial depression should be tested in the future.