Premium
Melatonin improved rat cardiac mitochondria and survival rate in septic heart injury
Author(s) -
Zhang Hongmin,
Liu Dawei,
Wang Xiaoting,
Chen Xiukai,
Long Yun,
Chai Wenzhao,
Zhou Xiang,
Rui Xi,
Zhang Qing,
Wang Hao,
Yang Quanhui
Publication year - 2013
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/jpi.12033
Subject(s) - melatonin , sepsis , medicine , cardiac function curve , mitochondrion , endocrinology , ejection fraction , heart rate , septic shock , oxidative stress , cardiology , heart failure , biology , blood pressure , biochemistry
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 (Cc OX ) 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 Cc OX activity was depressed during severe sepsis accompanied by myocardial depression characterized by the decline of EF . In septic rats, melatonin increased the Cc OX activity, improved heart systolic function, and lowered mortality rate. The clinical use of melatonin in septic myocardial depression should be tested in the future.