title: Rats in acute withdrawal from ethanol exhibit left ventricular systolic dysfunction and cardiac sympathovagal balance shift.
abstract: There is strong evidence that sympathovagal balance plays an important role in the progression of cardiac dysfunction in non-alcoholics. The purpose of this investigation was to determine whether a pattern of continuous ethanol intake and withdrawal modulates the cardiac sympathovagal balance and left ventricular (LV) systolic function in rats. Male Wistar rats were treated with a continuous ethanol liquid diet for 49 days, and then subjected to 1-day withdrawal and 21-day abstinence. Cardiac sympathovagal balance and LV systolic function were evaluated based on heart rate variability (HRV), Western blotting, and echocardiography. Longitudinal data obtained from the same rats showed that the 49-day continuous ethanol treatment induced LV systolic dysfunction, expressed by decreased fractional shortening and ejection fraction. At the 1-day withdrawal, LV systolic dysfunction was deteriorated, and the low-frequency power/high-frequency power (LF/HF) ratio in HRV was elevated because of the depressed HF and the increased LF. Western blot analysis showed an increased expression of myocardial tyrosine hydroxylase and a decreased expression of myocardial acetylcholine. All anomalies were recovered to baseline values with 21-day abstinence. We concluded that acute withdrawal from a 49-day continuous ethanol regimen is sufficient to promote the shift of cardiac sympathovagal balance toward sympathetic predominance and reduced vagal tone, contributing to the further deterioration of LV systolic function in rats. Those providing medical care for alcoholics should be aware of this enhanced susceptibility to LV systolic dysfunction with abrupt termination of a continuous ethanol regimen.
authors.affiliation: Department of Legal Medicine, Yamaguchi University Graduate School of Medicine, Minami-Kogushi, Ube, Yamaguchi, Japan. czhliu@yamaguchi-u.ac.jp
authors.forename: Jinyao
authors.initials: J
authors.lastname: Liu
authors.forename: Seiko
authors.initials: S
authors.lastname: Shirafuji
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Fujimiya
mesh_terms: D000818:Animals; D000431:Ethanol / Q000009:adverse effects*; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D008297:Male; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014630:Vagus Nerve / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced*; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D000431:Ethanol; D014446:Tyrosine 3-Monooxygenase