Submitted on September 9, 2006
Accepted on November 12, 2006
Magnesium attenuates isoproterenol-induced acute cardiac dysfunction and ß-adrenergic desensitization
Yin-Tie Jin1, NAOYUKI HASEBE2*, Tomoyuki Matsusaka1, Shunsuke Natori1, Takafumi Ohta1, Shiro Tsuji1, and Kenjiro Kikuchi1
1 DIVISION OF CARDIOLOGY, DEPARTMENT OF MEDICINE, ASAHIKAWA MEDICAL COLLEGE, ASAHIKAWA, Hokkaido, Japan
2 FIRST DEPARTMENT OF MEDICINE, ASAHIKAWA MEDICAL COLLEGE, 2-1-1-1, MIDORIGAOKAHIGASHI, ASAHIKAWA, 078-8510, Japan; DIVISION OF CARDIOLOGY, DEPARTMENT OF MEDICINE, ASAHIKAWA MEDICAL COLLEGE, ASAHIKAWA, Hokkaido, Japan
* To whom correspondence should be addressed. E-mail: haselove{at}asahikawa-med.ac.jp.
Sympathetic nervous activation is a crucial compensatory mechanism in heart failure. However, excess catecholamine may induce cardiac dysfunction and 
-adrenergic desensitization. While magnesium is known to be a cardioprotective agent, its beneficial effects on acute cardiac dysfunction remain to be elucidated. We examined the effects of magnesium on left ventricular (LV) dysfunction induced by a large dose of isoproterenol (ISO) in dogs. Sixteen anesthetized dogs underwent a continuous infusion of
ISO (1 µg/kg/min) with or without a magnesium infusion (1 mg/kg/min). The dose-response to small doses of ISO (0.025-0.2 µg/kg/min) was tested hourly. A large dose of ISO decreased LV systolic function, increased tau, and suppressed the dose-response to small doses of ISO in a time dependent manner. Magnesium significantly attenuated ISO-induced LV systolic and diastolic dysfunction, and preserved the dose-response to ISO. Serum ionized calcium significantly decreased with a large dose of ISO, but was fully maintained at baseline level with magnesium. A large dose of ISO increased serum lipid peroxide levels and serological markers of myocardial damage, which were significantly suppressed by magnesium. In conclusion, magnesium significantly attenuated excess ISO-induced acute cardiac dysfunction and -adrenergic desensitization.
