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Am J Physiol Heart Circ Physiol 292: H1593-H1599, 2007. First published November 17, 2006; doi:10.1152/ajpheart.00985.2006
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Magnesium attenuates isoproterenol-induced acute cardiac dysfunction and beta-adrenergic desensitization

Yin-Tie Jin, Naoyuki Hasebe, Tomoyuki Matsusaka, Shunsuke Natori, Takafumi Ohta, Shiro Tsuji, and Kenjiro Kikuchi

Department of Internal Medicine, Division of Cardiology, Asahikawa Medical College, Asahikawa, Hokkaido, Japan

Submitted 9 September 2006 ; accepted in final form 12 November 2006

Sympathetic nervous activation is a crucial compensatory mechanism in heart failure. However, excess catecholamine may induce cardiac dysfunction and beta-adrenergic desensitization. Although 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 in dogs. Sixteen anesthetized dogs underwent a continuous infusion of isoproterenol (1 µg·kg–1·min–1) with or without a magnesium infusion (1 mg·kg–1·min–1). The dose response to small doses of isoproterenol (0.025–0.2 µg·kg–1·min–1) was tested hourly. A large dose of isoproterenol decreased LV systolic function, increased the time constant of LV isovolumic relaxation, and suppressed the dose response to small doses of isoproterenol in a time-dependent manner. Magnesium significantly attenuated isoproterenol-induced LV systolic and diastolic dysfunction and preserved the dose response to isoproterenol. Serum-ionized calcium significantly decreased with a large dose of isoproterenol but was fully maintained at baseline level with magnesium. A large dose of isoproterenol increased serum lipid peroxide levels and serological markers of myocardial damage, which were significantly suppressed by magnesium. In conclusion, magnesium significantly attenuated excess isoproterenol-induced acute cardiac dysfunction and beta-adrenergic desensitization.

calcium overload; free radical; dog, left ventricular; tau


Address for reprint requests and other correspondence: N. Hasebe, Dept. of Internal Medicine, Division of Cardiology, Asahikawa Medical College, 2-1-1-1 Midorigaoka Higashi, Asahikawa, Hokkaido 078-8510 Japan (e-mail: haselove{at}asahikawa-med.ac.jp)






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