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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(More)
Nitric oxide (NO) inhalation therapy has been widely used in several diseases with pulmonary hypertension. However, application of NO inhalation therapy remains controversial in heart failure. Cardiovascular effects of inhaled NO (iNO) were evaluated in dogs before and after induction of heart failure with and without infusion of vasoactive agents. iNO did(More)
Jin YT, Hasebe N, Matsusaka T, Natori S, Ohta T, Tsuji S, Kikuchi K. Magnesium attenuates isoproterenol-induced acute cardiac dysfunction and -adrenergic desensitization. Am J Physiol Heart Circ Physiol 292: H1593–H1599, 2007. First published November 17, 2006; doi:10.1152/ajpheart.00985.2006.—Sympathetic nervous activation is a crucial compensatory(More)
Several clinical trials have demonstrated that angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor blocker (ARB) are equally effective in the treatment of chronic heart failure. However, this has not been confirmed for acute cardiac dysfunction. We examined whether ACEI or ARB prevents isoproterenol-induced acute left(More)
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