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CARDIOVASCULAR ANESTHESIA

The Effects of Dexmedetomidine on Left Ventricular Function During Hypoxia and Reoxygenation in Isolated Rat Hearts

Department of Anesthesiology, Nagasaki University School of Medicine, Nagasaki, Japan

Address correspondence and reprint requests to Sungsam Cho, MD, Department of Anesthesiology, Nagasaki University School of Medicine, 1–7–1 Sakamoto, Nagasaki 852–8501, Japan. Address e-mail to chos{at}net.nagasaki-u.ac.jp.

Hypoxia resulting from apnea in patients with sleep apnea is an important factor in heart disease. We designed the present study to determine whether dexmedetomidine (DEX) has a direct protective effect against hypoxia-reoxygenation-induced left ventricular dysfunction without systemic hemodynamic and humoral effects. Isolated rat hearts were exposed to 60-min hypoxia followed by 30-min reoxygenation with 0, 10, or 100 nM DEX prehypoxia administration (n = 7 each group). In a second experiment (n = 7), 100 nM DEX was administered posthypoxia. In a third experiment (n = 7 each group), an 2 antagonist, yohimbine was given with and without 100 nM DEX prehypoxia administration. DEX prehypoxia, but not posthypoxia, administration significantly improved the recovery of left ventricular developed pressure after reoxygenation (0, 10, 100 nM DEX prehypoxia or 100 nM DEX posthypoxia values were 53 ± 6, 64 ± 9, 78 ± 13, or 62 ± 12 mm Hg [mean ± sd]) and reversed by yohimbine, 58 ± 8 mm Hg, respectively. We conclude that DEX exerts the direct protective effect on the left ventricular dysfunction caused by hypoxia-reoxygenation through mainly 2-adrenergic stimulation before and during the hypoxic period.

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