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ANESTHETIC PHARMACOLOGY

Identification of the Central Imidazoline Receptor Subtype Involved in Modulation of Halothane-Epinephrine Arrhythmias in Rats

Kiyokazu Kagawa, MD^*, Yukio Hayashi, MD^*, Isao Itoh, MD^*, Mitsuo Iwasaki, MD^*, Koji Takada, MD^*, Takahiko Kamibayashi, MD^*, Atsushi Yamatodani, MD, and Takashi Mashimo, MD^*

Department of *Anesthesiology and Medical Physics School of Allied Health Sciences, Osaka University Faculty of Medicine, Japan

Address correspondence and reprint requests to Yukio Hayashi, MD, Department of Anesthesiology, Osaka University Faculty of Medicine (D-7), 2–2, Yamada-oka, Suita, Osaka 565–0871, Japan. Address e-mail to yhayashi{at}anes.med.osaka-u.ac.jp.

We previously reported that imidazoline receptors in the central nervous system are involved in modulation of halothane-epinephrine arrhythmias. These receptors have been subclassified as I₁ and I₂ subtypes, but it is not known which receptor subtype is involved in halothane-epinephrine-induced arrhythmias. We designed the present study to clarify the involvement of central imidazoline receptor subtype in the modulation of halothane-epinephrine-induced arrhythmias. Rats were anesthetized with halothane and monitored continuously for systemic arterial blood pressure and premature ventricular contractions. The arrhythmogenic dose of epinephrine was defined as the smallest dose that produces three or more premature ventricular contractions within a 15-s period. Intracisternal moxonidine dose-dependently inhibited the epinephrine-induced arrhythmias during halothane anesthesia. Intracisternal efaroxan, a selective I₁ antagonist with little affinity for I₂ subtype, but not rauwolscine, an ₂ antagonist without affinity for imidazoline receptors, blocked the antiarrhythmic effect of moxonidine. Intracisternal BU 224 and 2-BFI, selective I₂ ligands, also inhibited the epinephrine-induced arrhythmias dose-dependently; however, these effects were abolished by efaroxan. We conclude that central I₁, but not I₂, receptors play an important role in inhibition of halothane-epinephrine arrhythmia.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999