Dexmedetomidine Prevents Epinephrine-induced Arrhythmias Through Stimulation of Central α2 Adrenoceptors in Halothane-anesthetized Dogs

Hayashi, Yukio; Sumikawa, Koji; Maze, Mervyn; Yamatodani, Atsushi; Kamibayashi, Takahiko; Kuro, Masakazu; Yoshiya, Ikuto

doi:10.1097/00000542-199107000-00018

Cited by 80 publications

(52 citation statements)

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“…It may also be due to presynaptic-mediated reduction of noradrenaline release or a direct vagomimetic action [78]. Although bradycardia can be a problem with the administration of alpha-2 adrenoceptor agonists, dexmedetomidine has been shown to protect against adrenaline-induced arrhythmia during halothane anaesthesia in dogs [79]. This anti-arrhythmic action may be due to stimulation of imidazoline receptors.…”

Section: Cardiovascular System Effectsmentioning

confidence: 99%

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Khan¹,

Ferguson²,

Jones³

1999

Anaesthesia

605

423

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SummaryClonidine has proved to be a clinically useful adjunct in clinical anaesthetic practice as well as in chronic pain therapy because it has both anaesthetic and analgesic-sparing activity. The more selective alpha-2 adrenoceptor agonists, dexmedetomidine and mivazerol, may also have a role in providing haemodynamic stability in patients who are at risk of peri-operative ischaemia. The side-effects of hypotension and bradycardia have limited the routine use of alpha-2 adrenoceptor agonists. Investigations into the molecular pharmacology of alpha-2 adrenoceptors have elucidated their role in the control of wakefulness, blood pressure and antinociception. We discuss the pharmacology of alpha-2 adrenoceptors and their therapeutic role in this review.

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Section: Cardiovascular System Effectsmentioning

confidence: 99%

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Khan¹,

Ferguson²,

Jones³

1999

Anaesthesia

605

423

View full text Add to dashboard Cite

show abstract

“…Several previous reports have shown that the central nervous system (CNS) affects the genesis of different types of arrhythmias including this type (Waxman et al, 1989;Podrid et al, 1990;Chen et al, 1991;Hayashi et al, 1991a,c). Recently, we demonstrated that an a2-adrenoceptor agonist dexmedetomidine, which has a weak affinity for imidazoline receptors (Wikberg & Uhlen, 1990;Wikberg et al, 1991), inhibits adrenaline-induced arrhythmia under halothane anaesthesia through its action on the CNS (Hayashi et al, 1991b). Furthermore, our subsequent studies suggested that central imidazoline receptors are involved in the genesis of halothane-adrenaline-induced arrhythmia (Hayashi et al, 1993a), and that the inhibition of sympathetic neural activity is protective against this type of arrhythmia (Kamibayashi et al, 1992;.…”

Section: Introductionmentioning

confidence: 96%

Antiarrhythmic action of rilmenidine on adrenaline‐induced arrhythmia via central imidazoline receptors in halothane‐anaesthetized dogs

Mammoto

Kamibayashi

Hayashi

et al. 1996

British J Pharmacology

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To elucidate the role of central imidazoline receptors in the genesis of adrenaline‐induced arrhythmias under halothane anaesthesia, we investigated the effects of rilmenidine, a selective agonist at imidazoline receptors, on this type of arrhythmia in dogs. Rilmenidine (1, 3, 10 μg kg−1, i.v.) did not affect basal haemodynamic parameters (heart rate and blood pressure), but dose‐dependently inhibited adrenaline‐induced arrhythmias under halothane anaesthesia. Although, rilmenidine has a weak affinity for α2‐adrenoceptors, pretreatment with idazoxan (10 μg kg−1, intracistenally i.c.), an imidazoline receptor antagonist which has also α2‐adrenoceptor blocking potency, blocked the antiarrhythmic effect of rilmenidine (10 μg kg−1, i.v.). In contrast, pretreatment with rauwolscine (20 μg kg−1, i.c.), a classical α2‐adrenoceptor antagonist with little affinity for imidazoline receptors, did not affect the effect of rilmenidine (10 μg kg−1, i.v.). Furthermore, bilateral vagotomy completely blocked the antiarrhythmic action of rilmenidine (10 μg kg−1, i.v.). It is suggested that the antiarrhythmic action of rilmenidine is due to the activation of central imidazoline receptors and that vagal tone is critical for this action of rilmenidine.

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“…On the other hand, previous studies have indicated that dexmedetomidine can prevent epinephrineinduced arrhythmias in dog experiments [6][7][8]. Stabilization of the systemic circulation after CPR (due to a reduction in postcountershock arrhythmias) may contribute to the maintenance of adequate cerebral perfusion pressure.…”

Section: Introductionmentioning

confidence: 97%

Effects of dexmedetomidine on cerebral circulation and systemic hemodynamics after cardiopulmonary resuscitation in dogs

Iida

Ohata

et al. 2006

J Anesth

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Dexmedetomidine Prevents Epinephrine-induced Arrhythmias Through Stimulation of Central α2 Adrenoceptors in Halothane-anesthetized Dogs

Cited by 80 publications

References 0 publications

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Antiarrhythmic action of rilmenidine on adrenaline‐induced arrhythmia via central imidazoline receptors in halothane‐anaesthetized dogs

Effects of dexmedetomidine on cerebral circulation and systemic hemodynamics after cardiopulmonary resuscitation in dogs

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