Opposite to α2-adrenergic agonists, an imidazoline I1 selective compound does not influence reflex bradycardia in rabbits

Sy, Guata Yoro; Bousquet, Pascal; Feldman, Josiane

doi:10.1016/j.autneu.2005.12.003

Cited by 7 publications

(4 citation statements)

References 27 publications

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“…It has been demonstrated in human volunteers that their blood pressure increases, whereas their HR decreases, at high plasma concentration of dexmedetomidine (26). In another study on rabbit, activation of a 2 -adrenoceptor, not I 1 receptor, exaggerated a reflex bradycardia (27). Therefore, these observations suggest a possibility that the incomplete amelioration of the dexmedetomidineassociated decrease in HR by efaroxan may be influenced, at least in part, by a reflex bradycardia, which could be magnified by a 2 -adrenoceptor activation.…”

Section: Discussionmentioning

confidence: 98%

Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newborn rats during dexmedetomidine administration

Sato

Saiki

Tamiya

et al. 2017

Pediatric Anesthesia

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Section: Discussionmentioning

confidence: 98%

Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newborn rats during dexmedetomidine administration

Sato

Saiki

Tamiya

et al. 2017

Pediatric Anesthesia

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“…DXM was selected as the study drug as it is a high affinity a 2 -adrenergic agonist, with a K i value of 13.2 nmol/l for a 2 -ARs [17], and is highly selective for a 2 -ARs; it crosses the blood-brain barrier easily [8] and it has a marked central hypotensive effect [18,19]. In wild-type control animals, a standard dose of DXM elicited the expected biphasic effect on BP of a 2 -adrenergic agonists acting centrally: a transient increase in BP followed by longlasting and marked hypotensive activity.…”

Section: Discussionmentioning

confidence: 99%

The central hypotensive effect induced by α2-adrenergic receptor stimulation is dependent on endothelial nitric oxide synthase

Feldman

Fellmann²,

Bousquet³

2008

Journal of Hypertension

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“…by administration of dexmedetomidine alone) or without this enhancement (i.e. by administration of dexmedetomidine plus atipamezole or efaroxan) [35]. Further investigation of the mechanisms underlying the persistent drop in the PR is warranted.…”

Section: Plos Onementioning

confidence: 99%

Effect of dexmedetomidine on cardiorespiratory regulation in spontaneously breathing adult rats

et al. 2022

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Purpose We examined the cardiorespiratory effect of dexmedetomidine, an α2- adrenoceptor/imidazoline 1 (I1) receptor agonist, in spontaneously breathing adult rats. Methods Male rats (226−301 g, n = 49) under isoflurane anesthesia had their tail vein cannulated for drug administration and their tail artery cannulated for analysis of mean arterial pressure (MAP), pulse rate (PR), and arterial blood gases (PaO2, PaCO2, pH). After recovery, one set of rats received normal saline for control recording and was then divided into three experimental groups, two receiving dexmedetomidine (5 or 50 μg·kg−1) and one receiving normal saline (n = 7 per group). Another set of rats was divided into four groups receiving dexmedetomidine (50 μg·kg−1) followed 5 min later by 0.5 or 1 mg∙kg−1 atipamezole (selective α2-adrenoceptor antagonist) or efaroxan (α2-adrenoceptor/I1 receptor antagonist) (n = 6 or 8 per group). Recordings were performed 15 min after normal saline or dexmedetomidine administration. Results Compared with normal saline, dexmedetomidine (5 and 50 μg·kg−1) decreased respiratory frequency (fR, p = 0.04 and < 0.01, respectively), PR (both p < 0.01), and PaO2 (p = 0.04 and < 0.01), and increased tidal volume (both p = 0.049). Dexmedetomidine at 5 μg·kg−1 did not significantly change minute ventilation (V′E) (p = 0.87) or MAP (p = 0.24), whereas dexmedetomidine at 50 μg·kg−1 significantly decreased V′E (p = 0.03) and increased MAP (p < 0.01). Only dexmedetomidine at 50 μg·kg−1 increased PaCO2 (p < 0.01). Dexmedetomidine (5 and 50 μg·kg−1) significantly increased blood glucose (p < 0.01), and dexmedetomidine at 50 μg·kg−1 increased hemoglobin (p = 0.04). Supplemental atipamezole or efaroxan administration similarly prevented the 50 μg·kg−1 dexmedetomidine-related cardiorespiratory changes. Principal conclusion These results suggest that dexmedetomidine-related hypoventilation and hypertension are observed simultaneously and occur predominantly through activation of α2-adrenoceptors, but not I1 receptors, in spontaneously breathing adult rats.

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Opposite to α2-adrenergic agonists, an imidazoline I1 selective compound does not influence reflex bradycardia in rabbits

Cited by 7 publications

References 27 publications

Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newborn rats during dexmedetomidine administration

Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newborn rats during dexmedetomidine administration

The central hypotensive effect induced by α2-adrenergic receptor stimulation is dependent on endothelial nitric oxide synthase

Effect of dexmedetomidine on cardiorespiratory regulation in spontaneously breathing adult rats

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