Dexmedetomidine constant-rate infusion suppresses insulin secretion and impairs glucose tolerance in healthy dogs.

Clinically used low-dose dexmedetomidine CRI is unlikely to significantly impair glucose tolerance in healthy dogs.

This prospective, randomized, repeated-measures study investigated the metabolic effects of dexmedetomidine (DEX) constant-rate infusion (CRI) on glucose tolerance and insulin secretion in five healthy adult Beagles. Animals received four treatments in crossover fashion: low-dose DEX (1 µg/kg loading; 1 µg/kg/h CRI), medium-dose DEX (5 µg/kg loading; 5 µg/kg/h CRI), high-dose DEX (10 µg/kg loading; 10 µg/kg/h CRI), or saline control. An intravenous glucose tolerance test was administered 30 minutes after CRI initiation, with serial serum glucose and insulin measurements analyzed using linear mixed-effects models. DEX suppressed early-phase insulin secretion in a dose-dependent manner. Glucose disappearance rates were significantly reduced at medium (mean difference -1.37%/min; 95% CI, -2.32 to -0.42) and high doses (mean difference -1.45%/min; 95% CI, -2.36 to -0.54) compared to control. The low-dose treatment did not produce a meaningful difference in glucose disappearance rate (mean difference -0.68%/min; 95% CI, -1.63 to 0.27). No clinically relevant adverse events were recorded. These findings suggest that medium- and high-dose DEX CRI impairs glucose homeostasis primarily through suppression of insulin secretion, consistent with alpha-2 adrenoceptor-mediated inhibition of pancreatic beta cells. Importantly, the clinically employed low-dose regimen did not substantially alter glucose tolerance under controlled conditions, providing reassurance for routine clinical use. Clinicians should nonetheless remain vigilant regarding hyperglycemia when using DEX at higher infusion rates, particularly in patients with pre-existing metabolic or endocrine conditions.

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