American journal of veterinary research · 2026
Dexmedetomidine constant-rate infusion suppresses insulin secretion and impairs glucose tolerance in healthy dogs.
СтатьяRandomized Controlled Trial, VeterinaryНазвание и аннотация: Перевод в очереди
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Maeda Kenichi, Inada Misaki, Iwai Satomi, Okano Shozo
Аннотация
OBJECTIVE: To evaluate the effects of dexmedetomidine (DEX) constant-rate infusion (CRI) on glucose tolerance and metabolic responses in healthy dogs.
METHODS: In a prospective, randomized, repeated-measures study, 5 healthy adult Beagles received 4 treatments: 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. An IV glucose tolerance test was performed 30 minutes after CRI initiation. Serum glucose and insulin were measured. Data were analyzed using linear mixed-effects models, with treatment, time, and their interaction as fixed effects and dog as a random effect. Results are reported as effect sizes with 95% CIs.
RESULTS: DEX CRI suppressed insulin secretion in a dose-related manner during the early phase of the glucose tolerance test. Compared with control, glucose disappearance rate was reduced at medium (mean difference, -1.37%/min; 95% CI, -2.32 to -0.42) and high (mean difference, -1.45%/min; 95% CI, -2.36 to -0.54) infusion rates, whereas the low-dose treatment did not differ meaningfully (mean difference, -0.68%/min; 95% CI, -1.63 to 0.27). No clinically relevant adverse events occurred.
CONCLUSIONS: DEX CRI causes dose-related suppression of insulin secretion and impairs glucose tolerance at medium and high infusion rates in healthy dogs. In contrast, the clinically used low infusion rate did not substantially alter glucose tolerance under study conditions.
CLINICAL RELEVANCE: Medium- and high-dose DEX CRI may impair glucose tolerance in healthy dogs, whereas the clinically used low-dose regimen appears unlikely to disrupt glucose homeostasis under controlled conditions.
METHODS: In a prospective, randomized, repeated-measures study, 5 healthy adult Beagles received 4 treatments: 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. An IV glucose tolerance test was performed 30 minutes after CRI initiation. Serum glucose and insulin were measured. Data were analyzed using linear mixed-effects models, with treatment, time, and their interaction as fixed effects and dog as a random effect. Results are reported as effect sizes with 95% CIs.
RESULTS: DEX CRI suppressed insulin secretion in a dose-related manner during the early phase of the glucose tolerance test. Compared with control, glucose disappearance rate was reduced at medium (mean difference, -1.37%/min; 95% CI, -2.32 to -0.42) and high (mean difference, -1.45%/min; 95% CI, -2.36 to -0.54) infusion rates, whereas the low-dose treatment did not differ meaningfully (mean difference, -0.68%/min; 95% CI, -1.63 to 0.27). No clinically relevant adverse events occurred.
CONCLUSIONS: DEX CRI causes dose-related suppression of insulin secretion and impairs glucose tolerance at medium and high infusion rates in healthy dogs. In contrast, the clinically used low infusion rate did not substantially alter glucose tolerance under study conditions.
CLINICAL RELEVANCE: Medium- and high-dose DEX CRI may impair glucose tolerance in healthy dogs, whereas the clinically used low-dose regimen appears unlikely to disrupt glucose homeostasis under controlled conditions.