期刊
VETERINARY ANAESTHESIA AND ANALGESIA
卷 48, 期 3, 页码 314-323出版社
ELSEVIER
DOI: 10.1016/j.vaa.2020.12.007
关键词
alpha(2)-adrenoreceptor agonist; alpha(2)-adrenoreceptor antagonist; cardiac output; dexmedetomidine; minimum alveolar concentration; vatinoxan
资金
- Vetcare, Finland
The study found that the combined use of vatinoxan and dexmedetomidine can significantly reduce the requirement for sevoflurane in dogs while also improving cardiovascular function. The addition of vatinoxan can attenuate the adverse effects of dexmedetomidine, such as slowing heart rate and decreasing CO, and gradually restore cardiovascular variables to baseline levels.
Objective To evaluate the effects of combined infusions of vatinoxan and dexmedetomidine on inhalant anesthetic requirement and cardiopulmonary function in dogs. Study design Prospective experimental study. Methods A total of six Beagle dogs were anesthetized to determine sevoflurane minimum alveolar concentration (MAC) prior to and after an intravenous (IV) dose (loading, then continuous infusion) of dexmedetomidine (4.5 mu g kg(-1) hour(-1)) and after two IV doses of vatinoxan in sequence (90 and 180 mu g kg(-1) hour(-1)). Blood was collected for plasma dexmedetomidine and vatinoxan concentrations. During a separate anesthesia, cardiac output (CO) was measured under equivalent MAC conditions of sevoflurane and dexmedetomidine, and then with each added dose of vatinoxan. For each treatment, cardiovascular variables were measured with spontaneous and controlled ventilation. Repeated measures analyses were performed for each response variable; for all analyses, p < 0.05 was considered significant. Results Dexmedetomidine reduced sevoflurane MAC by 67% (0.64 +/- 0.1%), mean +/- standard deviation in dogs. The addition of vatinoxan attenuated this to 57% (0.81 +/- 0.1%) and 43% (1.1 +/- 0.1%) with low and high doses, respectively, and caused a reduction in plasma dexmedetomidine concentrations. Heart rate and CO decreased while systemic vascular resistance increased with dexmedetomidine regardless of ventilation mode. The co-administration of vatinoxan dose-dependently modified these effects such that cardiovascular variables approached baseline. Conclusions and clinical relevance IV infusions of 90 and 180 mu g kg(-1) hour(-1) of vatinoxan combined with 4.5 mu g kg(-1) hour(-1) dexmedetomidine provide a meaningful reduction in sevoflurane requirement in dogs. Although sevoflurane MAC-sparing properties of dexmedetomidine in dogs are attenuated by vatinoxan, the cardiovascular function is improved. Doses of vatinoxan >180 mu g kg(-1) hour(-1) might improve cardiovascular function further in combination with this dose of dexmedetomidine, but beneficial effects on anesthesia plane and recovery quality may be lost.
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