Effects of detomidine constant rate infusion on blood glucose and lactate in sevoflurane anesthetized horses

Abstract

Background: The drugs that promote sedation, analgesia, and anesthesia, as inhalatory agents, phenothiazines, benzodiazepines, alpha-2 adrenergic agonists, and opioids, can promote different kinds of side effects. The concept of a balanced anesthesia in equine was developed in order to minimize adverse effects inherent to anesthesia, creating a combination of lower doses of these drugs in comparison with the doses of each one used alone. Alpha-2-adrenoceptor agonists such as xylazine, detomidine, and others, are drugs used for standing sedation, analgesia, and reduction of volatile anesthetic requirement in the equine as well as an agent used to maintenance of arterial blood pressure during anesthesia. Alpha-2 agonists works stimulating receptors of autonomic neurons inducing reduction of heart rate, cardiac output and vascular resistance, hypertension, behavioral changes, and inhibition of insulin secretion. This reduction in insulin levels increases blood glucose concentration in horses due to its lower utilization in insulin-dependent tissues, as muscular and adipose tissues. Muscular tissue is capable to maintain a constant lactate production even in a well oxygenated environment in order to maintain its cellular activity, especially in cases when glucose is not available. To evaluate the effect on blood glucose and lactate, horses were submitted to one hour of detomidine constant rate infusion during sevofl urane inhalatory anesthesia with controlled ventilation, in order to assess blood concentration of glucose and lactate Materials, Methods & Results: Four adult horses were studied. Detomidine 20 µg.kg-1 was used as premedication followed by an association of ketamine and diazepam intravenously as anesthetic induction. After intubation, sevofl urane was vaporized at approximately 2.3 V%. Mechanical ventilation was established. After stabilization, an intravenous continuous rate infusion (CRI) of detomidine 5 µg.kg.h-1 was started. Venous blood samples were collected before premedication, prior to detomidine continuous infusion, 20, 40, and 60 min after beginning of infusion, in order to determination of glucose and lactate serum concentrations. After 60 min of detomidine infusion, the horses were allowed to recovery. There was statistical signifi cant hyperglycemia in the horses under CRI of detomidine. There was no signifi cant increase in blood lactate, despite of the hyperlactatemia in some animals. Discussion: Detomidine CRI of 5 µg.kg.h-1 does increase blood glucose levels over normal values but not to levels that could be toxic to tissues, mainly CNS. With low levels of serum insulin, body tissues, mainly muscular and adipose tissues, are unable to capture this available blood glucose and these cells depend on lactate metabolism. The lactate serum concentrations below normal range observed in studied horses suggest that all lactate produced by the tissues is being utilized in the energetic metabolism. In according to many authors, lactate is produced and utilized for mitochondrias as energetic source even in fully oxygenated tissues, which seems to be what happened in this experiment. The present study helps to understand energetic metabolism in horses under general inhaled anesthesia with detomidine CRI, a selective alpha-2-adrenoceptor agonist. In order to better evaluate energetic metabolism during inhaled anesthesia under detomidine infl uence, other studies are suggested, as prolonged anesthesia duration to evaluate a longer adrenergic stimulus induced by detomidine. Besides, other investigations with detomidine CRI in horses submitted to surgical procedures could provide different responses in energetic metabolism.