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Alpha-2 agonists have been widely used in equine anaesthesia since the clinical advent of xylazine in the 1970s (Clarke and Hall 1969; Kerr et al. 1972). Alpha-2 agonists produce sedation, muscle relaxation and analgesia by stimulation of α2 receptors centrally in the brain and spinal cord and peripherally (Hellyer et al. 2003). Two α2 agonists, xylazine and detomidine, are currently approved for use in the horse in the USA, while 2 additional drugs, romifidine and medetomidine, are approved for use in horses in other countries. Although differing in potency, α2 agonists share a common pharmacology. The degree of sedation, muscle relaxation and analgesia for a given drug is dose-dependent (England and Clarke 1996). Arterial blood pressure is initially increased due to drug-induced increases in peripheral vascular resistance (Wagner et al. 1991). The increases may be sustained (10–60 mins) when more potent α2 agonists like detomidine are used. Heart rate decreases, sinus arrhythmia and first and second degree atrioventricular blockade are common initial reflex mediated responses. Decreases in heart rate produce significant decreases in cardiac output, often to levels 50% of predrug values (Yamashita et al. 2000). Respiratory rate is usually decreased but this is offset by increases in tidal volume so that significant hypercarbia does not usually occur. Relaxation of the muscles of the upper airway occurs and can predispose the horse to respiratory stridor (Lavoie et al. 1992). Additional effects include sweating, ataxia, decreased salivation, decreased gastric secretions and gastrointestinal motility and increased urine volume. Swallowing is depressed; the passage of nasogastric tubes may therefore be more difficult and horses should be monitored for potential oesophageal obstruction. Other incidental effects of α2 agonist administration include increases in intrauterine pressure, hyperglycaemia and hypoinsulinaemia (von Reitzenstein et al. 2002). Alpha-2 agonists as analgesics |
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