Читать книгу Farm Animal Anesthesia - Группа авторов - Страница 32

Similar to cattle, small ruminants (e.g. sheep and goats) are very sensitive to xylazine, and goats are more sensitive than sheep [6]. Camelids (e.g. alpacas, llamas), though more sensitive to xylazine than horses, are not as sensitive as cattle and small ruminants. Therefore, the dose of xylazine required to produce a similar degree of sedation in goats is equal to or slightly less than that of cattle, whereas a slightly higher dose is required in camelids than in cattle and small ruminants. Compared to llamas, alpacas require dosages 10–15% higher than the recommended dose for llamas. Xylazine alone produces dose‐dependent CNS depression ranging from standing sedation to recumbency and immobilization in small ruminants and camelids. Extreme caution should be practiced when xylazine is used in animals with preexisting cardiopulmonary disease and urinary tract obstruction or in late pregnancy [33, 40, 74]. Severe hypoxemia and pulmonary edema have been implicated as the cause of death in sheep under xylazine sedation/anesthesia [75–78]. Lateral recumbency in conscious sheep has been reported to induce a significant decrease in PaO₂ [79]. Xylazine has been reported to cause hypoxemia in xylazine‐sedated standing sheep [80, 81]. Apparently, all α₂ agonists cause similar and significant decrease in PaO₂ in sheep without affecting the PaCO₂ [82]. Nolan et al. (1986) [83] demonstrated that xylazine‐induced increased airway pressure (from 13.7 to 35 mmHg) in sheep was a result of dose‐dependent stimulation of peripheral (postsynaptic) α₂ adrenoceptors located in the airway smooth muscles (0.002–0.02 mg/kg). The effect of xylazine on the airway smooth muscles occurred within 5 minutes following IV administration and lasted longer than 60 minutes, long after the measured cardiovascular variables had returned to baseline values [83]. Furthermore, severe pulmonary parenchymal damage was seen with substantial morphological changes, such as extensive damages to capillary endothelium and alveolar type I cells, intra‐alveolar hemorrhage, and interstitial and alveolar edema. Such changes occurred almost immediately following IV administration of 0.15 mg/kg of xylazine [84]. Bronchospasm and venospasm due to direct action of α₂ adrenoceptors on the vascular and bronchial smooth muscles, transient α₂‐induced platelet aggregation with pulmonary microembolism, and release of cytokines and other inflammatory mediators subsequent to α₂‐induced pulmonary intravascular macrophage activation have been suggested as the contributing factors for the development of hypoxemia in sheep [85].

Caudal epidural administration of xylazine (0.07–0.1 mg/kg), with or without lidocaine, induced long‐lasting somatic analgesia for open castration in rams (8 hours, without lidocaine) and correction of vaginal prolapse in ewes (24 hours, with 0.5 mg/kg of lidocaine) [86, 87]. However, visceral analgesia induced by epidural xylazine alone may not be sufficient for ligation of the spermatic cord [86].