超高压液相色谱串联四级杆飞行时间质谱法同时筛查牛肉中6种镇静剂

应用超高压液相色谱串联四级杆飞行时间质谱建立了同时筛查牛肉中6种镇静剂的新方法.样品经乙腈提取后,氨基柱净化,氮吹复溶后上机测定.空白样品在2、5和10 μg/kg三个不同添加浓度下测得6种镇静剂的回收率在60％～90％,6种镇静剂的检出限为0.5～1 μg/kg,且在2 ～50 ng/mL范围内线性关系良好,相关系数r2≥0.98.在2、5和10 μg/kg三个添加浓度下获得的6种镇静剂的精确分子量,其质量偏差绝对值均低于7×10-6,适用于牛肉中6种镇静剂的检测.     

The α2A‐adrenoceptor subtype plays a key role in the analgesic and sedative effects of xylazine

Xylazine, the classical α₂‐adrenoceptor (α₂‐AR) agonist, is still used as an analgesic and sedative in veterinary medicine, despite its low potency and affinity for α₂‐ARs. Previous pharmacological studies suggested that the α_2A‐AR subtype plays a role in mediating the clinical effects of xylazine; however, these studies were hampered by the poor subtype‐selectivity of the antagonists used and a lack of knowledge of their bioavailability in vivo. Here, we attempted to elucidate the role of the α_2A‐AR subtype in mediating the clinical effects of xylazine by comparing the analgesic and sedative effects of this drug in wild‐type mice with those in α_2A‐AR functional knockout mice using the hot‐plate and open field tests, respectively. Hippocampal noradrenaline turnover in both mice was also measured to evaluate the contribution of α_2A‐AR subtype to the inhibitory effect of xylazine on presynaptic noradrenaline release. In wild‐type mice, xylazine (10 or 30 mg/kg) increased the hot‐plate latency. Furthermore, xylazine (3 or 10 mg/kg) inhibited the open field locomotor activity and decreased hippocampal noradrenaline turnover. By contrast, all of these effects were abolished in α_2A‐AR functional knockout mice. These results indicate that the α_2A‐AR subtype is mainly responsible for the clinical effects of xylazine.     

Survival and behavioural responses of cool and warm water fish sedated with AQUI‐S®20E (10% eugenol) at high loading densities

This study evaluated the effects of AQUI‐S^®20E (10% eugenol) sedation on the survival and behaviour of yellow perch Perca flavescens (Mitchill) and Nile tilapia Oreochromis niloticus L. held in high loading densities. Fish were held in 0–300 mg L^?1 AQUI‐S^®20E (0–30 mg L^?1 eugenol) for up to 10 h in static tanks. At 17°C, yellow perch held in 200 and 300 mg L^?1 AQUI‐S^®20E were lightly sedated for up to 7 h. Yellow perch at 200 and 300 mg L^?1 AQUI‐S^®20E also had >95% mean survival 7‐days post exposure using loading densities up to 360 g L^?1. Nile tilapia were only sedated for ≤3 h in concentrations up to 300 mg L^?1 at 22°C and had >90% mean survival at loading densities ≤480 g L^?1. Ammonia in tanks increased significantly as loading density increased, but treatment with AQUI–S^®20E did not reduce ammonia accumulation. Results suggest that AQUI–S^®20E was effective to sedate yellow perch and Nile tilapia at high loading densities, but sedation varied with loading density and species.     

Sublingual administration of detomidine to calves prior to disbudding: a comparison with the intravenous route

ObjectiveTo study the effects of oromucosal detomidine gel administered sublingually to calves prior to disbudding, and to compare its efficacy with intravenously (IV) administered detomidine.Study designRandomised, prospective clinical study.AnimalsTwenty dairy calves aged 12.4 ± 4.4days (mean ± SD), weight 50.5 ± 9.0 kg.MethodsDetomidine at 80 μg kg^?1 was administered to ten calves sublingually (GEL) and at 30 μg kg^?1 to ten control calves IV (V. jugularis). Meloxicam (0.5 mg kg^?1) and local anaesthetic (lidocaine 3 mg kg^?1) were administered before heat cauterization of horn buds. Heart rate (HR), body temperature and clinical sedation were monitored over 240 minutes. Blood was collected from the V. cephalica during the same period for drug concentration analysis. Pharmacokinetic variables were calculated from the plasma detomidine concentration-time data using non-compartmental methods. Statistical analyses compared routes of administration by Student’s t-test and linear mixed models as relevant.ResultsThe maximum plasma detomidine concentration after GEL was 2.1 ± 1.2 ng mL^?1 (mean ±SD) and the time of maximum concentration was 66.0 ± 36.9 minutes. The bioavailability of detomidine was approximately 34% with GEL. Similar sedation scores were reached in both groups after administration of detomidine, but maximal sedation was reached earlier in the IV group (10 minutes) than in the GEL group (40 minutes). HR was lower after IV than GEL from 5 to 10 minutes after administration. All animals were adequately sedated, and we were able to administer local anaesthetic without resistance to all of the calves before disbudding.Conclusions and clinical relevanceOromucosally administered detomidine is an effective sedative agent for calves prior to disbudding.     

Effects of acepromazine and dexmedetomidine,followed by propofol induction and maintenance with isoflurane anaesthesia,on the microcirculation of Beagle dogs evaluated by sidestream dark field imaging: an experimental trial

ObjectiveTo investigate the effects of intramuscularly administered acepromazine or dexmedetomidine on buccal mucosa microcirculation in Beagle dogs.Study designExperimental, blinded, crossover study.AnimalsA group of seven Beagle dogs aged 7.5 ± 1.4 years (mean ± standard deviation).MethodsMicrocirculation was assessed on buccal mucosa using sidestream dark field videomicroscopy. After baseline measurements, 5 μg kg^–1 dexmedetomidine or 30 μg kg^–1 acepromazine were administered intramuscularly. After 10, 20 and 30 minutes, measurements were repeated. At 40 minutes after premedication, anaesthesia was induced with propofol intravenously and maintained with isoflurane. Measurements were repeated 50, 60 and 65 minutes after the injection of the investigated drugs. Analysed microcirculatory variables were: Perfused de Backer density, Perfused de Backer density of vessels < 20 μm, Proportion of perfused vessels and Proportion of perfused vessels < 20 μm. Heart rate (HR), systolic, diastolic (DAP) and mean (MAP) arterial pressures were recorded at the same time points. Macro- and microcirculatory variables were analysed using a linear mixed model with baseline as a covariate, treatment, trial period and repetition as fixed effects and time and dog as random effect. Results are presented as effect size and confidence interval; p values < 0.05 were considered significant.ResultsAfter acepromazine, Perfused de Backer density was greater during sedation and anaesthesia [3.71 (1.93–5.48 mm mm^–2, p < 0.0001) and 2.3 (0.86–3.75 mm mm^–2, p < 0.003)], respectively, than after dexmedetomidine. HR was significantly lower, whereas MAP and DAP were significantly higher with dexmedetomidine during sedation and anaesthesia (p < 0.0001 for all) compared with acepromazine.Conclusions and clinical relevanceThe sedative drugs tested exerted a significant effect on buccal mucosal microcirculation with a higher Perfused de Backer density after the administration of acepromazine compared with dexmedetomidine. This should be considered when microcirculation is evaluated using these drugs.     

超高效液相色谱-串联质谱法测定动物尿液中5种镇静剂类药物残留

为建立动物尿液中异丙嗪亚砜、异丙嗪、氯丙嗪、安眠酮和地西泮5种镇静剂类药物残留的超高效液相色谱-串联质谱(UPLC-MS/MS)检测方法,本研究以固相萃取为净化手段,采用HPLC-MS/MS检测猪、牛和羊尿液中5种镇静剂类药物的残留量。结果表明,尿液样品经离心,调节pH值,Oasis MCX固相萃取柱净化后,能够有效去除杂质,5种镇静剂在0.6~20.0 μg·L^-1范围内呈良好的线性关系,相关系数(R²)均大于0.993;5种镇静剂类药物的检出限和定量限分别为0.1和0.6 μg·L^-1,0.6、2.5和9.0 μg·L^-1 3个添加水平的回收率介于64.6%~110.2%之间,相对标准偏差(RSD)均小于6.0%。本研究结果为不同动物尿液中镇静剂类兽药残留的精准检测提供了技术支持。     

改良QuEChERS结合高效液相色谱-串联质谱法检测饲料中的7种镇静剂

本实验旨在建立以改良的QuEChERS作为前处理技术,结合高效液相色谱-串联质谱技术(HPLC-MS/MS)检测饲料中7种镇静剂的检测方法。样品加入乙腈提取,提取液经增强型基质去脂吸附剂(EMR-Lipid)脱脂,盐析后经PSA和C18吸附剂进一步净化浓缩,然后用高效液相色谱-串联质谱方法检测分析。结果表明:7种镇静剂为1~100μg/L时线性关系良好,相关系数均大于0.99,检出限为1.1~2.8μg/kg,定量限为3.7~9.3μg/kg。分别对配合饲料、浓缩饲料和预混合饲料进行3个水平的加标回收实验,平均回收率为84.7%~96.5%,相对标准偏差为3.2%~10.8%。该方法前处理方法快速、简便、灵敏度高,适用于饲料中多种残留镇静剂的同时测定。     

Effectiveness of eugenol sedation to reduce the metabolic rates of cool and warm water fish at high loading densities

Effects of eugenol (AQUI‐S^®20E, 10% active eugenol) sedation on cool water, yellow perch Perca flavescens (Mitchill), and warm water, Nile tilapia Oreochromis niloticus L. fish metabolic rates were assessed. Both species were exposed to 0, 10, 20 and 30 mg L^?1 eugenol using static respirometry. In 17°C water and loading densities of 60, 120 and 240 g L^?1, yellow perch controls (0 mg L^?1 eugenol) had metabolic rates of 329.6–400.0 mg O₂ kg^?1 h^?1, while yellow perch exposed to 20 and 30 mg L^?1 eugenol had significantly reduced metabolic rates of 258.4–325.6 and 189.1–271.0 mg O₂ kg^?1 h^?1 respectively. Nile tilapia exposed to 30 mg L^?1 eugenol had a significantly reduced metabolic rate (424.5 ± 42.3 mg O₂ kg^?1 h^?1) relative to the 0 mg L^?1 eugenol control (546.6 ± 53.5 mg O₂ kg^?1 h^?1) at a loading density of 120 g L^?1 in 22°C water. No significant differences in metabolic rates for Nile tilapia were found at 240 or 360 g L^?1 loading densities when exposed to eugenol. Results suggest that eugenol sedation may benefit yellow perch welfare at high densities (e.g. live transport) due to a reduction in metabolic rates, while further research is needed to assess the benefits of eugenol sedation on Nile tilapia at high loading densities.