Immobilization of African buffaloes (Syncerus caffer) using etorphine–midazolam compared with etorphine–azaperone

ObjectiveTo compare induction times and physiological effects of etorphine–azaperone with etorphine–midazolam immobilization in African buffaloes.Study designRandomized crossover study.AnimalsA group of 10 adult buffalo bulls (mean body weight 353 kg).MethodsEtorphine–azaperone (treatment EA; 0.015 and 0.15 mg kg^–1, respectively) and etorphine–midazolam (treatment EM; 0.015 and 0.15 mg kg^–1, respectively) were administered once to buffaloes, 1 week apart. Once in sternal recumbency, buffaloes were instrumented and physiological variables recorded at 5 minute intervals, from 5 minutes to 20 minutes. Naltrexone (20 mg mg^–1 etorphine dose) was administered intravenously at 40 minutes. Induction (dart placement to recumbency) and recovery (naltrexone administration to standing) times were recorded. Arterial blood samples were analysed at 5 and 20 minutes. Physiological data were compared between treatments using a general linear mixed model and reported as mean ± standard deviation. Time data were compared using Mann-Whitney U test and reported as median (interquartile range) with p ≤ 0.05.ResultsActual drug doses administered for etorphine, azaperone and midazolam were 0.015 ± 0.001, 0.15 ± 0.01 and 0.16 ± 0.02 mg kg^–1, respectively. Induction time for treatment EA was 3.3 (3.6) minutes and not different from 3.2 (3.2) minutes for treatment EM. The overall mean arterial blood pressure was significantly lower for treatment EA (102 ± 25 mmHg) than that for treatment EM (163 ± 18 mmHg) (p < 0.001). The PaO₂ for treatment EA (37 ± 12 mmHg; 5.0 ± 1.6 kPa) was not different from that for treatment EM (43 ± 8 mmHg; 5.8 ± 1.1 kPa). Recovery time was 0.8 (0.6) minutes for treatment EA and did not differ from 1.1 (0.6) minutes for treatment EM.Conclusions and clinical relevanceTreatment EA was as effective as treatment EM for immobilization in this study. However, systemic arterial hypertension was a concern with treatment EM, and both combinations produced clinically relevant hypoxaemia. Supplemental oxygen administration is recommended with both drug combinations.     

克伦特罗和苯二氮卓化合物F89对肉鸡生长、胴体组成和血液代谢物的影响

将β－受体激动剂克伦特罗（１ｍｇ／ｋｇ）和苯二氮卓化合物Ｆ８９（２ｍｇ／ｋｇ）同时添加在４１～５６,３８～５９和５～５６日龄红布罗肉鸡的日粮中,连续饲喂。饲养试验表明：试验组肉鸡的摄食量分别提高了４．４７％,３．３４％和５．３４％;增重分别提高了１３．６％（Ｐ＜０．０１）,８．７２％（Ｐ＜０．０５）和９．９６％（Ｐ＜０．０５）。屠宰试验表明：试验组肉鸡的胸肌率和腿肌率都有明显提高,从而改善了肉鸡胴体组成,提高了瘦肉率。肉鸡的胸肌增加伴随着ＲＮＡ含量增多,而总ＤＮＡ含量保持不变,因此,试验组肉鸡的胸肌ＲＮＡ／ＤＮＡ值上升。添喂Ｆ８９和ＣＬ后,肉鸡血清尿酸和雌激素（１７β－Ｅ２）含量显著降低,而游离脂肪酸和胰岛素含量显著上升。     

添加苯二氮化合物F89对皖西白鹅生长和代谢性能的影响

利用生理调节剂Ｆ８９提高皖西白鹅的摄食量,加速动物生长。日粮中添加２ｍｇ／ｋｇＦ８９,连续饲喂８～３５日龄皖西白鹅,日摄食量较对照组增加６．０２％,增重提高９．４０％,耗料比下降２．８９％。对育肥期鹅的增重也有明显影响。血液代谢物分析表明：饲喂Ｆ８９后,皖西白鹅血清中葡萄糖和尿酸浓度下降,β－脂蛋白浓度上升。提示Ｆ８９不仅能促进鹅的摄食量,而且可以影响鹅的代谢机能,促进生长     

Changes of mitochondrial peripheral-type benzodiazepine receptor during rat live regeneration

AIM: To investigate the expression profile of peripheral-type benzodiazepine receptor (PBR) involved in mitochondrial permeability transition (PT) regulation, and to observe the binding dynamic of the mitochondrial PBR with specificity ligand during rat live regeneration. METHODS: Liver regeneration model was produced by 70% partial hepatectomy (PH) performed in male SD rats. The animals of sham groups underwent the same surgical operations as PH groups did, but the liver lobes were not resected. The animals in the PH groups and corresponding sham groups were sacrificed at 3, 6, 12, 24, 48, 72, 120 and 168 hours after the operation. The livers were removed, weighted and processed for isolation of mitochondria. Semi-quantitative RT-PCR was performed to examine the expression level of PBR in 70% hepatectomized rat livers during the whole regeneration process and compared to that in the sham and normal groups. Compared with healthy rats, the kinetic parameters of PBR was evaluated by using a specific radioligand ［3H］-PK11195. RESULTS: Compared with healthy rats, the expression of PBR was unchanged. Meanwhile, the results obtained in the present experiments by scatchard analysis, Bmax of PK11195 for PBR significantly decreased, returned to normal level in 168 h after PH. Kd of PK11195 for PBR significantly decreased at 72 h and 168 h after PH of rat liver regeneration (P<0.01). CONCLUSION: The mRNA expression and evaluation of kinetic parameters of PBR may be related to the time-phase change of mitochondrial PT during rat liver regeneration after partial hepatectomy.     

Clinical evaluation of intranasal benzodiazepines, alpha-agonists and their antagonists in canaries

OBJECTIVE: To evaluate the effects of intranasal benzodiazepines (midazolam and diazepam), alpha(2)-agonists (xylazine and detomidine) and their antagonists (flumazenil and yohimbine) in canaries. STUDY DESIGN: Prospective randomized study. ANIMALS: Twenty-six healthy adult domesticated canaries of both sexes, weighing 18.3 +/- 1.0 g. METHODS: In Study 1 an attempt was made to determine the dose of each drug that allowed treated canaries to be laid in dorsal recumbency for at least 5 minutes, i.e. its effective dose. This involved the evaluation of various doses, during which equal volumes of the tested drug were administered slowly into each nostril. In study 2 the onset of action, duration and quality of sedation induced by each drug at its effective dose were evaluated. The efficacy of flumazenil and yohimbine in antagonizing the effects of the sedative drugs was also studied. RESULTS: In study 1 administration of 25 microL per nostril diazepam (5 mg mL(-1) solution) or midazolam (5 mg mL(-1) solution) to each bird caused adequate sedation within 1-2 minutes; birds did not move when placed in dorsal recumbency. After administration of 12 microL per nostril of either xylazine (20 mg mL(-1)) or detomidine (10 mg mL(-1)), birds seemed heavily sedated and assumed sternal recumbency but could not be placed in dorsal recumbency. Higher doses of xylazine (0.5 mg per nostril) or detomidine (0.25 mg per nostril) prolonged sedation but did not produce dorsal recumbency. In study 2 in all treatment groups, onset of action was rapid. Duration of dorsal recumbency was significantly longer (p < 0.05) with diazepam (38.4 +/- 10.5 minutes) than midazolam (17.1 +/- 2.2 minutes). Intranasal flumazenil (2.5 microg per nostril) significantly reduced recumbency time. Duration of sedation was longer with alpha(2)-agonists compared with benzodiazepines. Detomidine had the longest duration of effect (257.5 +/- 1.5 minutes) and midazolam the shortest (36.9 +/- 2.4 minutes). Nasally administered flumazenil significantly reduced the duration of sedation with diazepam and midazolam while yohimbine (120 microg per nostril) effectively antagonized the effects of xylazine and detomidine. CONCLUSION: Intranasal benzodiazepines produce rapid and effective sedation in canaries. Intranasal alpha(2) agonists produce sedation but not sustained recumbency. Specific antagonists are also effective when used by this route. Clinical relevance Intranasal sedative drug administration is an acceptable alternative method of drug delivery in canaries.     

Imidazenil,a new drug for the management of convulsions in organophosphate intoxication in rodents

The summary deals with the anti-convulsant and antilethal effects of a new benzodiazepine receptor partial agonist, imidazenil, in DFP intoxication. It has been demonstrated that imidazenil (2–5 mg kg⁻¹) significantly decreases convulsion intensity, rapidly inhibits seizure patterns in brain bioelectrical activity and significantly increases the anti-lethal efficacy of atropine plus obidoxime therapy. These effects are comparable to diazepam at 5 mg kg⁻¹. However, diazepam exhibits myorelaxant activity at therapeutic doses, which are only observed at 5–10 times the therapeutic doses of imidazenil.