Sedative and cardiorespiratory effects of low doses of xylazine with and without acepromazine in Nordestino donkeys.

BACKGROUND: Information on appropriate protocols for sedation of Nordestino donkeys is scarce. OBJECTIVES: To evaluate the sedative and cardiorespiratory effects of low doses of intravenous (i.v.) xylazine with and without acepromazine in 'Nordestino' donkeys. STUDY DESIGN: Seven healthy female Nordestino donkeys (150 ± 18 kg) were included in this blinded, randomised, crossover experiment. METHODS: Four treatments were administered, consisting of two i.v. injections, at baseline (T0, 1st injection) and 15 min later (T15, 2nd injection). Treatments included acepromazine 0.05 mg/kg bwt + saline (AS), saline + xylazine 0.5 mg/kg bwt (SX0.5), acepromazine + xylazine 0.25 mg/kg bwt (AX0.25) or acepromazine + xylazine 0.5 mg/kg bwt (AX0.5). Sedative and cardiorespiratory parameters were evaluated before T0 and 15, 20, 30, 45, 60, 75 and 90 min after treatment. Degree [height of head above ground (HHAG)] and quality of sedation [ataxia, responses to stimuli and visual analogue scale (VAS) scoring] and respiratory rate were evaluated by the main investigator in situ, and heart rate was measured by an assistant investigator. Three experienced evaluators assessed vídeos for ataxia and responses to stimuli. Normal data were analysed by repeated measures ANOVA, and non-normal by Kruskal-Wallis (P<0.05). RESULTS: HHAG was lower than baseline for 15 min after xylazine administration in AX0.25 and for 30 min in SX0.5 and AX0.5 groups. All treatments with xylazine increased VAS and ataxia scores in situ for 15 min after xylazine administration, with no differences between groups. Ataxia scores in situ were higher in SX0.5 and AX0.5 groups than AS for 15 and 30 min after xylazine administration, respectively. MAIN LIMITATIONS: Absence of a negative control group (saline-saline). CONCLUSION: Acepromazine added to xylazine at 0.25 mg/kg bwt produced briefer and milder sedation than xylazine at 0.5 mg/kg bwt.

Improving access to the control region and tRNA gene clusters of dipteran mitochondrial DNA.

Despite the successful use of universal primers for amplifying insect mtDNA, specific regions remain difficult to recover and demand the use of taxon-specific primers. In this work, we describe a new set of primers for efficiently amplifying and sequencing the mtDNA control region and three tRNA gene clusters of dipterans of medical and veterinary importance, including Muscidae, Calliphoridae, and Oestridae species. These new primers were useful for investigating the nucleotide information and the structural organization of dipteran mtDNA.

Automatic detection of K-complexes: validation in normals and dysthymic patients.

A model-based automatic K-complex (Kc) detector was applied to all-night single-channel sleep electroencephalographic (EEG) recordings from normal and dysthymic patients. The performance of the detector was analyzed in the two groups, and the differences obtained were discussed. The results showed that the detection rate of Kc in the normal group was around 92% through all stages of non-rapid eye movement (NREM) sleep, but with high numbers of "false" positives in stage 4 NREM, which reached 57%. In the dysthymic patients "true" detection included 85% of the Kc, but the percentage of "false" positives dropped to 25% in stage 4 NREM. Most of the "false" detections in the normal group were due to sharp delta activity during slow wave sleep (SWS). The results in the patient group were expected, because sleep in dysthymics showed a reduction in SWS when compared to normals. The behavior and automatic artifact rejection mechanisms of the detector are briefly presented. The model-based Kc detector performed significantly better than other automatic detectors described in the literature; it was found to be a useful tool for routine sleep EEG studies.

A model-based detector of vertex waves and K complexes in sleep electroencephalogram.

A model of sleep phasic events such as vertex waves, K complexes, delta waves and sleep spindles is proposed. It consists of feedback loops that are driven by white noise (simulating tonic delta and sigma activity) and by isolated random impulses, simulating vertex waves or K complexes, depending on the background tonic activity. A model-based method for the detection of sleep phasic events was implemented in a personal computer. Its performance was investigated using simulated and real whole-night EEG signals. The method was able to detect K complexes and vertex waves in a reliable way in spite of their variable shapes and in the presence of a variety of background activities. The detector appears to have superior performance to those so far reported in the literature. The performance of the detector was also compared to that of an electroencephalographer using normal sleep EEG records of 8 h duration from 6 subjects. The performance was satisfactory both in terms of accuracy and reliability. The problem of detecting K complexes in stages 3 and 4 of sleep is discussed.