Backgrounds, there are limited choice of analgesic agent in horse medicine, and mostly because of side effects usage of analgesics is contraindicated in horses. Objectives, introduction of compounds which have little side effects whith good analgesic affects. Methods, this study was undertakan in 6 healthy horses, in control group they received normal saline. In treatment group CRI of lidocaine and xylasine has been administered, and data was recorded at the beginning of infusion and 10, 20, 30, 40 and 50 minutes after starting the infusion at time 50 infusion was stopped and 15, 30 and 60 minutes after that data was recorded as well. Analgesic effect was evaluated by algometer. NIBP, Temperature, Heart rate, respiratory rate, sedation, intestinal sounds was evaluated at each time points. Results, 30 minutes after starting the infusion analgesic effect has started and there was significant difference between control and treatment group this effect last until the end of infusion and after the CRI this effect disappeared gradually. Conclusions, simultaneous infusion of xylasine and lidocanie has significant analgesic effect. But it needs more study in fields like laminitis cases to prove the efficacy of combination of xylazine and lidocaine.

Introduction: Tiletamine-xylazine-tramadol (XFM) has few side effects and can provide good sedation and analgesia. Adenosine 5’-monophosphate-activated protein kinase (AMPK) can attenuate trigeminal neuralgia. The study aimed to investigate the effects of XFM and its specific antagonist on AMPK in different regions of the brain. Material and Methods: A model of XFM in the rat was established. A total of 72 Sprague Dawley (SD) rats were randomly divided into three equally sized groups: XFM anaesthesia (M group), antagonist (W group), and XFM with antagonist interactive groups (MW group). Eighteen SD rats were in the control group and were injected intraperitoneally with saline (C group). The rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus, and brain stem were immediately separated, in order to detect AMPKα mRNA expression by quantitative PCR. Results: XFM was able to increase the mRNA expression of AMPKα1 and AMPKα2 in all brain regions, and the antagonist caused the opposite effect, although the effects of XFM could not be completely reversed in some areas. Conclusion: XFM can influence the expression of AMPK in the central nervous system of the rat, which can provide a reference for the future development of anaesthetics for animals.

Xylazine, a type of α₂-adrenoceptors, is a commonly used drug in veterinary medicine. Xylazine-induced changes in the content of amino acid neurotransmitters – glycine (Gly) and aspartic acid (Asp), in different brain regions and neurons were studied. Wistar rats were administered 50 mg/kg or 70 mg/kg of xylazine by intraperitoneal injection. In addition, in vitro experiments were conducted, in which neurons were treated with 15 μg/mL, 25 μg/mL, 35μg/mL, and 45 μg/mL of xylazine. Test methods were based on the enzyme-linked immunosorbent assays (ELISA). During anaesthesia, Asp levels in each brain area were significantly lower compared to the control group. Except for the cerebrum, levels of Gly in other brain areas were significantly increased during the anaesthesia period. In vitro, xylazine-related neuron secretion of Gly increased significantly compared to the control group at 60 min and 90 min. Moreover, xylazine caused a significant decrease in the levels of Asp secreted by neurons at 20 min, but gradually returned to the level of the control group. The data showed that during anaesthesia the overall levels of Asp decreased and overall levels of Gly increased. In addition, the inhibitory effect of xylazine on Asp and the promotion of Gly were dose-dependent. Our data showed that different effects of xylazine on excitatory and inhibitory neurotransmitters provided a theoretical basis for the mechanism of xylazine activity in clinical anaesthesia.

Xylazine, a type of α2-adrenoceptors, is a commonly used drug in veterinary medicine. Xylazine-induced changes in the content of amino acid neurotransmitters – glycine (Gly) and aspartic acid (Asp), in different brain regions and neurons were studied.

Introduction: Tiletamine-xylazine-tramadol (XFM) has few side effects and can provide good sedation and analgesia. Adenosine 5’-monophosphate-activated protein kinase (AMPK) can attenuate trigeminal neuralgia. The study aimed to investigate the effects of XFM and its specific antagonist on AMPK in different regions of the brain. Material and Methods: A model of XFM in the rat was established. A total of 72 Sprague Dawley (SD) rats were randomly divided into three equally sized groups: XFM anaesthesia (M group), antagonist (W group), and XFM with antagonist interactive groups (MW group). Eighteen SD rats were in the control group and were injected intraperitoneally with saline (C group). The rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus, and brain stem were immediately separated, in order to detect AMPKα mRNA expression by quantitative PCR. Results: XFM was able to increase the mRNA expression of AMPKα1 and AMPKα2 in all brain regions, and the antagonist caused the opposite effect, although the effects of XFM could not be completely reversed in some areas. Conclusion: XFM can influence the expression of AMPK in the central nervous system of the rat, which can provide a reference for the future development of anaesthetics for animals.

OBJECTIVE To examine the effects of imidazoline and nonimidazoline α-adrenergic agents on aggregation of feline platelets. SAMPLE Blood samples from 12 healthy adult cats. PROCEDURES In 7 experiments, the effects of 23 imidazoline and nonimidazoline α-adrenoceptor agonists or antagonists on aggregation and antiaggregation of feline platelets were determined via a turbidimetric method. Collagen and ADP were used to initiate aggregation. RESULTS Platelet aggregation was not induced by α-adrenoceptor agonists alone. Adrenaline and noradrenaline induced a dose-dependent potentiation of ADP- or collagen-induced aggregation. Oxymetazoline and xylometazoline also induced a small potentiation of ADP-stimulated aggregation, but other α-adrenoceptor agonists did not induce potentiation. The α2-adrenoceptor antagonists and certain imidazoline α-adrenergic agents including phentolamine, yohimbine, atipamezole, clonidine, medetomidine, and dexmedetomidine inhibited adrenaline-potentiated aggregation induced by ADP or collagen in a dose-dependent manner. The imidazoline compound antazoline inhibited adrenaline-potentiated aggregation in a dose-dependent manner. Conversely, α1-adrenoceptor antagonists and nonimidazoline α-adrenergic agents including xylazine and prazosin were ineffective or less effective for inhibiting adrenaline-potentiated aggregation. Moxonidine also was ineffective for inhibiting adrenaline-potentiated aggregation induced by collagen. Medetomidine and xylazine did not reverse the inhibitory effect of atipamezole and yohimbine on adrenaline-potentiated aggregation. CONCLUSIONS AND CLINICAL RELEVANCE Adrenaline-potentiated aggregation of feline platelets may be mediated by α2-adrenoceptors, whereas imidazoline agents may inhibit in vitro platelet aggregation via imidazoline receptors. Imidazoline α-adrenergic agents may have clinical use for conditions in which there is platelet reactivity to adrenaline. Xylazine, medetomidine, and dexmedetomidine may be used clinically in cats with minimal concerns for adverse effects on platelet function.

To investigate the effects of a xylazine infusion during isoflurane anesthesia on global perfusion parameters and gastrointestinal oxygenation and microperfusion, 8 adult warmblood horses were sedated with xylazine and anesthesia induced with midazolam and ketamine. Horses were mechanically ventilated during anesthesia. After 3 h of stable isoflurane anesthesia (FEIso 1.3 Vol %), a xylazine infusion with 1 mg/kg body weight (BW) per hour was started for 1 h and then stopped. Before, during, and after xylazine infusion, heart rate (HR), arterial blood pressure (MAP), cardiac output (CO), central venous pressure (CVP), and pulmonary artery pressure (PAP) were measured and systemic vascular resistance (SVR) was calculated. Arterial blood gases were taken and oxygen delivery (DO2) and alveolar dead space (VDalv) were calculated. Further intestinal oxygen and microperfusion were measured using white light spectroscopy and laser Doppler flowmetry. Surface probes were placed via median laparotomy on the stomach, the jejunum, and the colon. Wilcoxon rank-sum test was used to compare values over time (P < 0.05). During xylazine infusion, MAP, CVP, PAP, SVR, and VDalv increased significantly, whereas CO, DO2, and intestinal microperfusion decreased. Intestinal oxygenation remained unchanged. All parameters returned to pre-xylazine values within 1 h after stopping xylazine infusion. A xylazine infusion during constant isoflurane anesthesia in horses impairs global and intestinal perfusion without changing tissue oxygenation in normoxic healthy horses. Further studies are necessary, however, to evaluate whether a possible reduction of isoflurane concentration by xylazine infusion will ameliorate these negative effects.