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Amiodarone may prevent the tilmicosin-caused lethal toxicity

Er, Ayse; Tras, Bunyamin; Cetin, Gul; Dik, Burak.
Acta sci. vet. (Impr.); 42: Pub.1187-Dec. 12, 2014. graf
Artigo em Inglês | VETINDEX | ID: biblio-1457193

Resumo

Background: Tilmicosin is widely used in veterinary medicine and its accidental overdose by injection may cause death viacausing negative inotropy and positive chronotropy in both the treated animal and the veterinarian. In addition, there is noany antidote against to tilmicosin-caused death. Amiodarone blocks some channels in the heart, but it has much complexeffect including vagotonic, bradycardic etc on the heart. Considering vagotonic and bradycardic effects of amiodarone, ithas been hypothesised that amiodarone may prevent tilmicosin-caused death. The aim of this study was to determine theeffect of amiodarone on the survival rate of rats in tilmicosin-caused lethal toxicity.Materials, Methods & Results: Twenty female Wistar rats (body weight: 288 ± 33.8 g, age: 7-8 months) were used in thisstudy. The study protocol was approved by the Ethical Committee. Rats received food and water ad libitum. The rats weredivided into two groups containing 10 rats each. Rats in Group 1 were administered 360 mg/kg of tilmicosin in a singlesubcutaneous injection. Rats in Group 2 were administered 25 mg/kg of amiodarone via the tail vein at 8. min after thesingle subcutaneous injection of tilmicosin in a dose of 360 mg/kg. After the injections, deaths were recorded at 0, 2, 6, 10,12 and 24 h. At the end of the 24-h period, survival/death ratio was analysed by the Chi-square test. The level of statisticalsignifi cance was set at P < 0.05. The survival rate of Group 2 (40%) was statistically signifi cantly (P < 0.025) higher thanthat of Group 1 (0.0%). In control group all rats died at 10 h after subcutaneously tilmicosin injection. In Group 2 wereadministered 25 mg/kg of amiodarone (intravenously) at 8 min after the single subcutaneous injection of tilmicosin in adose of 360 mg/kg, and 2 rats died at 2 h and 4...
Biblioteca responsável: BR68.1
Localização: BR68.1