Qualls H J, Holbrook T C, Gilliam L L, Njaa B L, Panciera R J, Pope C N, Payton M E
Weatherford Equine Medical Center, PC, Weatherford, TX.
J Vet Intern Med. 2013 Sep-Oct;27(5):1179-84. doi: 10.1111/jvim.12164.
The efficacy of orally administered therapeutics for the treatment of cantharidin intoxication has not been evaluated in controlled studies.
To develop a model of acute cantharidin intoxication in laboratory rats and to evaluate in this model the relative efficacy of 3 gastrointestinal therapies used to treat equine cantharidin toxicosis.
Sixty-four male Sprague-Dawley rats.
A blinded, randomized, controlled study was performed on rats surgically implanted with telemetry transmitters for evaluating heart rate, locomotor activity, and body temperature. Orogastric administration of cantharidin was performed within 15 seconds before administration of mineral oil, activated charcoal, or smectite. Negative control groups received therapeutic agents alone. Urine was collected for cantharidin analysis. Rats were sacrificed 24 hours after intoxication, and tissues were collected for histopathologic evaluation. Data analysis included ANOVA procedures and contingency tables.
Six of 8 cantharidin-intoxicated rats treated with mineral oil died; bradycardia and hypothermia developed in the animals of this group 0-8 hours after intoxication. Rats treated with mineral oil had higher urine cantharidin concentrations than rats receiving cantharidin alone or with smectite (P = .04). The most severe hypothermia (30.6°C ± 1.0) developed in rats administered mineral oil at 4-8 hours after intoxication, whereas those treated with charcoal (35.2°C ± 0.8) had mean body temperatures higher than all other treatment groups (P = .03). Survival times in the charcoal (P = .16) and smectite (P = .12) treatment groups were not statistically different from negative controls.
Mineral oil is often used in the treatment of equine cantharidin toxicosis. Our findings suggest that mineral oil increases cantharidin absorption, worsening morbidity and fatality in rats.
口服治疗剂用于治疗斑蝥素中毒的疗效尚未在对照研究中得到评估。
建立实验室大鼠急性斑蝥素中毒模型，并在该模型中评估3种用于治疗马斑蝥素中毒的胃肠道疗法的相对疗效。
64只雄性斯普拉格-道利大鼠。
对手术植入遥测发射器以评估心率、运动活动和体温的大鼠进行一项盲法、随机、对照研究。在给予矿物油、活性炭或蒙脱石前15秒内通过口胃管给予斑蝥素。阴性对照组仅接受治疗剂。收集尿液进行斑蝥素分析。中毒24小时后处死大鼠，收集组织进行组织病理学评估。数据分析包括方差分析程序和列联表。
8只接受矿物油治疗的斑蝥素中毒大鼠中有6只死亡；该组动物在中毒后0 - 8小时出现心动过缓和体温过低。接受矿物油治疗的大鼠尿液中斑蝥素浓度高于单独接受斑蝥素或与蒙脱石联合接受斑蝥素治疗的大鼠（P = 0.04）。中毒后4 - 8小时接受矿物油治疗的大鼠出现最严重的体温过低（30.6°C ± 1.0），而接受活性炭治疗的大鼠（35.2°C ± 0.8）平均体温高于所有其他治疗组（P = 0.03）。活性炭（P = 0.16）和蒙脱石（P = 0.12）治疗组的存活时间与阴性对照组无统计学差异。
矿物油常用于治疗马斑蝥素中毒。我们的研究结果表明，矿物油会增加斑蝥素的吸收，使大鼠的发病率和死亡率恶化。
