Stress or excitement is a concern when performing endocrine tests on fractious horses. Sedation may be a solution; however, perturbation of test results may preclude useful information. Thyrotropin-releasing hormone (TRH) is a known stimulator of prolactin, thyroid-stimulating hormone (TSH), melanocyte-stimulating hormone (MSH), and ACTH. Thyrotropin-releasing hormone–induced ACTH is a diagnostic tool for the assessment of endocrinopathies such as pituitary pars intermedia dysfunction. It is unknown if drugs commonly used for sedation alter endocrine responses. The objective of this study was to assess the effects of detomidine (DET) and butorphanol on endocrine responses to TRH. Nine light horse mares were used in a replicated 3 × 3 Latin square with the following treatments: saline, DET, and detomidine + butorphanol (DET/BUT), all administered intravenously at 0.01 mg/kg BW. A 1-wk washout period was allowed between phases, all of which were performed in December. Blood samples were collected at −10 and 0 min before treatment and 5 and 10 min post-treatment. Administration of 1 mg TRH occurred 10 min post-treatment, and blood sampling continued 5, 10, 20, and 30 min post-TRH. Data were analyzed by ANOVA as a replicated Latin square with repeated sampling. Plasma prolactin increased (P < 0.0001) after TRH in all groups, rapidly peaking at 5 min in drug-treated mares and 40 min in saline-treated mares. The peak prolactin response to TRH was 2-fold higher (P < 0.0001) in saline-treated mares compared with those drug-treated. A peak rise in plasma TSH was observed in DET/BUT-treated mares 10 min after TSH and was greater (P ≤ 0.007) compared with DET- and saline-treated mares. Plasma MSH was stimulated (P = 0.001) by DET and DET/BUT before TRH, and the peak MSH response to TRH was greater (P < 0.0001) in drug-treated mares, although not hastened as observed with prolactin and TSH. A peak rise in ACTH was observed in drug-treated mares 5 min after administration of TRH, whereas a peak rise was observed in control mares 10 min post-TRH and was almost 2-fold lower (P = 0.05) than the peak observed in DET and DET/BUT-treated mares. Basal ACTH concentrations were not affected by DET or DET/BUT, indicating that sedation with these compounds may be achieved when needing to measure basal plasma ACTH. Treatment with DET and DET/BUT did alter the prolactin, TSH, MSH, and ACTH responses to TRH; therefore, the use of these drugs may not be advisable when assessing endocrine responses to TRH stimulation.

在对脾气暴躁的马进行内分泌测试时，压力或兴奋是一个问题。镇静可能是一种解决方案；然而，测试结果的扰动可能会排除有用的信息。促甲状腺激素释放激素 (TRH) 是催乳素、促甲状腺激素 (TSH)、促黑素细胞激素 (MSH) 和促肾上腺皮质激素 (ACTH) 的已知刺激剂。促甲状腺激素释放激素诱导的 ACTH 是评估内分泌疾病（如垂体中间部功能障碍）的诊断工具。目前尚不清楚常用于镇静的药物是否会改变内分泌反应。本研究的目的是评估地托咪定 (DET) 和布托啡诺对 TRH 内分泌反应的影响。在重复的 3 × 3 拉丁方格中使用了九匹轻马，并进行了以下处理：盐水、DET 和地托咪定 + 布托啡诺 (DET/BUT)，均以 0.01 mg/kg BW 静脉内给药。阶段之间允许有 1 周的冲洗期，所有这些都在 12 月进行。在治疗前-10 分钟和0 分钟以及治疗后5 和10 分钟收集血样。在治疗后 10 分钟施用 1 mg TRH，并在 TRH 后 5、10、20 和 30 分钟继续采血。数据通过方差分析作为重复抽样的复制拉丁方进行分析。血浆催乳素升高（数据通过方差分析作为重复抽样的复制拉丁方进行分析。血浆催乳素升高（数据通过方差分析作为重复抽样的复制拉丁方进行分析。血浆催乳素升高（P < 0.0001) 在所有组的 TRH 后，药物治疗的母马在 5 分钟和生理盐水治疗的母马中在 40 分钟时迅速达到峰值。与药物治疗的母马相比，​​生理盐水治疗的母马对 TRH 的催乳素峰值反应高 2 倍（P < 0.0001）。在 TSH 后 10 分钟，在 DET/BUT 处理的母马中观察到血浆 TSH 的峰值升高，并且与 DET 和盐水处理的母马相比更大（P ≤ 0.007）。TRH前DET和DET/BUT刺激血浆MSH（P = 0.001），MSH对TRH的反应峰值更大（P< 0.0001) 在药物治疗的母马中，虽然不像催乳素和 TSH 观察到的那样加速。在 TRH 给药后 5 分钟，在药物治疗的母马中观察到 ACTH 的峰值升高，而在 TRH 给药后 10 分钟，在对照母马中观察到了峰值升高，并且几乎比在TRH 中观察到的峰值低 2 倍（P = 0.05） DET 和 DET/BUT 处理的母马。基础 ACTH 浓度不受 DET 或 DET/BUT 的影响，表明当需要测量基础血浆 ACTH 时，可以使用这些化合物实现镇静。DET 和 DET/BUT 治疗确实改变了催乳素、TSH、MSH 和 ACTH 对 TRH 的反应；因此，在评估内分泌对 TRH 刺激的反应时，可能不建议使用这些药物。