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首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >Effect of resiniferatoxin on the noxious heat threshold temperature in the rat: a novel heat allodynia model sensitive to analgesics
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Effect of resiniferatoxin on the noxious heat threshold temperature in the rat: a novel heat allodynia model sensitive to analgesics

机译：树脂毒素对大鼠有害热阈温度的影响：一种新型的对镇痛药敏感的热异常性疼痛模型

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class="enumerated" style="list-style-type:decimal">An increasing-temperature hot plate (ITHP) was introduced to measure the noxious heat threshold (45.3±0.3°C) of unrestrained rats, which was reproducible upon repeated determinations at intervals of 5 or 30 min or 1 day.Morphine, diclofenac and paracetamol caused an elevation of the noxious heat threshold following i.p. pretreatment, the minimum effective doses being 3, 10 and 200 mg kg−1, respectively.Unilateral intraplantar injection of the VR1 receptor agonist resiniferatoxin (RTX, 0.048 nmol) induced a profound drop of heat threshold to the innocuous range with a maximal effect (8–10°C drop) 5 min after RTX administration. This heat allodynia was inhibited by pretreatment with morphine, diclofenac and paracetamol, the minimum effective doses being 1, 1 and 100 mg kg−1 i.p., respectively.The long-term sensory desensitizing effect of RTX was examined by bilateral intraplantar injection (0.048 nmol per paw) which produced, after an initial threshold drop, an elevation (up to 2.9±0.5°C) of heat threshold lasting for 5 days.The VR1 receptor antagonist iodo-resiniferatoxin (I-RTX, 0.05 nmol intraplantarly) inhibited by 51% the heat threshold-lowering effect of intraplantar RTX but not α,β-methylene-ATP (0.3 μmol per paw). I-RTX (0.1 or 1 nmol per paw) failed to alter the heat threshold either acutely (5–60 min) or on the long-term (5 days). The heat threshold of VR1 receptor knockout mice was not different from that of wild-type animals (45.6±0.5 vs 45.2±0.4°C).In conclusion, the RTX-induced drop of heat threshold measured by the ITHP is a novel heat allodynia model exhibiting a high sensitivity to analgesics.
机译：class =“ enumerated” style =“ list-style-type：decimal”> <！-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 引入了一个高温热板（ITHP）来测量未受约束的大鼠的有害热量阈值（45.3±0.3°C），该阈值可以在5、30分钟或1天的间隔中重复测定后重现。 < li>吗啡，双氯芬酸和扑热息痛引起腹腔注射后有害热阈值升高预处理，最小有效剂量分别为3、10和200 mg kg −1 。 单侧li骨内注射VR1受体激动剂类树脂毒素（RTX，0.048 nmol）诱导RTX给药后5分钟，热量阈值急剧下降至无害范围，达到最大效果（下降8–10°C）。可以通过吗啡，双氯芬酸和扑热息痛的预处理抑制这种热异常性疼痛，其最低有效剂量分别为1、1和100 mg kg −1 ip。 长期通过双足底内注射（每爪0.048 nmol）检查RTX的感觉减敏作用，初始阈值下降后，RTX持续5天升高（高达2.9±0.5°C）。 < li> VR1受体拮抗剂碘-树脂毒素（I-RTX，足底内0.05 nmol）抑制足底内RTX降低热阈值的作用达51％，但抑制α，β-亚甲基-ATP（每爪0.3μmol）。 I-RTX（每爪0.1或1 nmol）无法急性（5-60分钟）或长期（5天）改变热阈值。 VR1受体敲除小鼠的热阈值与野生型动物没有差别（45.6±0.5 vs 45.2±0.4°C）。 总而言之，RTX诱导的热阈值下降是通过ITHP是一种新型的热痛觉过敏模型，对止痛药具有很高的敏感性。

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