Evidence that chronic hyperprolactinemia effects skin temperature regulation through an opioid mechanism.
Evidence that chronic hyperprolactinemia effects skin temperature regulation through an opioid mechanism.
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有证据表明，慢性高催乳素血症通过阿片类药物机制影响皮肤温度调节。
DOI：
10.1159/000123999
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发表时间：
1984
影响因子：
4.1
通讯作者：
Millard,WJ
中科院分区：
文献类型：
--
作者：
Simpkins,JW;Taylor,ST;Gabriel,SM;Katovich,MJ;Millard,WJ
本研究旨在评价由MtTWI 5肿瘤诱导的慢性高泌乳素血症（HYP）对雌性大鼠对纳洛酮阻断阿片受体的体温调节反应的影响。长期服用吗啡和HYP都会导致轻度体温过高，直肠温度（Tr）升高0.8-1.0 °C即可证明这一点。纳洛酮催促吗啡戒断引起尾部皮肤温度（TST）迅速升高（4.9 ± 0.76 °C），随后Tr下降（-2.8 °C）。同样，纳洛酮给药的HYP大鼠引起了一个戏剧性的TST反应，这是一致的严重HYP的发作。纳洛酮的这种作用在肿瘤生长7周时最大，此时观察到4.8 ± 0.3 °C的TST反应，但在肿瘤接种前或肿瘤接种后1周时不明显，此时血清催乳素水平较低。在慢性HYP中，纳洛酮的TST反应表现出明显的脉冲，幅度为3.4 ± 0.4 °C，频率为2.2 ± 0.5脉冲/120 min。似乎HYP大鼠中阿片受体的阻断诱导了皮肤温度调节的不稳定性，如TST峰的反复发作所示。慢性HYP对TST对纳洛酮反应的影响不受卵巢切除术的影响，表明卵巢分泌物的变化不参与反应。在肿瘤生长4周时，下丘脑内侧基底部、视前区-下丘脑前部和垂体神经中间叶的β-内啡肽免疫反应性浓度分别下降59%、28%和47%。此时，垂体前叶免疫反应性β-内啡肽的浓度没有显著改变。总的来说，这些数据表明：（1）HYP可以诱导核心体温和皮肤温度对纳洛酮的反应发生改变，这与在吗啡依赖大鼠中观察到的相似;（2）慢性HYP导致下丘脑和垂体神经中间叶中免疫反应性β-内啡肽的耗竭;（3）慢性HYP max通过对含β-内啡肽的神经元的作用发挥这些作用。
Studies were undertaken to evaluate the effects of chronic hyperprolactinemia (HYP) induced by the MtTWI5 tumor on the thermoregulatory response of female rats to blockade of opiate receptors with naloxone. Both chronic administration of morphine and HYP cause a mild hyperthermia as evidenced by a 0.8–1.0 °C elevation in rectal temperature (Tr). Naloxone-precipitated morphine withdrawal caused a prompt increase (4.9 ± 0.76 °C) in tail skin temperature (TST) and a subsequent decline in Tr(-2.8 °C). Similarly, naloxone administration to HYP rats caused a dramatic TST response which was coincident with the onset of severe HYP. This effect of naloxone was maximal at 7 weeks of tumor growth when a TST response of 4.8 ± 0.3 °C was observed but was not evident prior to or 1 week following tumor inoculation, when serum prolactin levels were low. The TST response to naloxone in chronic HYP exhibited distinct pulses with an amplitude of 3.4 ± 0.4 °C and a frequency of 2.2 ± 0.5 pulses per 120 min. It appears that blockade of opiate receptors in HYP rats induces instability in the regulation of skin temperature as evident by recurrent episodes of TST surges. These effects of chronic HYP on the TST response to naloxone were not influenced by ovariectomy, suggesting that changes in ovarian secretions were not involved in the response. At 4 weeks of tumor growth, immunoreacitve β-endorphin concentrations in the medial basal hypothalamus, preoptic area-anterior hypothalamus and the neurointermediate lobe of the pituitary were decreased by 59, 28 and 47%, respectively. Anterior pituitary concentration of immunoreactive β-endorphin were not significantly altered at this time. Collectively, these data indicate that (1) HYP can induce alterations in core body temperature and skin temperature responses to naloxone which are similar to those observed in morphine-dependent rats; (2) chronic HYP causes depletion of imunoreactive β-endorphin in the hypothalamus and the neurointermediate lobe of the pituitary, and (3) chronic HYP max exert these effects by an action on β-endorphin containing neurons.