Jansson A, Andersson K, Bjelke B, Eneroth P, Fuxe K
Department of Histology and Neurobiology, Karolinska Institute, Stockholm, Sweden.
Acta Physiol Scand. 1992 Apr;144(4):453-62. doi: 10.1111/j.1748-1716.1992.tb09320.x.
The purpose of this paper was to study the possible long-term effects of postnatal exposure to cigarette smoke. Male Sprague-Dawley rats were exposed to the smoke from 2 cigarettes (Kentucky reference IR-1 type) every morning from day 1 after birth for a period of 5, 10 or 20 days. The rats were decapitated 24 hours (5, 10 and 20 days of exposure), 1 week (20 days of exposure) or 7 months (20 days of exposure) after the last exposure. Using the Falck-Hillarp methodology in combination with quantitative histofluorimetry catecholamine levels and changes in catecholamine utilization (alpha MT-induced CA fluorescence disappearance) in discrete hypothalamic catecholamine nerve terminal systems were analysed. Serum prolactin, LH, TSH and corticosterone levels were determined by means of radioimmunoassay procedures. In the postnatal period serum LH levels were significantly increased 24 hours after a 10 and 20 day exposure to cigarette smoke. In adult life after a 20-day postnatal exposure to cigarette smoke a highly significant increase was observed in serum prolactin levels, which were unaltered by this exposure when measured in the postnatal period. Twenty-four hours following a 20-day postnatal exposure, catecholamine utilization was increased in the medial palisade zone of the median eminence and substantially reduced in the parvocellular and magnocellular parts of the paraventricular hypothalamic nucleus. One week and 7 months following a 20-day postnatal exposure to cigarette smoke no alterations were observed in catecholamine levels or utilization in various hypothalamic areas including the median eminence. All the above changes were observed in the presence of an unaltered development of body weight. The results indicate that marked but temporary increases in LH secretion occur 24 hours after a postnatal exposure to cigarette smoke, while increase in prolactin secretion only develop in adult life, when the maturational processes of the brain and/or the anterior pituitary gland are completed. Changes in catecholamine levels and utilization are found in discrete hypothalamic nerve terminal networks but do not play a major role in mediating the above changes in anterior pituitary function and are probably the result of a withdrawal phenomenon.
本文旨在研究出生后暴露于香烟烟雾可能产生的长期影响。从出生后第1天起，每天早晨让雄性斯普拉格-道利大鼠暴露于2支香烟（肯塔基参考IR-1型）的烟雾中，持续5、10或20天。在最后一次暴露后24小时（暴露5、10和20天）、1周（暴露20天）或7个月（暴露20天）将大鼠断头。采用福尔克-希拉尔普方法结合定量组织荧光测定法，分析了离散的下丘脑儿茶酚胺神经末梢系统中的儿茶酚胺水平及儿茶酚胺利用情况的变化（α-甲基酪氨酸诱导的儿茶酚胺荧光消失）。通过放射免疫测定法测定血清催乳素、促黄体生成素、促甲状腺激素和皮质酮水平。在出生后阶段，暴露于香烟烟雾10天和20天后24小时，血清促黄体生成素水平显著升高。在出生后暴露于香烟烟雾20天后的成年期，观察到血清催乳素水平显著升高，而在出生后阶段测量时，该暴露对其无影响。出生后暴露20天后24小时，正中隆起内侧栅栏区的儿茶酚胺利用增加，而下丘脑室旁核小细胞部和大细胞部的儿茶酚胺利用则大幅减少。出生后暴露于香烟烟雾20天后1周和7个月，在包括正中隆起在内的各个下丘脑区域，未观察到儿茶酚胺水平或利用情况的改变。所有上述变化均在体重发育未受影响的情况下观察到。结果表明，出生后暴露于香烟烟雾24小时后，促黄体生成素分泌会出现显著但暂时的增加，而催乳素分泌增加仅在成年期出现，此时大脑和/或垂体前叶的成熟过程已完成。在离散的下丘脑神经末梢网络中发现儿茶酚胺水平和利用情况发生了变化，但在介导上述垂体前叶功能变化中不起主要作用，可能是戒断现象的结果。
