Maritz G S, van Wyk G
Department of Physiological Sciences, University of Bellville, South Africa.
Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1997 Jun;117(2):159-65. doi: 10.1016/s0742-8413(96)00052-7.
The aims of this study were (1) to determine and quantify the adverse effects of maternal nicotine exposure during pregnancy and lactation on neonatal rat lung development, and (2) to establish whether ascorbic acid will protect the neonatal rat lung against the adverse effects of maternal nicotine exposure. Pregnant rats received nicotine (1 mg/kg body mass/day) subcutaneously during gestation and lactation. A second group received nicotine and ascorbic acid (1 mg/kg body mass/day). The control animals received saline subcutaneously. The results illustrate that maternal nicotine exposure results in (a) a decreased (P < 0.001) radial alveolar count (RAC), (b) an increase (P < 0.001) in destructive index (DI), (c) an increased (P < 0.001) linear intercept (Lm), (d) an increased (P < 0.001) abnormal alveolar attachment index (AAA) (e) and an increase in septal cellularity. Ascorbic acid does not protect fetal lung development against the adverse effects of maternal nicotine exposure. However, after birth ascorbic acid prevents further deterioration of the DI, AAA and Lm, whereas the RAC and thus the number of alveoli was even higher than in control neonatal rat lung. No further increase in cellularity occurred. The reason for this response to ascorbic acid supplementation is under investigation.
（1）确定并量化孕期和哺乳期母体尼古丁暴露对新生大鼠肺发育的不良影响；（2）确定抗坏血酸是否能保护新生大鼠肺免受母体尼古丁暴露的不良影响。怀孕大鼠在妊娠期和哺乳期皮下注射尼古丁（1毫克/千克体重/天）。第二组大鼠接受尼古丁和抗坏血酸（1毫克/千克体重/天）。对照动物皮下注射生理盐水。结果表明，母体尼古丁暴露导致：（a）肺泡径向计数（RAC）降低（P<0.001）；（b）破坏指数（DI）升高（P<0.001）；（c）线性截距（Lm）增加（P<0.001）；（d）异常肺泡附着指数（AAA）增加（P<0.001）；（e）隔细胞增多。抗坏血酸不能保护胎儿肺发育免受母体尼古丁暴露的不良影响。然而，出生后抗坏血酸可防止DI、AAA和Lm进一步恶化，而RAC以及肺泡数量甚至高于对照新生大鼠肺。细胞增多情况未进一步增加。补充抗坏血酸产生这种反应的原因正在研究中。
