Szakmáry E, Morvai V, Náray M, Ungváry G
National Institute of Occupational Health, Budapest, Hungary.
Acta Physiol Hung. 1995;83(1):3-12.
Non-pregnant and pregnant CFY rats were given 3 mg/kg nickel chloride or physiological saline by gavage daily for eight days during days 7-14 of organogenesis. The haemodynamic investigations were carried out using 113Sn labelled microspheres. Nickel concentrations in maternal and fetal blood, as well as in amniotic fluid were determined by atomic absorption spectrophotometry. It was found, that nickel crossed the placenta, appeared in the fetal blood and amniotic fluid, where its concentration depended on the dose given to the pregnant animal and the nickel concentration of the maternal blood. Nickel chloride influenced neither the systemic haemodynamic parameters (arterial blood pressure, total peripheral resistance--TPR, cardiac index) nor the values of the organ (including the placenta) circulation indices, neither in the pregnant nor in the non-pregnant animals. It is concluded that in the pathomechanism of embryotoxicity (causing weight gain retardation) and teratogenicity (causing major anomalies of the uropoietic apparatus) of nickel, demonstrated earlier, the assumed effects of nickel on maternal and placental circulation probably do not play role (as such effects could not be detected). The direct embryo-damaging effect of nickel crossing the placenta (direct cytotoxic effect) may be held responsible for the embryotoxicity and teratogenicity of nickel.
在器官形成的第7至14天期间，对未怀孕和怀孕的CFY大鼠每天经口灌胃给予3mg/kg氯化镍或生理盐水，持续8天。使用113Sn标记的微球进行血流动力学研究。通过原子吸收分光光度法测定母体和胎儿血液以及羊水中的镍浓度。结果发现，镍穿过胎盘，出现在胎儿血液和羊水中，其浓度取决于给予怀孕动物的剂量和母体血液中的镍浓度。氯化镍对未怀孕和怀孕动物的全身血流动力学参数（动脉血压、总外周阻力——TPR、心脏指数）以及器官（包括胎盘）循环指数的值均无影响。结论是，在先前已证明的镍的胚胎毒性（导致体重增加迟缓）和致畸性（导致泌尿生殖系统主要异常）的发病机制中，镍对母体和胎盘循环的假定作用可能并不起作用（因为未检测到此类作用）。镍穿过胎盘的直接胚胎损伤作用（直接细胞毒性作用）可能是镍的胚胎毒性和致畸性的原因。
