Ylikorkala O, Viinikka L, Lehtovirta P
Obstet Gynecol. 1985 Jul;66(1):102-5.
To study the effect of nicotine on fetal prostacyclin and thromboxane A2, specimens from the umbilical arteries of infants born to healthy nonsmoking mothers were superfused in the absence or presence of nicotine (50 to 10,000 micrograms/mL), and the releases of 6-keto-prostaglandin F1alpha (a break-down product of prostacyclin) and thromboxane B2 (a metabolite of thromboxane A2) were measured. The baseline production of 6-keto-prostaglandin F1alpha (63.9 +/- 8.8 ng/minute per gram of dry weight tissue, mean +/- SE, N = 10) or that of thromboxane B2 (1.3 +/- 0.2 ng/minute per gram, N = 10) were unaffected by nicotine. To study the effect of nicotine on thromboxane A2 synthesis by the fetal platelets, thrombin-induced platelet aggregation and consequent thromboxane A2 synthesis were allowed to occur in the whole cord blood in the absence or presence of nicotine (10 to 500 micrograms/mL). Nicotine inhibited concentration dependently platelet thromboxane A2 synthesis from the baseline level (107.3 +/- 7.1 ng/mL) by 15 to 93%. This inhibition was also seen in thromboxane A2 synthesis starting from exogenous arachidonic acid, suggesting that nicotine inhibits either cyclooxygenase and/or thromboxane A2 synthetase in the fetal platelets. Thus, nicotine is hardly responsible for maternal smoking-induced changes in fetal prostacyclin formation.
为研究尼古丁对胎儿前列环素和血栓素A2的影响，将健康非吸烟母亲所生婴儿的脐动脉标本在无尼古丁或有尼古丁（50至10,000微克/毫升）的情况下进行灌流，并测定6-酮-前列腺素F1α（前列环素的分解产物）和血栓素B2（血栓素A2的代谢产物）的释放量。尼古丁对6-酮-前列腺素F1α的基础生成量（每克干重组织63.9±8.8纳克/分钟，平均值±标准误，N = 10）或血栓素B2的基础生成量（每克1.3±0.2纳克/分钟，N = 10）均无影响。为研究尼古丁对胎儿血小板血栓素A2合成的影响，在无尼古丁或有尼古丁（10至500微克/毫升）的情况下，使凝血酶诱导的血小板聚集及随之的血栓素A2合成在全脐带血中发生。尼古丁浓度依赖性地抑制血小板血栓素A2从基础水平（107.3±7.1纳克/毫升）合成，抑制率为15%至93%。从外源性花生四烯酸起始的血栓素A2合成中也可见到这种抑制作用，这表明尼古丁抑制胎儿血小板中的环氧化酶和/或血栓素A2合成酶。因此，尼古丁几乎与母亲吸烟引起的胎儿前列环素形成变化无关。
