Kurki T, Viinikka L, Ylikorkala O
I Department of Obstetrics and Gynecology, University of Central Hospital of Helsinki, Finland.
Am J Obstet Gynecol. 1992 Jan;166(1 Pt 1):150-4. doi: 10.1016/0002-9378(92)91851-z.
We studied the role of smooth muscle-relaxing prostacyclin and its endogenous antagonist, thromboxane A2, in preterm labor by assessing the urinary output of the breakdown products of prostacyclin (6-keto-prostaglandin F1 alpha and 2,3-dinor-6-keto-prostaglandin F1 alpha) and those of thromboxane A2 (thromboxane B2, 2,3-dinor-thromboxane B2).
Thirty-three women in preterm labor between 25 and 34 weeks of gestation were studied before, during, and after treatment with indomethacin (n = 16) or nylidrin (n = 17). Urinary prostanoid levels were determined by high-performance liquid chromatography followed by radioimmunoassay, and the excretion was expressed as nanograms of prostanoids per millimole of creatinine. Statistical analyses were done by paired and unpaired Student t test, by Spearman's correlation, and by Wilcoxon signed-rank test.
Preterm labor was accompanied by a median 32% higher output of prostacyclin and thromboxane A2 metabolites as compared with those in 25 controls. At 8 hours after the start of treatment indomethacin induced maximal drops in 6-keto-prostaglandin F1 alpha (70%), in dinor-6-keto-prostaglandin F1 alpha (60%), in thromboxane B2 (85%), and in dinor-thromboxane B2 (95%) excretion. Within 1 week after the cessation of indomethacin, output of prostacyclin metabolites had recovered to pretreatment values, whereas output of thromboxane A2 metabolites was yet lower than the pretreatment value. Nylidrin induced no change in the output of prostacyclin and thromboxane A2 metabolites.
Threatened preterm labor is associated with a rise in prostacyclin and thromboxane A2 synthesis. Indomethacin inhibits more thromboxane A2 than does prostacyclin synthesis. These findings may explain the fetal vascular changes during maternal indomethacin treatment.
通过评估前列环素（6-酮-前列腺素F1α和2,3-二去甲-6-酮-前列腺素F1α）和血栓素A2（血栓素B2、2,3-二去甲-血栓素B2）分解产物的尿量，研究平滑肌舒张性前列环素及其内源性拮抗剂血栓素A2在早产中的作用。
对33例妊娠25至34周早产的妇女在使用吲哚美辛（n = 16）或尼立替林（n = 17）治疗前、治疗期间和治疗后进行研究。通过高效液相色谱法继以放射免疫测定法测定尿类前列腺素水平，排泄量以每毫摩尔肌酐中类前列腺素的纳克数表示。采用配对和非配对学生t检验、Spearman相关性分析和Wilcoxon符号秩检验进行统计分析。
与25例对照相比，早产时前列环素和血栓素A2代谢产物的尿量中位数高32%。在治疗开始后8小时，吲哚美辛使6-酮-前列腺素F1α（70%）、2,3-二去甲-6-酮-前列腺素F1α（60%）、血栓素B2（85%）和2,3-二去甲-血栓素B2（95%）的排泄量最大幅度下降。在吲哚美辛停药后1周内，前列环素代谢产物的尿量恢复到治疗前水平，而血栓素A2代谢产物的尿量仍低于治疗前水平。尼立替林未引起前列环素和血栓素A2代谢产物尿量的变化。
先兆早产与前列环素和血栓素A2合成增加有关。吲哚美辛对血栓素A2合成的抑制作用比对前列环素合成的抑制作用更强。这些发现可能解释了母体使用吲哚美辛治疗期间胎儿血管的变化。
