The Effect And Mechanism Of Alcohol On Embryo Transport

IntroductionEctopic pregnancy is a serious gynecological and obstetrical diseases, of which tubal pregnancy is the most common and severe one. Although the root cause of its occurrence is still unknown, but the embryo retention in the fallopian tubes is a major cause of tubal pregnancy occurred. Modern medical research has proven, gynecological inflammation, history of tubal ligation and abortion, are the three main reasons of tubal pregnancy. Most studies have demonstrated that alcohol consumption is not only associated with cardiovascular disease, liver disease and mental illness, but also the decreased human fertility. The research of alcohol consumption during pregnancy on offspring development has become a hot modern research, however, the relationship between alcohol consumption and embryo transport of oviduct or early embryo development in the oviduct has not yet been investigated. This experiment will explore the influence of alcohol intake in early pregnancy on the embryo transport in the fallopian tubes and its mechanism. Furthermore, it would propose new ideas for the mechanism of tubal pregnancy.Materials and MethodsHuman fallopian tubes were obtained from ectopic pregnancy surgery, hysterectomy and postpartum tubal sterilization surgery. Wistar rats and BABL/c mice were purchased from the Animal Center of Shandong University School of Medicine. In acute and chronic alcohol intake experiment, BABL/c mice were injected different drugs orally, for 3 days and 30 days respectively. Tension recording was used in recording the change of the oviduct muscle strips. Western blot was used in analysis of nitric oxide synthase (NOS) activity. NO assay kit was used in the measurement of NO levels in fallopian tube. Hematoxylin-eosin staining and scanning electron microscope (SEM) were used to detect the morphology of mouse oviduct; BABLA/c mouse uterus and tubal were removed to count embryos.ResultsIn this study, ethanol concentration-dependently suppressed the spontaneous motility of isolated human oviduct strips, which was largely attenuated in the present of L-NAME, a classical NOS competitive inhibitor. Notably, alcohol intake delayed transport and development of preimplantation embryo, and impaired oviductal epithelium. The experiment of NO experiments in human and BABL/c mice oviduct proved that alcohol consumption can make oviduct tissue NOS activity increased and increased NO release; L-NAME can activity reduced the release of NO. Interesting to note, admin istration of L-NAME, largely rescues either the embryo transport retention or asynchronous development in acute alcohol intake group but not in chronic alcohol intake group. In chronic alcohol intake experiment, hematoxylin-eosin staining and scanning electron microscopy (SEM) proved chronic alcohol intake could alter the tubal morphology. It suggests that the mechanism of acute and chronic alcohol intake is not exactly the same in retarding embryo transport in oviducts.ConclusionCollectively, the findings suggest that alcohol can lead to an increase of NO release in oviducts and impair the spontaneous contractions of the fallopian tubes. Chronic alcohol intake would alter the fallopian tube morphology. Alcohol intake retards embryo transport in oviducts. This suggests that there is a certain relationship between tubal pregnancy and alcoholism.