AI Article Synopsis
- The study aimed to investigate whether aquaporin 1 knockout mice have increased amniotic fluid volume.
- The research involved creating transgenic mice lacking aquaporin 1, measuring amniotic fluid parameters after cesarean sections, and analyzing the data for differences between these mice and control groups.
- Results showed that the knockout mice had significantly greater amniotic fluid volume and lower osmolality compared to the wild-type and heterozygote mice, suggesting a link between aquaporin 1 channels and amniotic fluid regulation, which could relate to human conditions like idiopathic polyhydramnios.
Article Abstract
Objective: To test the hypothesis that amniotic fluid volume is increased in aquaporin 1 knockout mice.
Study Design: Transgenic mice deficient in aquaporin 1 protein were generated by targeted gene disruption, as described previously. After a cesarean section was performed, intact, individual gestational sacs were removed from the uterus and weighed. Amniotic fluid volume, osmolality, and fetal and placental weights were determined. Data were analyzed by a 1-way analysis of variance for ranks; Dunn's post hoc test was used to analyze significant trends.
Results: Analysis of 16 litters showed 35 wild-type, 52 heterozygote, and 33 aquaporin 1 knockout mice. The knockout mice had a greater volume of amniotic fluid and lower amniotic fluid osmolality than their wild-type and heterozygote counterparts. There were no significant differences in fetal or placental weights among the groups.
Conclusions: Aquaporin 1 null fetuses produce a greater volume of more dilute amniotic fluid. Our findings show that aquaporin 1 water channels in fetal membranes may contribute to amniotic fluid volume regulation. We speculate that idiopathic polyhydramnios may be associated with a deficiency of aquaporin 1 channels in human fetal membranes. Transgenic aquaporin 1 knockout mice provide a unique animal of polyhydramnios.
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| http://dx.doi.org/10.1016/j.ajog.2005.02.046 | DOI Listing |
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