Acetylcholine increase in amniotic fluid of experimental rats for intrauterine growth retardation.
Previous reports from this laboratory have demonstrated evidence for synthesis and release of acetylcholine (ACh) and catecholamines (CAs) by human amniotic epithelial cells (HAEC) and the presence of ACh and CAs in amniotic fluid. To study the physiological role of amniotic ACh, we used an experimental pregnant rat model for intrauterine growth retardation. Prior to this experiment, we confirmed the presence of choline acetyltransferase in the HAEC by immunocytochemical staining. Amniotic fluid was collected at 48 and 72 h after a transient ligation of the uterine vessels near the lower and upper ends of the right horn of the pregnant rat. The ACh concentration in the amniotic fluid from rats received intrauterine ischemia increased with time to a greater degree compared with the control rat, although the increase was not statistically significant. These results suggest that intrauterine hypoxic conditions cause a tendency to increase ACh concentrations in the amniotic fluid.
Horikoshi
Tsuguhiro
T
Department of Inherited Metabolic Disease, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-0032, Japan.
Fujii
Takeshi
T
Kawashima
Koichiro
K
Sakuragawa
Norio
N
D000109:Acetylcholine / Q000096:biosynthesis / Q000378:metabolism*; D000653:Amniotic Fluid / Q000378:metabolism*; D000818:Animals; D000911:Antibodies, Monoclonal; D002395:Catecholamines / Q000096:biosynthesis; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004847:Epithelial Cells / Q000378:metabolism; D005321:Extraembryonic Membranes / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D007150:Immunohistochemistry; D007511:Ischemia / Q000503:physiopathology; D008026:Ligation; D011247:Pregnancy; D051381:Rats; D014599:Uterus / Q000098:blood supply
D000911:Antibodies, Monoclonal; D002395:Catecholamines; D002795:Choline O-Acetyltransferase; D000109:Acetylcholine