AIMS: The purpose of this study was to investigate the proliferation of smooth muscle cells in umbilical vessels of fetuses affected by intrauterine growth restriction (IUGR) and to compare the findings with gestational age-matched control cases. METHODS: Sixty umbilical cords from fetuses at 36-37 weeks gestation were examined. Fetuses were divided into three groups: group I, appropriate for dates birthweight; group II, IUGR with reassuring fetal status; and group III, IUGR with abnormal umbilical Doppler waveforms. Umbilical cords were immunostained with an antibody to proliferating cell nuclear antigen and Ki-67; stained smooth muscle cells were subsequently counted. Smooth muscle cell density was determined by counting the total number of cells in a representative area of vessel wall and the wall thickness of each vessel was also measured. RESULTS: Proliferation marker-positive cells were increased in the umbilical vessels of group II compared to group I, and there were more proliferating smooth muscle cells in the umbilical vessels of group III compared to the other two groups. The umbilical vessels of group III showed the highest smooth muscle cell density, but the wall thickness of all vessels was significantly thinner in group III than the other two groups. CONCLUSIONS: This study showed overproliferation of smooth muscle cells in the umbilical vessel walls associated with IUGR. It is hypothesised that hypoxia might induce this overproliferation given the further proliferation in IUGR fetuses with abnormal umbilical Doppler waveforms. Coexistence of a high cell density and lean vessel walls suggests small smooth muscle cells in umbilical vessels with IUGR.
AIMS: The purpose of this study was to investigate the proliferation of smooth muscle cells in umbilical vessels of fetuses affected by intrauterine growth restriction (IUGR) and to compare the findings with gestational age-matched control cases. METHODS: Sixty umbilical cords from fetuses at 36-37 weeks gestation were examined. Fetuses were divided into three groups: group I, appropriate for dates birthweight; group II, IUGR with reassuring fetal status; and group III, IUGR with abnormal umbilical Doppler waveforms. Umbilical cords were immunostained with an antibody to proliferating cell nuclear antigen and Ki-67; stained smooth muscle cells were subsequently counted. Smooth muscle cell density was determined by counting the total number of cells in a representative area of vessel wall and the wall thickness of each vessel was also measured. RESULTS: Proliferation marker-positive cells were increased in the umbilical vessels of group II compared to group I, and there were more proliferating smooth muscle cells in the umbilical vessels of group III compared to the other two groups. The umbilical vessels of group III showed the highest smooth muscle cell density, but the wall thickness of all vessels was significantly thinner in group III than the other two groups. CONCLUSIONS: This study showed overproliferation of smooth muscle cells in the umbilical vessel walls associated with IUGR. It is hypothesised that hypoxia might induce this overproliferation given the further proliferation in IUGR fetuses with abnormal umbilical Doppler waveforms. Coexistence of a high cell density and lean vessel walls suggests small smooth muscle cells in umbilical vessels with IUGR.