Introduction The decrease in uterineartery pulsatility index (UtAPI) on the border of the first and second trimester is a well-established clinical marker of physiological placentation. This decline is due to the development of the specialized
The present study examines the direct effect of luteinising hormone (LH) on the reactivity of the porcine uterine artery to norepinephrine (NE). Three-mm-long arterial segments collected during the luteal phase of the oestrous cycle were mounted in an organ bath for isometric tension recording. After 30 min of equilibration in optimal passive tone, one part of the vessels was treated with 10 ng/ml of LH in PBS (experimental), while a second part of the arterial segments was treated with 10 ng/ml of bovine serum albumin (BSA) in PBS (control). After 30 min of equilibration, NE was given to each organ bath in a cumulative concentration manner, ranging between 1 × 10
mol/l to 3 × 10
mol/l. NE caused a dose-dependent contraction of all experimental and control arteries. The addition of LH caused a rightward shift of the dose-response curve to NE. The corresponding EC
values were 2.17 (± 0.39) μmol/l in PBS-pretreated vessels and 3.35 (± 0.41) μmol/l in LH-pretreated vessels (P < 0.05). The results of the present study demonstrate that LH attenuates the vascular response to NE in third-order branches of the uterine artery. Therefore, it can be suggested that besides the known effect of LH-hCG on the formation of vasoactive eicosanoids, an additional mechanism is involved in the direct action of LH on blood flow in the uterine arteries in pigs.
treatment and three control groups), each group consisting of two rats. The rats of the treatment groups underwent unilateral ligation of the right uterineartery, which supplies one uterine horn, on pregnancy day 7, 12, or 17 (designated as HI 7 , HI 12
. Carbon-monoxide (CO) decreases placental vascular impedance. We assessed the consequences of smoking-induced temporary maternal CO-increase on fetal and placental circulation.
. In a prospective study twenty-nine smoking pregnant women and their fetuses were evaluated. We determined the changes in maternal blood CO levels after smoking, and the concomitant changes in maternal and fetal circulation. Changes in fetal heart rate, uterine artery (UTA), middle cerebral artery (MCA), and descending aorta (DA) flow were measured by Doppler velocimetry. Changes in maternal CO level and umbilical flow value were assessed by paired t-test. The correlation between CO level and placental flow was assessed by partial correlation test.
. CO level increased (mean±SD 1.7±0.65% vs. 2.36±0.89, p<0.0001). Nicotine-related maternal circulatory parameters changed significantly, but uterine flow values remained unchanged. Fetal heart rate increased, while flow in MCA and DA showed no change. CO-dependent umbilical artery impedance remained unchanged (Pulsatility Index: 0.956±0.18 vs. 0.948±0.21). Partial correlation between CO level and umbilical arterial impedance showed no significance (r:−0.324).
. Despite significant CO elevation, the mainly CO-regulated placental flow remained unchanged.
gynaecology. [Szülészet-nőgyógyászati ultrahang-diagnosztika.] White Golden Book Kft., Budapest, 2006. [Hungarian]
Ferrazzi, E., Rigano, S., Padoan, A., et al.: Uterineartery blood flow volume in pregnant women with an