Effect of human chorionic gonadotropin on uterine blood flow in intact and ovariectomized gilts.

This experiment was designed to test the hypothesis that human chorionic gonadotropin (hCG) can directly influence uterine blood flow in pigs. In the study, 18 crossbred gilts (95-100 kg) which had exhibited at least one estrous cycle were used: 8 cyclic gilts in the luteal phase of the estrous cycle and 10 gilts ovariectomized (OVX) three weeks before the experiment began. The OVX animals received i.m. injections of 1 mg estradiol benzoate and 50 mg progesterone daily for five consecutive days before transducer implantation. Precalibrated electromagnetic blood flow transducers were surgically implanted around the uterine artery under general anaesthesia. Beginning at 120 min (0 h) following the placement of probes, i.e. after recording had stabilized, blood flow values were recorded at 10 min intervals for the next 360 min. At 0 h, cyclic (n = 4) and OVX (n = 5) gilts received a bolus injection (5 ml) of 1000 IU hCG intravenously through an indwelling catheter and then the same dose of hCG continuously during 4 hours in 40 ml of saline. The remaining cyclic (n = 4) and OVX (n = 5) gilts were infused with saline only and served as control. The mean (SEM) uterine blood flow at 0 h in cyclic (n = 8) and OVX (n = 10) gilts was 104.0 +/- 25.7 and 58.6 +/- 6.0 ml/min, respectively. Because of the variability of initial blood flow, especially in the cyclic gilts, hCG induced changes were expressed as a percent change from the initial flow and were compared to pretreatment period 0 (-30 - 0 h). hCG produced a significant increase in the uterine blood flow in both treated groups (p < 0.05) reaching at 70 min 110.2 +/- 3.4 vs 80.0 +/- 10.5 and 122.4 +/- 12.1 vs 90.6 +/- 3.8, and then at 230 min 116.7 +/- 9.3 vs 62.0 +/- 10.0 and 121.8 +/- 13.2 vs 85.4 +/- 2.3 percent of initial blood flow in cyclic and OVX gilts, respectively. A comparison of nine 30-min periods (periods 1-9) to period 0 showed a significant decrease of uterine blood flow in both (cyclic and ovariectomized) saline control groups in periods 2-9 (50-360 min). The comparison of the same periods in cyclic and ovariectomized hCG treated gilts revealed a significant increase during periods 7-9 (250-360 min) and in period 6, 9 (210-240 and 330-360 min), respectively. Serum estradiol levels increased significantly from 7.4 +/- 1.5 to 351.9 +/- 50.2 pg/ml in cyclic, and from 43.3 0 +/- 7.0 to 224.8 +/- 24.1 in OVX hCG treated gilts at 180 and 120 min, respectively, and returned to the levels of the control groups 240-300 min after the beginning of hCG infusion. Those results indicate that the early response in uterine blood flow is produced directly by hCG, which overcomes the inhibitory pharmacological effect of pentobarbital on uterine blood flow. The second phase of response to hCG could be caused by estradiol which significantly increased an hour earlier before uterine blood flow elevation. We have also shown a novel source of estradiol in castrated pigs which is released by hCG.