초록 열기/닫기 버튼
Objective We investigated the in vivo tocolytic effect of Clostridium botulinum toxin A (BoNT/A) on mifepristone-induced preterm labor in rats. Methods On day 17 of gestation, an incision was made to expose the uterus, and BoNT/A (normal saline or 20 units) was injected into the uterine horns. On day 18, mifepristone was used to induce uterine contractions. Electrical activity of uterine contractions was measured via electromyography on day 19. Results In rats treated with 20 units of BoNT/A, the amplitude of uterine contractions was significantly decreased by 45.2 ± 18.4 (P<0.05) from baseline, respectively. The total duration of uterine contractions was significantly decreased by 51.7 ± 7.9 (P<0.01), respectively. The frequency of contraction bursts after treatment with 20 units of BoNT/A was decreased by 5.6 ± 16.3 from the baseline (P=0.4). Conclusion In rats undergoing mifepristone-induced preterm labor, BoNT/A significantly inhibited uterine contractility. The decrease in uterine activity was mainly caused by a decline in the duration and intensity rather than frequency of uterine contractions.
Objective We investigated the in vivo tocolytic effect of Clostridium botulinum toxin A (BoNT/A) on mifepristone-induced preterm labor in rats. Methods On day 17 of gestation, an incision was made to expose the uterus, and BoNT/A (normal saline or 20 units) was injected into the uterine horns. On day 18, mifepristone was used to induce uterine contractions. Electrical activity of uterine contractions was measured via electromyography on day 19. Results In rats treated with 20 units of BoNT/A, the amplitude of uterine contractions was significantly decreased by 45.2 ± 18.4 (P<0.05) from baseline, respectively. The total duration of uterine contractions was significantly decreased by 51.7 ± 7.9 (P<0.01), respectively. The frequency of contraction bursts after treatment with 20 units of BoNT/A was decreased by 5.6 ± 16.3 from the baseline (P=0.4). Conclusion In rats undergoing mifepristone-induced preterm labor, BoNT/A significantly inhibited uterine contractility. The decrease in uterine activity was mainly caused by a decline in the duration and intensity rather than frequency of uterine contractions.
목적우리는 클로스트리디움 보툴리눔 독소 A형(BoNT/A)이 미페프리스톤으로 유발된 조기진통 쥐 모델에 대해 자궁수축억제 효과가 있는지 in vivo 연구를 실시하였다. 연구방법임신 17일, 개복 후 자궁 양측 뿔에 식염수 또는 20 유니트의 BoNT/A를 투여하였다. 임신 18일, 미페프리스톤을 근주하여 자궁의 조기진통을 유발시켰다. 임신 19일, 근전도검사기를 통하여 자궁수축 활동을 측정하였다. 결과BoNT/A 20 유니트를 투여한 군은 자궁수축 강도가 BoNT/A를 투여하지 않은 군에 비해 45.2% (P＜0.05)로 유의하게 감소하였으며, 자궁수축 기간은 51.6% (P＜0.01)로 유의하게 감소하였다. 하지만 자궁수축 빈도에 대한 감소는 5.6% (P = 0.4)로 유의하게 감소는 없었다. 결론미페프리스톤으로 유발된 조기진통 쥐 모델에서 BoNT/A는 자궁의 수축력을 유의하게 감소시켰다. 자궁수축의 감소는 자궁수축 빈도에대한 억제효과보다는 자궁수축의 기간 및 강도의 억제효과가 유의했다.
키워드열기/닫기 버튼
클로스트리디움 보툴리눔 독소 A형, 조기진통억제제, 조기진통, 미페프리스톤, 쥐
