Morishita F, Kawarabayashi T, Sakamoto Y, Shirakawa K
Department of Obstetrics and Gynecology, School of Medicine, Fukuoka University, Japan.
Am J Obstet Gynecol. 1995 Jan;172(1 Pt 1):186-95. doi: 10.1016/0002-9378(95)90111-6.
Periodic uterine relaxation in labor relieves the fetus from hypoxia related to sustained contractions. A reduction in intracellular calcium is essential for relaxation. Therefore we aimed to clarify the extrusion mechanisms of intracellular calcium ions in pregnant human myometrium.
Isometric contraction of small muscle bundles obtained from human myometrium at term was recorded. High-potassium and sodium-free solutions could induce stable contractures that revealed initial phasic contractions followed by tonic contractions. The effects of external calcium, external magnesium, nifedipine, and calcium adenosine triphosphatase inhibitors on both contractures were then examined.
Because maximum tonic contraction was induced by 48 mmol/L potassium, this concentration was used. Both contractures depended on external calcium concentrations. Nifedipine, 10(-7) mol/L inhibited both initial phasic contractions and the tonic phase of the high-potassium contracture; however, it could not suppress the tonic phase of the sodium-free contracture. Calcium adenosine triphosphatase inhibitors, cyclopiazonic acid and lauryl sulfate, potentiated the tensions of tonic phases in both contractures; the effect of lauryl sulfate was stronger than that of cyclopiazonic acid. When external magnesium was gradually increased (from 0 to 9.6 mmol/L), both phasic contractions and the tonic phase of the high-potassium contracture transiently increased, followed by a reduction of tension, whereas the tonic phase of the sodium-free contracture was markedly inhibited by magnesium in a dose-dependent manner.
The presence of the sodium-calcium exchange mechanism and the specific inhibitory effect of magnesium were indicated in human myometrium during pregnancy. These mechanisms might prevent the long tonic contractions, to protect the fetus from hypoxia during pregnancy and parturition.
分娩时子宫周期性松弛可使胎儿免受与持续性宫缩相关的缺氧影响。细胞内钙减少是松弛的关键。因此,我们旨在阐明妊娠子宫肌层细胞内钙离子的排出机制。
记录足月时从人子宫肌层获取的小肌肉束的等长收缩。高钾和无钠溶液可诱导稳定的挛缩,表现为初始的相性收缩继以强直性收缩。然后检测了细胞外钙、细胞外镁、硝苯地平和钙腺苷三磷酸酶抑制剂对两种挛缩的影响。
由于48 mmol/L钾可诱导最大强直性收缩,故采用该浓度。两种挛缩均依赖于细胞外钙浓度。10(-7) mol/L硝苯地平可抑制初始相性收缩和高钾挛缩的强直期;然而,它不能抑制无钠挛缩的强直期。钙腺苷三磷酸酶抑制剂环匹阿尼酸和月桂醇硫酸酯可增强两种挛缩强直期的张力;月桂醇硫酸酯的作用强于环匹阿尼酸。当细胞外镁逐渐增加(从0至9.6 mmol/L)时,高钾挛缩的相性收缩和强直期均短暂增加,随后张力降低,而无钠挛缩的强直期则被镁以剂量依赖性方式显著抑制。
妊娠人子宫肌层存在钠钙交换机制及镁的特异性抑制作用。这些机制可能防止长时间强直性收缩,以保护胎儿在妊娠和分娩期间免受缺氧影响。