目的:由于分娩缺血期间子宫细胞外pH值降低,但是它对子宫肌层收缩的影响在很大程度上是未知的,有必要阐明其生理效应和作用机制。此外,目前尚不清楚细胞外酸化的任何影响是否受到怀孕的影响,因此,我们还确定了妊娠如何影响酸化反应。
方法:非妊娠,mid-,从人道杀死的小鼠中获得足月妊娠子宫肌层条带。宫缩记录在自发状态下,去极化,和催产素刺激的条件。在HEPES缓冲的生理盐水中,灌注液的细胞外pH从7.4变为6.9或7.9。使用SNARF测量细胞内pH,使用Indo-1测量细胞内钙。使用适当的t检验检验统计学差异。
结果:细胞外酸化显著增加了孕妇自发收缩的频率和幅度,但不是没有怀孕,子宫肌层,而碱化减少收缩。细胞内酸化,通过丁酸钠,妊娠组织中的力暂时增加。当细胞外pH酸化时,细胞内pH逐渐酸化,但是在细胞内pH发生任何显着变化之前,细胞外酸化会增加收缩力。如果子宫肌力是由催产素或高K去极化驱动的,然后细胞外pH没有进一步增加力。细胞内钙的变化反映了自发收缩的妊娠子宫肌层中的力的变化,如果硝苯地平阻止了钙的进入,细胞外酸化不能引起力的上升。
结论:胞外酸化增加兴奋性,钙进入,从而迫使怀孕的小鼠子宫肌层,这可能有助于增加分娩期间的收缩,当缺血性疾病和酸血症发生时。
As
uterine extracellular pH decreases during the ischemic conditions of labor, but its effects on myometrial contraction are largely unknown, there is a need to elucidate its physiological effects and mechanisms of action. Furthermore, it is not known if any of the effects of extracellular acidification are affected by pregnancy, thus we also determined how gestation affects the response to acidification.
Nonpregnant, mid-, and term-pregnant myometrial strips were obtained from humanely killed mice. Contractions were recorded under spontaneous, depolarized, and oxytocin-stimulated conditions. The extracellular pH of the perfusate was changed from 7.4 to 6.9 or 7.9 in HEPES-buffered physiological saline. Intracellular pH was measured using SNARF, and intracellular calcium was measured using Indo-1. Statistical differences were tested using the appropriate t-test.
Extracellular acidification significantly increased the frequency and amplitude of spontaneous contractions in pregnant, but not nonpregnant, myometrium, whereas alkalinization decreased contractions. Intracellular acidification, via Na-butyrate, transiently increased force in pregnant tissue. Intracellular pH was gradually acidified when extracellular pH was acidified, but extracellular acidification increased contractility before any significant change in intracellular pH. If myometrial force was driven by oxytocin or high-K depolarization, then extracellular pH did not further increase force. Intracellular calcium changes mirrored those of force in the spontaneously contracting pregnant myometrium, and if calcium entry was prevented by nifedipine, extracellular acidification could not induce a rise in force.
Extracellular acidification increases excitability, calcium entry, and thus force in pregnant mouse myometrium, and this may contribute to increasing contractions during labor when ischemic conditions and acidemia occur.