Sibley C P, Ward B S, Glazier J D, Moore W M, Boyd R D
Am J Physiol. 1986 Mar;250(3 Pt 2):R474-84. doi: 10.1152/ajpregu.1986.250.3.R474.
Electrical activity generated by pieces of pig placenta, taken from anesthetized animals and mounted in Ussing chambers, has been investigated. Ten minutes after the start of voltage clamping, potential difference (PD; fetal side positive, open circuit), short circuit current (SCC), and resistance were 5.9 +/- 0.4 (SE) mV, 8.6 +/- 0.5 microA X cm-2, and 720 +/- 45 omega X cm2, respectively (n = 50). Ouabain (10(-4) M) added to the fetal side caused a maximum decline in PD and SCC from the time of addition of -3.7 +/- 0.98 mV and -3.9 +/- 1.4 microA X cm-2 (n = 6); epinephrine (10(-5) M) added to the fetal side caused increases of +1.0 +/- 0.2 mV and +4.0 +/- 1.4 microA X cm-2, respectively (n = 14). Drug concentrations for 50% maximum response for the effect of a series of adrenergic agonists on SCC were (in M) isoproterenol 1.2 +/- 0.05 X 10(-8), norepinephrine 6.1 +/- 0.3 X 10(-8), epinephrine 2.4 +/- 0.1 X 10(-7), and phenylephrine 4.7 +/- 0.2 X 10(-5), suggesting the involvement of fetally oriented beta-adrenergic receptors. Fetal epinephrine (10(-5) M) also stimulated net Na+ flux (Jnet) toward the fetal side to an extent equal to its effect on SCC. In control experiments Jnet was small but was inhibited by fetal side ouabain (10(-4) M) to produce a maternally directed Jnet, significantly different to the SCC. Replacement of Na+ by choline reduced SCC markedly but did not abolish it. In the absence of Na+, epinephrine had no effect on SCC. These results suggest that active Na+ transfer is not completely responsible for the control electrical activity of pig placenta. Epinephrine, however, modulates SCC entirely by stimulating net Na+ transfer toward the fetal side.
对取自麻醉动物并置于尤斯灌流小室中的猪胎盘组织所产生的电活动进行了研究。电压钳制开始10分钟后，电位差（PD；胎儿侧为正，开路）、短路电流（SCC）和电阻分别为5.9±0.4（SE）mV、8.6±0.5μA·cm⁻²和720±45Ω·cm²（n = 50）。向胎儿侧加入哇巴因（10⁻⁴M）后，从加入之时起，PD和SCC最大下降幅度分别为-3.7±0.98 mV和-3.9±1.4μA·cm⁻²（n = 6）；向胎儿侧加入肾上腺素（10⁻⁵M）后，分别使PD和SCC增加了+1.0±0.2 mV和+4.0±1.4μA·cm⁻²（n = 14）。一系列肾上腺素能激动剂对SCC产生50%最大反应的药物浓度（以M计）分别为：异丙肾上腺素1.2±0.05×10⁻⁸、去甲肾上腺素6.1±0.3×10⁻⁸、肾上腺素2.4±0.1×10⁻⁷、苯肾上腺素4.7±0.2×10⁻⁵，提示存在面向胎儿的β-肾上腺素能受体参与其中。胎儿侧肾上腺素（10⁻⁵M）还使净Na⁺通量（Jnet）向胎儿侧的方向增加，其程度与其对SCC的作用相当。在对照实验中，Jnet很小，但胎儿侧哇巴因（10⁻⁴M）可抑制Jnet，从而产生指向母体的Jnet，这与SCC有显著差异。用胆碱替代Na⁺可显著降低SCC，但并未使其完全消失。在无Na⁺的情况下，肾上腺素对SCC无影响。这些结果表明，主动Na⁺转运并非猪胎盘控制电活动的唯一原因。然而，肾上腺素完全通过刺激净Na⁺向胎儿侧的转运来调节SCC。
