Rhee J W, Longo L D, Pearce W J, Bae N H, Valenzuela G J, Ducsay C A
Department of Physiology, Loma Linda University, School of Medicine, California 92350, USA.
Am J Physiol. 1996 Mar;270(3 Pt 1):E477-82. doi: 10.1152/ajpendo.1996.270.3.E477.
Mechanisms involving the timing of normal parturition are not well understood in most animal species. To gain a greater understanding of the mechanisms, we employed hypoxia to perturb the normal system of parturition. The present study was designed to investigate the effects of chronic hypoxia on myometrial contractility in the near-term pregnant rat. Rats were exposed to room air (control) or to continuous hypoxia (10.5% O2) either from experimental days 19 through 21 (2-day exposure) or from experimental days 15 through 21 (6-day exposure). On day 21, blood was collected for hormone assays, and the uterine horns were collected from each dam. One horn was snap-frozen in liquid nitrogen for oxytocin (OT) receptor analysis, and the other was used for in vitro assessment of myometrial contractile responses to cumulative doses of OT or arginine vasopressin (AVP). Hypoxic exposure resulted in approximately 60% reduction of the maximal myometrial contractile response to OT and a significant reduction in OT binding sites from 256.9 +/- 34.9 to 84.9 +/- 21.3 fmol/mg protein (P<0.01). In contrast, the contractile response to AVP was unaffected after exposure to chronic hypoxia (P> 0.05). Additionally, we observed no difference in the plasma concentrations of estrogen, progesterone, and corticosterone. We conclude that chronic hypoxia decreased the effectiveness of OT-specific contractile mechanisms, at least partially through a decrease in OT binding sites.
在大多数动物物种中，正常分娩时机所涉及的机制尚未得到充分理解。为了更深入了解这些机制，我们采用缺氧来扰乱正常的分娩系统。本研究旨在调查慢性缺氧对近足月妊娠大鼠子宫肌层收缩性的影响。大鼠在实验第19天至21天（2天暴露）或实验第15天至21天（6天暴露）期间，暴露于室内空气（对照组）或持续缺氧环境（10.5%氧气）。在第21天，采集血液进行激素测定，并从每只母鼠身上采集子宫角。一个子宫角在液氮中速冻用于催产素（OT）受体分析，另一个用于体外评估子宫肌层对累积剂量的OT或精氨酸加压素（AVP）的收缩反应。缺氧暴露导致子宫肌层对OT的最大收缩反应降低约60%，OT结合位点从256.9±34.9 fmol/mg蛋白显著减少至84.9±21.3 fmol/mg蛋白（P<0.01）。相比之下，暴露于慢性缺氧后，对AVP的收缩反应未受影响（P>0.05）。此外，我们观察到雌激素、孕酮和皮质酮的血浆浓度没有差异。我们得出结论，慢性缺氧降低了OT特异性收缩机制的有效性，至少部分是通过OT结合位点的减少实现的。
