Department of Obstetrics and Gynecology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Am J Obstet Gynecol. 2011 Aug;205(2):155.e12-7. doi: 10.1016/j.ajog.2011.03.020. Epub 2011 Mar 16.
At-term pregnancy-induced vasodilation is the resultant of endothelium-dependent vasodilation, decreased myogenic reactivity, increased compliance, and reduced sensitivity to vasoconstrictor agents. We hypothesized that these vascular changes are already present at mid-gestation.
In 20 mid-pregnant and 20 nonpregnant Wistar Hannover rats, we measured vascular responses of isolated mesenteric arteries and kidney.
In the pregnant rats compared with the nonpregnant rats, mesenteric flow-mediated vasodilation and renal perfusion flow increased 1.52-fold (from 47±5 to 31±4 μL/min) and 1.13-fold (from 12.8±0.1 to 14.4±0.1 mL/min), respectively. Nitric oxide inhibition reduced mesenteric flow-mediated vasodilation to a similar extent in the pregnant and nonpregnant rats; it completely blocked the pregnancy-induced increase in renal perfusion flow. Pregnancy did not change mesenteric artery sensitivity to phenylephrine, myogenic reactivity, nor vascular compliance.
At mid-gestation, alterations in rat mesenteric vascular tone depend primarily on flow-mediated endothelium-dependent changes and not on changes in α-adrenergic vasoconstrictor sensitivity, myogenic reactivity, or vascular compliance.
足月妊娠诱导的血管舒张是内皮依赖性血管舒张、肌原性反应性降低、顺应性增加以及对血管收缩剂敏感性降低的结果。我们假设这些血管变化在妊娠中期就已经存在。
在 20 例中孕期和 20 例非孕期 Wistar 汉诺威大鼠中，我们测量了分离的肠系膜动脉和肾脏的血管反应。
与非孕期大鼠相比，孕期大鼠的肠系膜血流介导的血管舒张和肾灌注血流分别增加了 1.52 倍（从 47±5 增加到 31±4 μL/min）和 1.13 倍（从 12.8±0.1 增加到 14.4±0.1 mL/min）。一氧化氮抑制对孕期和非孕期大鼠的肠系膜血流介导的血管舒张的抑制作用相似；它完全阻断了妊娠引起的肾灌注血流增加。妊娠并未改变肠系膜动脉对苯肾上腺素的敏感性、肌原性反应性或血管顺应性。
在妊娠中期，大鼠肠系膜血管张力的改变主要依赖于血流介导的内皮依赖性变化，而不是α-肾上腺素能血管收缩剂敏感性、肌原性反应性或血管顺应性的变化。
