Ni Y, Meyer M, Osol G
Department of Molecular Physiology, University of Vermont College of Medicine, Burlington 05405, USA.
Am J Obstet Gynecol. 1997 Apr;176(4):856-64. doi: 10.1016/s0002-9378(97)70611-2.
The purpose of this study was to determine the influence of endothelium-released nitric oxide on uterine arterial tone and reactivity during pregnancy.
The effects of pregnancy on endothelial function were evaluated in isolated pressurized rat uterine arteries from late-pregnant rats (day 19 to 20) versus age-matched nonpregnant controls. The effects of nitric oxide synthase inhibition (N(omega)-nitro-L-arginine) on arterial tone and reactivity under basal and activated (phenylephrine) conditions were determined, as was arterial reactivity to endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside) vasodilators, by evaluating changes in lumen diameter.
(1) Maximal constriction to N(omega)-nitro-L-arginine was significantly enhanced under basal (nonstimulated) conditions in arteries from late-pregnant versus nonpregnant rats (changes in lumen diameter 37% +/- 8% vs 9.3 +/- 6.2%, respectively, p < 0.05). (2) Nitric oxide synthase blockade with 1 nmol/L N(omega)-nitro-L-arginine significantly increased phenylephrine sensitivity in arteries from late-pregnant animals (median effective concentration 115 +/- 23 nmol/L vs 33 +/- 8 nmol/L, control vs treated vessels, p < 0.05) but was without statistically significant effect on arteries from nonpregnant animals (control 255 +/- 164 nmol/L, treated 250 +/- 102 nmol/L, p > 0.05). (3) The threshold concentration of acetylcholine required to elicit endothelium-dependent dilation was significantly lower in late-pregnant versus nonpregnant arteries (1.4 +/- 0.2 nmol/L vs 12.2 +/- 3.8 nmol/L, p < 0.05). (4) Vascular smooth muscle sensitivity to an exogenous nitrodilator (sodium nitroprusside) was identical in late-pregnant versus nonpregnant vessels.
Endothelial vasodilator influences are augmented during pregnancy under basal, activated (phenylephrine), and chemically provoked (acetylcholine) conditions in uterine arteries by enhanced release of nitric oxide.
本研究旨在确定内皮释放的一氧化氮对孕期子宫动脉张力和反应性的影响。
在来自妊娠晚期大鼠（第19至20天）与年龄匹配的未孕对照大鼠的离体加压子宫动脉中，评估妊娠对内皮功能的影响。通过评估管腔直径的变化，确定一氧化氮合酶抑制（N（ω）-硝基-L-精氨酸）在基础和激活（去氧肾上腺素）条件下对动脉张力和反应性的影响，以及动脉对内皮依赖性（乙酰胆碱）和内皮非依赖性（硝普钠）血管舒张剂的反应性。
（1）在基础（未刺激）条件下，妊娠晚期大鼠动脉对N（ω）-硝基-L-精氨酸的最大收缩作用比未孕大鼠显著增强（管腔直径变化分别为37%±8%和9.3±6.2%，p<0.05）。（2）用1 nmol/L N（ω）-硝基-L-精氨酸阻断一氧化氮合酶，显著增加了妊娠晚期动物动脉对去氧肾上腺素的敏感性（半数有效浓度为115±23 nmol/L对33±8 nmol/L，对照血管与处理血管，p<0.05），但对未孕动物的动脉无统计学显著影响（对照255±164 nmol/L，处理250±102 nmol/L，p>0.05）。（3）引起内皮依赖性舒张所需的乙酰胆碱阈值浓度在妊娠晚期动脉中比未孕动脉显著更低（1.4±0.2 nmol/L对12.2±3.8 nmol/L，p<0.05）。（4）妊娠晚期与未孕血管对外源性血管舒张剂（硝普钠）的血管平滑肌敏感性相同。
在基础、激活（去氧肾上腺素）和化学激发（乙酰胆碱）条件下，孕期子宫动脉中一氧化氮释放增加，从而增强了内皮舒张因子的影响。
