Langer B, Barthelmebs M, Grima M, Coquard C, Imbs J L
Service de Gynécologie-Obstètrique II, CHU de Hautepierre, Strasbourg, France.
Obstet Gynecol. 1993 Sep;82(3):380-6.
To evaluate the vascular reactivity to vasoconstrictor drugs and the local role of angiotensin I-converting enzyme in the rat utero-feto-placental unit.
The experiments were carried out in vitro on a new model of the isolated perfused uterine horn from 19 nonpregnant and 16 pregnant rats.
Norepinephrine, angiotensin II, and angiotensin I induced concentration-dependent vasoconstriction in non-pregnant uteri (50% effective concentration = 271 +/- 63, 9.9 +/- 3.7, and 1.7 +/- 0.8 x 10(-9) mol/L, respectively; n = 4-5, mean +/- standard error of the mean). In pregnant uteri, the maximum vasoconstrictor effects of norepinephrine (increase in perfusion pressure 132 +/- 6 versus 186 +/- 20 mmHg in pregnant and nonpregnant, respectively) and angiotensin II (37 +/- 9 versus 89 +/- 4 mmHg), but not angiotensin I, were significantly lower. The vasoconstrictor effect of angiotensin I was inhibited by saralasin, an antagonist of the angiotensin II receptors, and by ramiprilat, a converting-enzyme inhibitor.
The isolated perfused rat utero-feto-placental unit is a useful experimental model for studying uterine vascular reactivity during pregnancy. Our in vitro results confirm vascular refractoriness to norepinephrine and angiotensin II during pregnancy and demonstrate local angiotensin II synthesis in the rat uterine vascular bed.
评估大鼠子宫 - 胎儿 - 胎盘单位对血管收缩药物的血管反应性以及血管紧张素I转换酶的局部作用。
实验在19只未孕大鼠和16只孕鼠的离体灌注子宫角新模型上进行。
去甲肾上腺素、血管紧张素II和血管紧张素I在未孕子宫中诱导浓度依赖性血管收缩(半数有效浓度分别为271±63、9.9±3.7和1.7±0.8×10⁻⁹ mol/L;n = 4 - 5,均值±均值标准误)。在孕子宫中,去甲肾上腺素(灌注压升高分别为132±6 mmHg和186±20 mmHg,孕鼠和未孕鼠)和血管紧张素II(37±9 mmHg和89±4 mmHg)的最大血管收缩作用显著降低,但血管紧张素I没有。血管紧张素I的血管收缩作用被血管紧张素II受体拮抗剂沙拉新和转换酶抑制剂雷米普利拉抑制。
离体灌注大鼠子宫 - 胎儿 - 胎盘单位是研究孕期子宫血管反应性的有用实验模型。我们的体外实验结果证实孕期对去甲肾上腺素和血管紧张素II存在血管不应性,并证明大鼠子宫血管床中存在局部血管紧张素II合成。