ATTENUATION OF THE VASOCONSTRICTOR EFFECTS OF THROMBOXANE AND ENDOTHELIN BY NITRIC-OXIDE IN THE HUMAN FETAL-PLACENTAL CIRCULATION
ATTENUATION OF THE VASOCONSTRICTOR EFFECTS OF THROMBOXANE AND ENDOTHELIN BY NITRIC-OXIDE IN THE HUMAN FETAL-PLACENTAL CIRCULATION
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DOI：
10.1016/0002-9378(92)91863-6
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发表时间：
1992-01-01
影响因子：
9.8
通讯作者：
BROCKMAN, DE
中科院分区：
文献类型：
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作者：
MYATT, L;BREWER, AS;BROCKMAN, DE
目的：我们假设内皮源性舒张因子一氧化氮可能有助于降低静息血管张力，并可能减弱人胎儿-胎盘循环中的血管收缩作用。采用离体人胎盘子叶进行双重灌流，观察了N-单甲基-L-精氨酸和N-硝基-L-精氨酸对离体人胎盘子叶细胞增殖的影响。（3 × 10（-4）mol/L），它们是L-精氨酸的非代谢类似物，L-精氨酸是一氧化氮合酶的底物，分别用U46619（10（-8）mol/L）或ET-1（10（-8）mol/L）预收缩胎-胎盘循环，建立胎-胎盘微循环收缩模型。 配对t检验比较抑制前后的反应。 三硝酸甘油（10（-6）mol/L）、乙酰胆碱（10（-4）mol/L）、钙离子载体A23187（10（-6）mol/L）和组胺（10（-8）~ 10（-4）mol/L）对收缩前胎儿-胎盘循环的影响也被测定。N-单甲基-L-精氨酸和N-硝基-L-精氨酸（3 x 10（-4）mol/L）静息灌注压升高（p < 0.06），和N-硝基-L-精氨酸迅速和显着增加灌注压在胎儿胎盘循环预收缩与U46619（p < 0.0004）或内皮素-1（p < 0.06）。 加入硝酸甘油（10（-6）mol/L）产生的一氧化氮减弱了U46619（p < 0.026）或内皮素-1（p < 0.01）的缩血管作用。 无论是乙酰胆碱，也没有钙离子载体A23187对胎儿胎盘循环的影响，而缓激肽进一步增加灌注压。 组胺仅在高于其它系统释放一氧化氮的浓度（10（-6）~ 10（-4）mol/L）时才使预收缩的制品松弛.结论：对胎儿-胎盘循环中一氧化氮产生的刺激可能是流体动力学的. 一氧化氮似乎有助于维持基础血管张力，并减弱血管收缩剂在该循环中的作用。
OBJECTIVE: We hypothesized that the endothelial-derived relaxing factor nitric oxide may contribute to low resting vascular tone and may attenuate vasoconstrictor action in the human fetal-placental circulation.STUDY DESIGN: Isolated human placental cotyledons were dually perfused in vitro, and the effects of N-monomethyl-L-arginine and N-nitro-L-arginine (3 x 10(-4) mol/L), which are nonmetabolizable analogs of L-arginine, the substrate for nitric oxide synthase, on resting perfusion pressure and on the fetal-placental circulation preconstricted with U46619 (10(-8) mol/L) or endothelin-1 (10(-8) mol/L) were established. Responses before and after inhibition were compared by paired t test. The effects of glyceryl trinitrate (10(-6) mol/L), acetylcholine (10(-4) mol/L), the calcium ionophore A23187 (10(-6) mol/L), and histamine (10(-8) to 10(-4) mol/L) were also determined in the preconstricted fetal-placental circulation.RESULTS: Both N-monomethyl-L-arginine and N-nitro-L-arginine (3 x 10(-4) mol/L) increased resting perfusion pressure (p < 0.06), and N-nitro-L-arginine promptly and significantly increased perfusion pressure in the fetal-placental circulation preconstricted with U46619 (p < 0.0004) or endothelin-1 (p < 0.06). Nitric oxide generated by addition of glyceryl trinitrate (10(-6) mol/L) attenuated the vasoconstrictor effects of U46619 (p < 0.026) or endothelin-1 (p < 0.01). Neither acetylcholine nor the calcium ionophore A23187 had an effect on the fetal-placental circulation, whereas bradykinin further increased perfusion pressure. Histamine only relaxed the preconstricted preparations at concentrations (10(-6) to 10(-4) mol/L) above those shown to release nitric oxide in other systems.CONCLUSION: The stimulus to nitric oxide generation in the fetal-placental circulation may be hydrodynamic. Nitric oxide appears to contribute to maintenance of basal vascular tone and to attenuate the actions of vasoconstrictors in this circulation.