Saha P R, Alsip N L, Henzel M K, Asher E F
Center for Applied Microcirculatory Research, University of Louisville, School of Medicine, KY 40292, USA.
J Reprod Fertil. 1998 Mar;112(2):211-6. doi: 10.1530/jrf.0.1120211.
The importance of nitric oxide (NO) and dilator prostaglandins in uterine resistance arterioles was investigated. In pentobarbital anaesthetized rats at dioestrus-2, the uterine microcirculation in vivo was transilluminated by a fibreoptic probe and microvessels (circumferential arterioles) viewed by video microscopy. Arteriolar diameters were measured while increasing concentrations of acetylcholine (ACh), serotonin (5-HT), phenylephrine (PE), or angiotensin II (AII) were applied topically (suffused) over the uterus. Agonists were applied alone or with ibuprofen (IBU; cyclooxygenase inhibitor), N omega-nitro-L-arginine (L-NA; nitric oxide synthase inhibitor) or both. Circumferential arterioles were dilated by ACh and 5-HT (10(-8)-10(-4) mol l-1) and constricted by PE (10(-8)-10(-5) mol l-1) and AII (10(-11)-10(-7) mol l-1). Suffusion of L-NA or L-NA with ibuprofen (10(-4) mol l-1 each) abolished ACh-induced dilation; ibuprofen alone blocked dilation at higher ACh concentrations. Serotonin-induced relaxation was significantly attenuated by L-NA alone or in combination with ibuprofen. Vasoconstriction induced by PE was enhanced by L-NA alone and L-NA with ibuprofen, but ibuprofen alone had no effect. In contrast, AII-induced constriction was enhanced significantly by ibuprofen or L-NA and further enhanced when both ibuprofen and L-NA were present. These results suggest that ACh can release either nitric oxide (NO) or cyclooxygenase products to cause uterine arteriolar dilation and that 5-HT-induced uterine microvascular relaxation is mediated via NO only. They also suggest that PE-induced vasoconstriction is attenuated by the release of NO but not cyclooxygenase products and that constrictor responses evoked by AII are attenuated by both NO and dilator prostaglandin release. Thus, both nitric oxide and dilator prostaglandins are important in the control of uterine microvessels.
研究了一氧化氮（NO）和扩张性前列腺素在子宫阻力小动脉中的重要性。在处于动情周期二期的戊巴比妥麻醉大鼠中，用光纤探头对子宫体内微循环进行透照，并通过视频显微镜观察微血管（环行小动脉）。在向子宫局部（灌注）施加浓度不断增加的乙酰胆碱（ACh）、血清素（5 - HT）、去氧肾上腺素（PE）或血管紧张素II（AII）的同时，测量小动脉直径。激动剂单独使用或与布洛芬（IBU；环氧化酶抑制剂）、Nω-硝基-L-精氨酸（L-NA；一氧化氮合酶抑制剂）或两者联合使用。环行小动脉可被ACh和5 - HT（10⁻⁸ - 10⁻⁴ mol/L）扩张，被PE（10⁻⁸ - 10⁻⁵ mol/L）和AII（10⁻¹¹ - 10⁻⁷ mol/L）收缩。灌注L-NA或L-NA与布洛芬（各10⁻⁴ mol/L）可消除ACh诱导的扩张；单独使用布洛芬在较高ACh浓度时可阻断扩张。单独使用L-NA或L-NA与布洛芬联合使用可显著减弱5 - HT诱导的舒张。单独使用L-NA或L-NA与布洛芬联合使用可增强PE诱导的血管收缩，但单独使用布洛芬无效。相比之下，布洛芬或L-NA可显著增强AII诱导的收缩，当布洛芬和L-NA同时存在时进一步增强。这些结果表明，ACh可释放一氧化氮（NO）或环氧化酶产物以引起子宫小动脉扩张，且5 - HT诱导的子宫微血管舒张仅通过NO介导。它们还表明，PE诱导的血管收缩可被NO释放减弱，但不能被环氧化酶产物减弱，且AII引起的收缩反应可被NO和扩张性前列腺素释放同时减弱。因此，一氧化氮和扩张性前列腺素在子宫微血管的控制中都很重要。
