在豚鼠中,通过剪切应力依赖性和非依赖性机制释放的一氧化氮可减轻过敏性肝静脉收缩。

IF 2.4 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Toshishige Shibamoto, Zonghai Ruan, Sen Cui, Yasutaka Kurata, Tomonobu Koizumi, Keishi Kubo
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引用次数: 3

摘要

1. 用离体卵清蛋白致敏豚鼠肝脏研究了剪切应力在一氧化氮(NO)介导的过敏性静脉收缩衰减中的作用。2. 豚鼠皮下注射1毫克卵清蛋白,使其主动致敏。致敏2周后,在恒流量或恒灌注压条件下向肝脏灌注稀释后的血液。恒定的流量会导致收缩过程中剪切应力的增加,而恒定的灌注压力可以阻止剪切应力的变化。采用双闭塞技术估计肝窦压力,评估肝窦前后收缩情况。2 .将卵清蛋白(4 μ g)注入灌注液,体积为40 mL,诱导肝脏过敏反应。在恒定流量或恒定压力下,过敏反应引起的静脉收缩主要是窦前而不是窦后,尽管恒定压力下的过敏性静脉收缩明显大于恒定流量下的静脉收缩。当通过维持恒定的灌注压力来保持剪切应力恒定时,NO合成酶抑制剂诺美加-硝基-L-精氨酸甲酯(L- name, 100微mol/L)在过敏反应引起的鼻窦收缩前和后均具有相似的增强作用。这表明肝过敏反应剪切应力独立产生NO,导致窦前和窦后血管的扩张程度相似。相反,当剪切应力在恒定流量下升高时,L-NAME优先增强了过敏性窦前收缩。4. 肝过敏反应可以以剪切应力无关的方式增加NO的产生,并且在窦前和窦后都类似地扩张,而以剪切应力依赖的方式产生的NO主要减弱剪切应力优先增加的窦前静脉收缩。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anaphylactic hepatic venoconstriction is attenuated by nitric oxide released via shear stress-dependent and -independent mechanisms in Guinea pig.

1. The role of shear stress in nitric oxide (NO)-mediated attenuation of anaphylactic venoconstriction was studied using an isolated ovalbumin-sensitized guinea pig liver. 2. Guinea pigs were actively sensitized by a subcutaneous injection of 1 mg ovalbumin. Two weeks after sensitization, the livers were perfused with diluted blood under constant flow or constant perfusion pressure. The constant flow could result in increased shear stress during constriction, while the constant perfusion pressure could prevent changes in shear stress. Using the double occlusion technique to estimate the hepatic sinusoidal pressure, pre- and postsinusoidal constriction was evaluated. Hepatic anaphylaxis was induced by an injection of ovalbumin (4 microg) into the perfusate, the volume of which was 40 mL. 3. Under either constant flow or pressure, anaphylaxis caused venoconstriction of predominantly presinusoids over postsinusoids, although anaphylactic venoconstriction under constant pressure was significantly greater than that under constant flow. When shear stress was held constant by maintaining constant perfusion pressure, a NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME, 100 micromol/L), potentiated similarly both pre- and postsinusoidal constriction induced by anaphylaxis. This suggests that hepatic anaphylaxis shear stress-independently generates NO, resulting in dilatation of both pre- and postsinusoidal vessels in a similar magnitude. In contrast, when shear stress was allowed to rise under constant flow, anaphylactic presinusoidal constriction was preferentially potentiated by L-NAME. 4. Hepatic anaphylaxis can increase NO production in a shear stress-independent manner and dilates similarly both pre- and postsinusoids, while NO produced in a shear stress-dependent manner attenuates predominantly venoconstriction of the presinusoids where shear stress is preferentially increased.

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来源期刊
Clinical and Experimental Pharmacology and Physiology
Clinical and Experimental Pharmacology and Physiology PHARMACOLOGY & PHARMACY-PHYSIOLOGY
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128
期刊介绍: Clinical and Experimental Pharmacology and Physiology is an international journal founded in 1974 by Mike Rand, Austin Doyle, John Coghlan and Paul Korner. Our focus is new frontiers in physiology and pharmacology, emphasizing the translation of basic research to clinical practice. We publish original articles, invited reviews and our exciting, cutting-edge Frontiers-in-Research series’.
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