门静脉的形态功能特征和反应性

Victor Ojog
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引用次数: 0

摘要

背景:门静脉是人体最神秘的血管,因为它通过以卡亚尔细胞为代表的特殊起搏器机制来调节自身的收缩性能。与一般动脉系统,特别是肝脏系统相比,对各种代谢介质和天然血管促进剂在门静脉血路控制中的作用的研究要少得多。对门静脉在不同预处理条件下的结构、功能和反应性进行的研究带来了一些与动脉系统相同但又不同的证据。一氧化氮的产生较高,部分原因是精氨酸酶的表达减少,但肌肉介质变薄。指向肝门的周期性自发收缩是门静脉(PV)的特征,纵向肌纤维被认为是造成这一现象的原因。卡贾尔细胞的自发性节律振荡是由钙离子浓度增加导致其去极化引发的。苯肾上腺素的血管收缩效应取决于 ET-1 受体的活性。在体内或体外,乙酰胆碱诱导的皮层收缩具有特征性,这种效应被认为依赖于 ET-1。结论:确定门静脉对不同旁分泌、内分泌和血流动力学刺激作用的主要特殊性,是预测可能导致门静脉高压的收缩障碍的重要工具。同样,胆碱能和肾上腺素能刺激之间,以及 Ang II 和 ET-1 作用之间的相互作用已得到充分证实,这必须为门静脉反应性疾病的药物调节提供支持。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Morphofunctional traits and reactivity of the portal vein
Background: Portal vein is the most enigmatic vessel of our body because it regulates own contractile performances using a special pace-maker mechanism represented by cells of Cajal. The contribution of various metabolic mediators and natural vasotropic agents in the control of the portal blood circuit is much less studied compared to the arterial system in general and the hepatic system in particular. The studies designed on the structure, function, and reactivity of the portal vein in different preconditioning have brought some common but also distinct evidence of the arterial system. Nitric oxide production is higher partly due to reduced arginase expression, but muscular media is thinner. Periodic spontaneous contractions directed towards the liver gate are characteristic for portal vein (PV), and the longitudinal muscle fibers are considered to be responsible for this phenomenon. Spontaneous rhythmic oscillations of the cells of Cajal are triggered by increasing calcium ion concentration leading to their depolarization. PV constrictor effect of phenylephrine is dependent on the activity of receptors to ET-1. For PV is characterized the acetylcholine induced contraction either in vivo or in vitro, and this effect is thought to be dependent on ET-1. Conclusions: The establishment of main particularities of portal vein reactivity of action of different paracrine, endocrine, and hemodynamical stimuli represents an important tool for prediction of contractile disorders leading plausible to portal hypertension. Likewise, a well proven interplay between cholinergic and adrenergic stimulations and on the other hand between Ang II and ET-1 actions must be a support for pharmacological modulating of portal vein reactivity disorders.
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