Nitric oxide and portal hypertension
Nitric oxide and portal hypertension
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DOI：
10.1023/a:1021957818240
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发表时间：
2002-12-01
影响因子：
3.6
通讯作者：
Bosch, J
中科院分区：
文献类型：
--
作者：
González-Abraldes, J;García-Pagán, JC;Bosch, J
在肝硬化中，肝阻力增加是导致门静脉高压的初始现象。这主要是由于肝硬化引起的肝内微循环的结构扭曲。然而，与其他血管疾病相似，肝脏的结构变化与一氧化氮（NO）产生不足有关，这导致血管张力增加，肝阻力和门静脉压力进一步增加。正在开发新的治疗策略，以选择性地向肝脏提供NO，克服全身血管扩张剂的有害作用。另一方面，内脏动脉循环中发生了一个明显相反的过程，其中NO的产生增加。这导致内脏血管扩张和随后的门静脉流入增加，这有助于门静脉高压。门静脉高压症中全身性阻断NO可减弱高动力循环，但其增加肝脏阻力的作用可能会抵消减少门静脉流入的益处，从而阻止门静脉压力的有效降低。此外，不能排除NO阻断可能对肝硬化进展具有有害作用，这引起了对它们在肝硬化患者中使用的谨慎。
In liver cirrhosis, an increase in hepatic resistance is the initial phenomenon leading to portal hypertension. This is primarily due to the structural distortion of the intrahepatic microcirculation caused by cirrhosis. However, similar to other vascular conditions, architectural changes in the liver are associated with a deficient nitric oxide (NO) production, which results in an increased vascular tone with a further increase in hepatic resistance and portal pressure. New therapeutic strategies are being developed to selectively provide the liver with NO, overcoming the deleterious effects of systemic vasodilators. On the other hand, a strikingly opposite process occurs in splanchnic arterial circulation, where NO production is increased. This results in splanchnic vasodilatation and subsequent increase in portal inflow, which contributes to portal hypertension. Systemic blockade of NO in portal hypertension attenuates the hyperdynamic circulation, but its effects increasing hepatic resistance may offset the benefit of reducing portal inflow, thus preventing an effective reduction of portal pressure. Moreover, it cannot be ruled out that NO blockade may have a deleterious action on cirrhosis progression, which raises caution about their use in patients with cirrhosis.