Lee F Y, Lin H C, Tsai Y T, Chang F Y, Lu R H, Hou M C, Li C P, Chu C J, Wang S S, Lee S D
Department of Medicine, Veterans General Hospital-Taipei, Taiwan, Republic of China.
Am J Gastroenterol. 1997 Nov;92(11):2080-4.
Nitric oxide has been proposed as being responsible for the hyperdynamic circulation observed in portal hypertensive states. Substance P, a neuropeptide partly cleared by liver, induces vasodilation through the activation of the endothelial nitric oxide pathway. This study investigated the plasma levels of substance P in cirrhotic patients and the relationship of these levels to systemic and portal hemodynamics.
Sixty-four patients with cirrhosis and 53 healthy controls had blood samples taken for determining plasma values of substance P by ELISA. Systemic and portal hemodynamics were measured on the same day of blood sampling using a Swan-Ganz catheterization and thermodilution technique.
Plasma levels of substance P were higher in cirrhotic patients than in healthy controls (45.7 +/- 2.0 vs 32.9 +/- 1.0 pg/ml, p < 0.001) and directly correlated with Child-Pugh's score (r = 0.52, p < 0.0001). Compared with compensated cirrhotic patients, decompensated cirrhotic patients had higher plasma levels of substance P accompanied by a lower systemic vascular resistance and higher hepatic venous pressure gradient. There was no significant correlation between plasma levels of substance P and systemic vascular resistance and hepatic venous pressure gradient. In addition, no significant difference in plasma levels of substance P was observed between cirrhotic patients with and cirrhotic patients without a hepatic venous pressure gradient > 12 mm Hg or between patients with and patients without large esophageal varices.
Plasma levels of substance P are increased in patients with cirrhosis and may contribute to the pathogenesis and/or maintenance of hyperdynamic circulation in decompensated patients. The severity of cirrhosis is more important than portal hypertension and the severity of esophageal varices for the development of increased plasma substance P levels.
一氧化氮被认为是门静脉高压状态下高动力循环的成因。P物质是一种部分由肝脏清除的神经肽，可通过激活内皮一氧化氮途径诱导血管舒张。本研究调查了肝硬化患者血浆P物质水平及其与全身和门静脉血流动力学的关系。
64例肝硬化患者和53例健康对照者采集血样，采用酶联免疫吸附测定法（ELISA）测定血浆P物质值。在采血当天，使用Swan-Ganz导管插入术和热稀释技术测量全身和门静脉血流动力学。
肝硬化患者血浆P物质水平高于健康对照者（45.7±2.0对32.9±1.0 pg/ml，p<0.001），且与Child-Pugh评分直接相关（r=0.52，p<0.0001）。与代偿期肝硬化患者相比，失代偿期肝硬化患者血浆P物质水平较高，同时全身血管阻力较低，肝静脉压力梯度较高。血浆P物质水平与全身血管阻力和肝静脉压力梯度之间无显著相关性。此外，肝静脉压力梯度>12 mmHg的肝硬化患者与无此情况的肝硬化患者之间，以及有大食管静脉曲张的患者与无大食管静脉曲张的患者之间，血浆P物质水平无显著差异。
肝硬化患者血浆P物质水平升高，可能参与失代偿期患者高动力循环的发病机制和/或维持过程。对于血浆P物质水平升高的发生，肝硬化的严重程度比门静脉高压和食管静脉曲张的严重程度更重要。
