Kurokawa H, Sekiyama T, Katsuta Y, Aramaki T
First Department of Internal Medicine, Nippon Medical School, Japan.
Nihon Ika Daigaku Zasshi. 1995 Feb;62(1):2-12. doi: 10.1272/jnms1923.62.2.
Portal and systemic hemodynamic responses to a very low dose of nitroglycerin were studied in patients with portal hypertension and cirrhosis, and compared with those to a high dose of this compound. A 0.15 mg dose of nitroglycerin was given sublingually to 10 patients (LDG), and 0.3 mg to another 10 (HDG). Hemodynamic measurements were performed by means of hepatic venous and right cardiac catheterization before and 5 min after nitroglycerin administration. The wedged hepatic venous pressure decreased after dosing by 7.9% (p < 0.01) in LDG, and by 15.3% (p < 0.01) in HDG. Hepatic blood flow with ICG did not change in either group. In LDG, azygos blood flow remained unchanged, in contrast to a significant decrease by 10.1% (p < 0.05) in HDG. Mean arterial pressure fell by 3.6% (p < 0.05) in LDG and by 18.6% (p < 0.01) in HDG. Cardiac index did not change in LDG, but decreased by 11.4% (p < 0.05) in HDG. In both groups, mean pulmonary arterial pressure and pulmonary capillary wedge pressure fell significantly by the same amount. In HDG, a significant correlation between changes in wedged hepatic venous pressure and azygos blood flow (r = 0.70, p < 0.05) was observed. This suggested that splanchnic vasoconstriction mediated by a high-pressure, rather than a low-pressure, baroreceptor reflex was the main contributor to a decrease in portal venous blood flow, resulting in a reduction in wedged hepatic venous pressure; whereas a slight but significant fall of wedged hepatic venous pressure induced by a very low dose of nitroglycerin might have been due to venodilatation in the portal system and the hepatic vascular bed. These data suggest that, even with a very low dose of nitroglycerin, partial improvement of the hepatic circulation can be expected with minimal change in the systemic circulation in patients with cirrhosis and portal hypertension.
研究了门静脉高压和肝硬化患者对极低剂量硝酸甘油的门静脉和全身血流动力学反应，并与高剂量该化合物的反应进行了比较。向10例患者（低剂量组，LDG）舌下给予0.15mg硝酸甘油，向另外10例患者（高剂量组，HDG）舌下给予0.3mg。在给予硝酸甘油前及给药后5分钟，通过肝静脉和右心导管插入术进行血流动力学测量。低剂量组给药后楔入肝静脉压下降7.9%（p<0.01），高剂量组下降15.3%（p<0.01）。两组中吲哚菁绿测定的肝血流量均未改变。低剂量组奇静脉血流量保持不变，而高剂量组则显著下降10.1%（p<0.05）。低剂量组平均动脉压下降3.6%（p<0.05），高剂量组下降18.6%（p<0.01）。低剂量组心脏指数未改变，高剂量组下降11.4%（p<0.05）。两组中，平均肺动脉压和肺毛细血管楔压均显著下降相同幅度。在高剂量组中，观察到楔入肝静脉压变化与奇静脉血流量之间存在显著相关性（r=0.70，p<0.05）。这表明，由高压而非低压压力感受器反射介导的内脏血管收缩是门静脉血流量减少、导致楔入肝静脉压降低的主要原因；而极低剂量硝酸甘油引起的楔入肝静脉压轻微但显著下降可能是由于门静脉系统和肝血管床的静脉扩张。这些数据表明，即使使用极低剂量的硝酸甘油，对于肝硬化和门静脉高压患者，在全身循环变化最小的情况下，也可预期肝循环得到部分改善。
