丹参等活血化淤中药对门脉高压血流动力学影响的临床与实验研究

目的探讨丹参、当归等及硝苯啶对门脉高压血流动力学的影响。方法采用血管插管测定胆管结扎肝硬化犬门脉系统压力变化；超声多普勒观测肝硬化患者门脉血流动力学变化。结果（１）静脉滴注丹参、当归后，肝硬化犬门静脉压（Ｐｐｖ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜０．０５～０．０１），平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞０．０５），硝苯啶则使Ｐｐｖ，ＷＨＶＰ，ＭＡＰ．ＨＲ显著降低（Ｐ＜０．０５）。（２）丹参、丹参＋硝苯啶．丹参＋水＋硝苯啶口服药１０－１２周，能显著降低肝硬化患者门静脉内径（Ｄｐｖ）、脾静脉内径（Ｄｓｖ）．门静脉血流量（Ｑｐｖ），脾静脉血流量（Ｑｓｖ）（Ｐ＜０．０５－０．０１，当归作用较弱。结论对比表明，丹参、当归等中药较硝苯啶对门脉压力作用为慢，但较持久，无副反应。     

丹参对门脉高压血流动力学影响的实验与临床研究

为研究丹参对肝硬化门脉血流动力学的影响，利用血管插管测定用药前后胆管结扎肝硬化犬门脉系统压力变化，超声多普勒监测肝硬化患者用药后门静脉系统血流动力的改变。结果：（１）丹参静脉给药可使肝硬化犬门静脉压（ＰＰＶ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜０．０５～０．０１），而平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞０．０５）；（２）丹参长期口服（１０～１２周），可显著降低肝硬化患者（Ｃｈｉｌｄ－ＰｕｇｈＡ、Ｂ级）门静脉内径（ＤＰＶ）、脾静脉内径（ＤＳＶ）、门静脉血流量（ＱＰＶ）、脾静脉血流量（ＱＳＶ）（Ｐ＜０．０５～０．０１），并对患者乏力、厌食、腹胀及肝功能（ＡＬＴ）具有部分改善作用，未见副作用。本研究表明，丹参为安全有效的降低门静脉压力药物，值得对其做进一步研究。     

Wedged hepatic venous pressure adequately reflects portal pressure in hepatitis C virus-related cirrhosis

Wedged hepatic venous pressure (WHVP) is equivalent to portal venous pressure in patients with alcoholic liver diseases. However, it may underestimate portal pressure in nonalcoholics, which is important because hepatitis C virus (HCV) infection is a frequent cause of chronic liver disease. We investigated the agreement between directly measured portal pressure and WHVP in alcoholic and HCV-related liver diseases. Seventy-one patients with liver disease resulting from HCV infection (n = 32), alcohol (n = 25), or both (n = 14) underwent simultaneous measurements of WHVP (by hepatic vein catheterization) and portal pressure (by direct puncture). In 9 patients, measurements were repeated 20 minutes after acute iv propranolol administration. WHVP showed an excellent agreement with portal pressure in patients with cirrhosis resulting from either HCV, alcohol or both (intraclass correlation coefficient: 0.94, 0.93, and 0.97, respectively; P <.001). A discrepancy of >/=5 mm Hg was observed in 7 cases. WHVP underestimated portal pressure in only 1 case and exceeded portal pressure by >/=5 mm Hg in 6 patients. The WHVP response to propranolol closely and significantly correlated with changes in portal pressure (intraclass correlation coefficient: 0.87; P <.004). The simple and safe measurement of WHVP accurately reflects portal pressure in alcoholic and HCV-related liver disease. This technique also allows us to accurately assess the portal pressure response to propranolol in both alcoholic and HCV-related cirrhosis.     

Long-term haemodynamic effects of a 4-week regimen of nipradilol, a new beta-blocker with nitrovasodilating properties, in patients with portal hypertension due to cirrhosis. A comparative study with propranolol.

To study the long-term effects of pharmacological combination therapy, a comparison was made of the haemodynamic changes in patients with cirrhosis and portal hypertension following a 4-week treatment of propranolol or nipradilol, a new nonselective beta-blocker with nitrovasodilating effect. Nipradilol (12 mg/dag, n = 12) significantly diminished wedged hepatic venous pressure (WHVP, 25 +/- 16%), the hepatic venous pressure gradient (HVPG, 20 +/- 12%), and estimated hepatic blood flow (EHBF, 18 +/- 16%). Propranolol (30 mg/day, n = 11) also caused a significant reduction in WHVP (22 +/- 21%) and HVPG (24 +/- 21%), but not in EHBF. The percentage of portal pressure reduction and the frequency of nonresponders did not differ between the nipradilol and propranolol groups. Both agents reduced heart rate by approx. 20%. Nipradilol, however, did not cause a significant reduction in cardiac index (CI) versus a 14% reduction by propranolol. Pulmonary capillary wedge pressure and central venous pressure, an index of preload, were decreased slightly in the nipradilol group. When nonresponders were excluded, there was a significant correlation of the percentage of reduction between WHVP and CI or systemic vascular resistance, in the nipradilol group. These results indicate that nipradilol may have potent hypotensive effects on portal hypertension, similar but not superior to propranolol. Nipradilol, at the dosage used in the present study, did not appear to exert a nitrovasodilating effect to enhance the portal pressure reduction induced by beta-blocking action.     

Effects of somatostatin on hepatic haemodynamics in the cirrhotic rat

Reports on the effects of somatostatin on hepatic haemodynamics in the cirrhotic patient have provided conflicting results. Therefore, we studied the effects of different modes and rates of somatostatin administration on hepatic haemodynamics in the cirrhotic rat. Portal pressure (PP), wedged hepatic venous pressure (WHVP), portal venous flow (PVF), liver blood flow (LBF) and systemic blood pressure were measured in rats with dimethylnitrosamine-induced cirrhosis. Somatostatin was administered as a rapid injection, a continuous infusion or as a bolus dose followed by a constant infusion. One group of rats with a previously constructed portacaval shunt received a bolus dose of somatostatin followed by a constant infusion. A rapid injection of somatostatin was attended by a rapid and significant fall in all the haemodynamic parameters measured (p less than 0.01). Continuous infusion of somatostatin [4 or 8 micrograms/kg body weight (BW) h] resulted in a gradual but significant reduction in PP, WHVP, PVF and LBF (p less than 0.05), but had no effect on systemic blood pressure. A bolus dose of somatostatin (2, 4 or 8 micrograms/kg BW over 2 min) resulted in a rapid decrease in PP, WHVP, PVF and LBF (p less than 0.01), the decreases being maintained by continuous infusion. In rats with a portacaval shunt a bolus dose of somatostatin (8 micrograms/kg BW) resulted in a rapid fall in WHVP and LBF, the decrease being maintained by a continuous infusion (8 micrograms/kg BW/h).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of nifedipine on hepatic venous pressure gradient and portal vein blood flow in patients with cirrhosis

Abstract We investigated the effects of nifedipine on splanchnic haemodynamics in 13 patients with cirrhosis and portal hypertension, and in 10 control subjects using hepatic venous catheterization and pulsed Doppler ultrasound. There were no significant changes in systemic or splanchnic haemodynamics in control patients. In contrast, systemic vascodilatation, evidenced by significant decreases in mean arterial pressure and systemic vascular resistance, was observed in patients 20 min after sublingual application of 10 mg nifedipine. Moreover, hepatic venous pressure gradient and portal vein blood flow significantly increased after nifedipine administration. There was a significant correlation between the percentage increases in portal vein blood flow and in hepatic venous pressure gradient. However, no correlation was found between the percentage change in cardiac output and that in portal vein blood flow. Thus the increase in portal vein blood flow appears to be related to splanchnic arterial vasodilatation by nifedipine. Consequently, nifedipine has deleterious effects on portal haemodynamics in patients with cirrhosis. As nifedipine may potentially increase the risk of variceal haemorrhage in patients with less advanced varices, this drug should be used with caution in patients with chronic liver disease.     

Hepatic venous pressure gradient measurement: Time to learn!

Portal hypertension is a clinical syndrome defined by a pathological increase in portal pressure. The development of cirrhosis of the liver is characterized by clinical manifestations related to portal hypertension like esophageal varices, ascites, bleeding, and encephalopathy. Direct measurement of portal pressure is invasive, inconvenient, and clinically impractical. Currently, the most commonly used parameter is the Hepatic Venous Pressure Gradient (HVPG), i.e., the difference between the wedged (WHVP) and the free hepatic venous pressures. HVPG represents the gradient between pressures in the portal vein and the intra-abdominal portion of inferior vena cava. When blood flow in a hepatic vein is stopped by a wedged catheter, the proximal static column of blood transmits the pressure from the preceding communicated vascular territory (hepatic sinusoids) to the catheter. Thus, WHVP reflects hepatic sinusoidal pressure and not the portal pressure itself. In the normal liver, due to pressure equilibration through interconnected sinusoids, wedged pressure is slightly lower than portal pressure, though this difference is clinically insignificant. In liver cirrhosis, the static column created by balloon inflation cannot be decompressed at the sinusoidal level due to disruption of the normal intersinusoidal communications; therefore, WHVP gives an accurate estimation of portal pressure in cirrhosis. The normal HVPG value is between 1 to 5 mmHg. Pressure higher than this defines the presence of portal hypertension, regardless of clinical evidence. HVPG >/= 10 mmHg (termed clinically significant portal hypertension) is predictive of the development of complications of cirrhosis, including death. HVPG above 12 mmHg is the threshold pressure for variceal rupture. The main advantages of HVPG are its simplicity, reproducibility, and safety. This review summarizes the technique of the HVPG measurement.     

Effects of isosorbide dinitrate on portal hypertension in alcoholic cirrhosis

It has recently been reported that vasodilators lower portal pressure in patients with cirrhosis. This effect, however, is not definitively proven. The effect of isosorbide dinitrate (5 mg sublingually) on splanchnic and systemic hemodynamics was investigated in 13 patients with alcoholic cirrhosis and portal hypertension. The administration of isosorbide dinitrate reduced hepatic venous pressure gradient by 34% (P less than 0.001), mean arterial pressure by 30% (P less than 0.001), cardiac index by 17% (P less than 0.001) and systemic vascular resistance by 11% (P = 0.05). Hepatic blood flow was not affected by the treatment. Significant correlations were found between the decrease in hepatic venous pressure gradient and that of cardiac index (P less than 0.05) and mean arterial pressure (P less than 0.05). These data indicate that isosorbide dinitrate lowers portal pressure in patients with cirrhosis. Decrease in cardiac output, rise in splanchnic arterial vascular resistance and decrease in porto-hepatic resistance seem to participate in determining the effect.     

Low-dose midazolam sedation: an option for patients undergoing serial hepatic venous pressure measurements

The hepatic venous pressure gradient (HVPG) is becoming increasingly used clinically. It is useful in the differential diagnosis of portal hypertension and provides a prognostic index in cirrhotic patients. Performance of serial measurements has been shown to be useful in guiding pharmacological therapy of portal hypertension and variceal hemorrhage. The technique is safe to perform; however, many patients are anxious and reluctant to undergo serial measurements. The effects of sedatives on portal pressure measurements have not yet been defined. The objective of this study was to evaluate the effects of midazolam on the HVPG. Twenty patients with compensated cirrhosis were included in this prospective, double-blind study. The HVPG was determined by subtracting the free hepatic venous pressure (FHVP) from the wedged hepatic venous pressure (WHVP). Patients were randomized to receive either placebo, 0.02 mg/kg midazolam, or 0.03 mg/kg midazolam, administered intravenously over 3 minutes. Immediately after drug administration and every 3 minutes thereafter, for a total of 30 or 40 minutes, measurements were repeated. Three hours later, patients were asked to state whether the sedative affected their state of comfort/relaxation. The effects of both doses of midazolam on HVPG did not differ significantly from those of placebo. Furthermore, neither dose of midazolam induced significant changes in HVPG as compared with baseline values. However, higher-dose midazolam (0.03 mg/kg) was associated with significant reductions in FHVP from baseline and a tendency for a reduction in WHVP. Both doses significantly increased patient comfort and relaxation during the test. Midazolam, used at a dose of 0.02 mg/kg, is effective in increasing patient comfort and relaxation during hepatic venous pressure measurements, without significantly affecting pressures (HVPG, WHVP, or FHVP). It is therefore an acceptable option for patients undergoing serial hepatic venous pressure measurements.     

Effect and mechanism of action of isosorbide-5-mononitrate.

Nitrates have been shown to decrease portal pressure in cirrhotic patients with portal hypertension and this has been attributed to decreased portal venous resistance. We studied the effect and mechanism of action of oral administration of isosorbide-5-mononitrate (Is-5-Mn) (20 mg), which, unlike the dinitrate, does not require hepatic biotransformation to a vasoactive metabolite on portal and systemic haemodynamics in 11 patients with portal hypertension complicating cirrhosis. A significant reduction in portal pressure gradient (WHVP-FHVP) (from 23.9 (3.4) to 21.8 (3.4) mmHg: p less than 0.005) occurred 60 minutes after Is-5-Mn due entirely to a fall in WHVP, associated with decreased estimated liver blood flow (from 1940 (159) to 1639 (179) ml/min: p less than 0.05). Right atrial and pulmonary artery pressures and cardiac index fell significantly whilst mean arterial pressure remained unaffected. Heart rate and the calculated systemic vascular resistance index increased significantly. Significant correlations existed between the reduction in portal pressure gradient and fall in cardiac index (r = 0.65, p less than 0.05) and increase in systemic vascular resistance index (r = 0.72, p less than 0.02). The observed decrease in estimated liver blood flow, in association with an increase in systemic vascular resistance index, suggests that baroreceptor mediated splanchnic vasoconstriction may be one of the factors responsible for the fall in portal pressure, rather than portal venous dilatation.     

Presinusoidal portal hypertension in non-alcoholic cirrhosis

The simultaneous measurement of wedged hepatic vein pressure (WHVP) and portal vein pressure (PVP) was performed in 156 cirrhotic patients. In the 110 alcoholic cirrhotic patients (97 micronodular and 13 macronodular cirrhosis), WHVP and PVP were closely related (25.8 +/- 6.3 vs. 25.9 +/- 6.3 mm Hg; p = not statistically significant). The difference between the two parameters was greater than 4 mm Hg in only six patients. In the 46 patients with nonalcoholic cirrhosis (41 macronodular and 1 micronodular cirrhosis; 4 primary biliary cirrhosis), PVP was significantly higher than was WHVP (25.8 +/- 6.2 vs. 21.7 +/- 6.8 mm Hg; p less than 0.001); in 20 patients, PVP exceeded WHVP by more than 4 mm Hg, and the mean difference was 7.5 mm Hg. There was no correlation between the porto-hepatic gradient and total hepatic blood flow measured by the indocyanine green single injection method or the portal fraction of total hepatic blood flow measured by indicator dilution curves. It is concluded that: (i) measurement of WHVP in alcoholic cirrhosis provides a reliable estimate of the severity of the portal hypertension, and (ii) hemodynamic evaluation of nonalcoholic cirrhosis should include PVP measurement in order to avoid underestimation of the porto-hepatic gradient.     

Wedged Hepatic Venous Pressure Does Not Reflect Portal Pressure in Patients with Cirrhosis and Hepatic Veno–Venous Communications

Some cirrhotic patients have hepatic veno–venous communications (HVVC) and large porto-systemic collaterals. However, the relationship between wedged hepatic vein pressure (WHVP) and portal vein pressure (PVP) in such patients is not clear. The aim of this study was to determine the relationships between simultaneously measured WHVP and PVP, and occluded hepatic and splenic portal venography in 100 cirrhotic patients (40 alcoholic and 60 hepatitis C virus (HCV)-related cirrhosis). PVP and WHVP were closely related in both groups (alcoholic-cirrhosis: 27.8 ± 4.7 and 27.5 ± 4.8 mmHg, HCV-cirrhosis: 27.3 ± 3.7 and 26.2 ± 4.4 mmHg, respectively). Occluded hepatic venography revealed that 13 of the 100 patients had HVVC (alcoholic-cirrhosis: 4, HCV-cirrhosis: 9). In patients with HVVC, PVP (27.9 ± 3.0 mmHg) was significantly higher than WHVP (21.9 ± 3.3 mmHg, P < 0.001). Large porto-systemic collaterals did not affect the relationship. We conclude that HVVC affects the relationship between PVP and WHVP. When WHVP is measured, occluded hepatic venography should be examined to detect HVVC.     

Comparison between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis

Portal vein pressure and wedged hepatic vein pressure were measured simultaneously in 21 patients with hepatitis B-related cirrhosis of the liver and were compared to pressure measured in six patients with idiopathic portal hypertension. No significant difference in the portal venous pressure gradient was found between patients with cirrhosis and those with idiopathic portal hypertension (17.3 +/- 4.3 mmHg (mean +/- S.D.) vs. 19.7 +/- 3.1 mmHg, P greater than 0.05). However, the difference between the portal and the hepatic venous pressure gradient was significantly smaller in patients with cirrhosis than in idiopathic portal hypertension patients (1.3 +/- 1.7 vs. 10.8 +/- 2.1 mmHg, P less than 0.001). An excellent correlation was found between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis (r = 0.94, P less than 0.001). There was no linear relationship between the portal venous pressure gradient and varix size or bleeding episodes. We concluded that a close agreement existed between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related liver cirrhosis. Therefore, measurement of wedged hepatic vein pressure reliably reflects portal vein pressure in these patients.     

Portohepatic Gradient and Portal Hemodynamics in Patients with Cirrhosis Due to Hepatitis C Virus Infection

We evaluated the agreement between wedgedhepatic vein pressure (WHVP), portal vein pressure(PVP), and its relationship with portal hemodynamics in21 patients with HCVrelated cirrhosis with esophageal varices. Direct measurements of theportohepatic gradient (HVPG) were obtained byultrasound-guided fine needle puncture of the righthepatic and the portal veins. In five cases PVP was6.4-10.4 mm Hg higher than WHVP. In 12 cases measurements weresimilar (WHVP-PVP 3 mm Hg). In the remaining fourcases WHVP was 3.6-9.6 mm Hg higher than PVP. WHVP andPVP agreement was not related to HVPG mean value,Child-Pugh score, or grading of esophageal varices. Bycontrast, the difference between WHVP and PVP wasinversely related to the portal flow velocity (P =0.053) and directly related to the portal vascularresistance (P = 0.02). Whereas the portal branches werevisualized in patients with WHVP lower or similar toPVP, a predominant left portosystemic collateral flowwas observed in patients with WHVP > PVP. Our data point out that, in patients with cirrhosis dueto hepatitis C virus infection, discrepant HVPG valuesreflect true hemodynamic differences.     

Low doses of isosorbide mononitrate attenuate the postprandial increase in portal pressure in patients with cirrhosis

Postprandial hyperemia is associated with a significant increase in portal pressure in cirrhosis, which may contribute to progressive dilation and rupture of gastroesophageal varices. In cirrhosis, an insufficient hepatic production of nitric oxide (NO) may impair the expected hepatic vasodilatory response to increased blood flow, further exaggerating the postprandial increase in portal pressure. This study was aimed at investigating whether low doses of an oral NO donor might counteract the postprandial peak in portal pressure. Twenty-three portal hypertensive cirrhotics, 8 of them under propranolol therapy, were randomized to receive orally 5-isosorbide mononitrate (ISMN; 10 mg; n = 11) or placebo (n = 12) and a standard liquid meal 15 minutes later. Hepatic venous pressure gradient (HVPG), mean arterial pressure (MAP), and hepatic blood flow (HBF) were measured at baseline and 15, 30, and 45 minutes after a meal. ISMN significantly attenuated the postprandial increase in portal pressure as compared with placebo (peak HVPG increase: 2.4 +/- 1.4 mm Hg vs. 5.2 +/- 2.1 mm Hg, P =.002). Percentual increases in HBF were similar in both groups. MAP decreased slightly in ISMN group (-7.5% +/-.5%; P <.01 vs. baseline). These effects were also observed in patients on chronic propranolol therapy. In conclusion, hepatic NO supplementation by low doses of ISMN effectively reduces the postprandial increase of portal pressure in cirrhosis, with only a mild effect on arterial pressure. The same was observed in patients receiving propranolol. Our results suggest that therapeutic strategies based on selective hepatic NO delivery may improve the treatment of portal hypertension.     

门静脉高压患者门静脉压力与血流动力学的相关性研究

目的 探讨门静脉高压患者门静脉血流动力学的变化特点及其与门静脉压力的相互关系。方法 采用彩色多普勒超声对４１例肝硬化门静脉高压患者（Ｃｈｉｌｄ Ａ、Ｂ级３１例、Ｃ级１０例）于手术前检测门静脉（ＰＶ）、脾静脉（ＳＶ）和肠系膜上静脉（ＳＭＶ）的内径和血流速度，再计算出相关的面积和血流量；于手术时对３１例ＣｈｉｌｄＡ十Ｂ级患者直接测量门静脉压力。３２例健康人和２６例慢性乙型肝炎患者（慢肝组）作为对照。结累 门静脉高压两组患者ＰＶ、ＳＶ和ＳＭＶ内径（ｃｍ）分别为１．５１和１．５２、１．３２和１．３４及１．１５和１．１５较慢肝组和正常组明显增宽，ｒ分别为１．３１和１．１６、０．９６和０．７９及０．９１和０．８２（Ｐ＜０．０１）；血流速度较正常组和慢肝组明显减慢（Ｐ＜０．０１）；门静脉高压Ｃ级组门静脉血流速度（ｃｍ／ｓ）为４．６５较门静脉高压Ａ十Ｂ级组（６．４２）明显减慢（Ｐ＜０．０１），而两组 ＳＶ和 ＳＭＶ的血流速度则差异无显著意义（Ｐ＞０．０５）；门静脉高压 Ａ＋Ｂ级组三条静脉的血流量明显大于正常组和慢肝组（Ｐ＜０．０１或Ｐ＜０．０５）；门静脉高压Ｃ级组门静脉血流量明显小于Ａ十Ｂ级组（Ｐ＜０．０１）；而ＳＶ和ＳＭＶ的血流     

Comparison of portal pressure with intravascular esophageal variceal pressure (IEVP) directly measured with a flexible indwelling needle

Intravascular esophageal variceal pressure (IEVP) was measured using a flexible indwelling needle and compared with wedged hepatic venous pressure (WHVP) in 38 patients with liver cirrhosis. There was a high correlation between IEVP and WHVP; the former was lower than the latter, indicating the presence of a pressure gradient. Bleeders with a history of esophageal variceal rupture showed higher IEVP value than non-bleeders without a history of rupture, even though no difference in WHVP was observed. IEVP in the post-endoscopic injection sclerotherapy (EIS) group, even in those with endoscopic findings of large varices, was lower than that in the untreated groups. These results suggest that IEVP is a factor in the hemodynamics of patients with portal hypertension and that its measurement may be helpful in elucidating the pathophysiology of esophageal varices.     

Discrepancy between wedged hepatic venous pressure and portal venous pressure after acute propranolol administration in patients with alcoholic cirrhosis

In patients with alcoholic cirrhosis, wedged hepatic venous pressure closely reflects portal venous pressure. This study was carried out to determine if propranolol-induced reductions in portal venous pressure are accurately evaluated by the measurement of wedged hepatic venous pressure. Hepatic venous cannulation and percutaneous transhepatic catheterization of the portal vein were simultaneously performed in 7 patients with alcoholic cirrhosis. One hour after oral administration of 40 mg of propranolol, wedged hepatic and portal venous pressures significantly decreased from 24.3 +/- 3.5 (mean +/- SD) to 19.0 +/- 3.0 mmHg, and from 24.7 +/- 3.9 to 22.4 +/- 3.6 mmHg, respectively. Although no significant difference was found between baseline wedged hepatic and portal venous pressures, a significant difference was found between these pressures after propranolol administration. We concluded that during acute administration of a drug acting on the splanchnic circulation, the measurement of wedged hepatic venous pressure may not provide a reliable estimation of the magnitude of the changes in portal venous pressure. There is, however, no evidence that the direction of the changes might not be adequately assessed by wedged hepatic venous pressure measurement.     

Effects of vaso-active agents on hepatic function and blood gases in patients with cirrhosis: A study of vasopressin and nitroglycerin

The effects of vaso-active agents on hepatic function and splanchnic oxygenation were studied in 17 patients with cirrhosis and portal hypertension. Eight patients received vasopressin (0.3 iu/min) and nine patients received nitroglycerin (50 micrograms/min). Both drugs caused a significant reduction in the portal venous pressure gradient. Vasopressin infusion significantly decreased intrinsic clearance of indocyanine green (-23%, P less than 0.01). This may be due to a decreased hepatic perfusion (-28%, P less than 0.01) and portal venous oxygenation (-15% in portal venous oxygen tension, P less than 0.05). In contrast, no changes in hepatic perfusion and portal venous oxygenation were observed after nitroglycerin infusion. Nitroglycerin did not decrease intrinsic clearance of indocyanine green. These results suggest that vasodilators, rather than vasoconstrictors, might be welcome in the treatment of patients with cirrhosis and portal hypertension.     

Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis

Hepatic venous catheterization is widely used to assess portal pressure. However, it remains unclear whether wedged hepatic venous pressure is a close indicator of portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis. To address this issue, we analyzed the data from our previous published studies. Forty patients with nonalcoholic cirrhosis (HBV infection in five, HCV infection in 28, and cryptogenic in seven) were available in this analysis. A vasoconstrictor (N=14), vasodilator (N=10), or combination (N=16) was administered. The agreement of the changes between portal and wedged hepatic venous pressures during pharmacological manipulation was assessed by an intraclass correlation coefficient. The intraclass correlation coefficient in each subgroup was more than 0.60 (0.62 in vasoconstrictor group, 0.87 in vasodilator group, and 0.73 in combination group). When the analysis was performed according to the cause of liver disease, the values were 0.67 in HBV infection, 0.73 in HCV infection, and 0.74 in cryptogenic cirrhosis. These results suggest that wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in patients with nonalcoholic cirrhosis.