Ultrasonographic splanchnic arterial flow measurement in severe acute pancreatitis

INTRODUCTION: Duplex ultrasonographic technology is now capable of detecting flow signals in the various splanchnic vessels and calculating the concomitant flow velocities using fast-Fourier transformation. AIM: To use Doppler sonography to investigate how splanchnic hemodynamics vary during the early stage of severe acute pancreatitis. METHODOLOGY: Six patients with severe acute pancreatitis (age, 59.0 +/- 6.57 years; four men, two women) and seven with mild to moderate acute pancreatitis (age, 60.1 +/- 7.41 years; five men, two women) were examined with Doppler sonography immediately after disease onset. The maximum velocity, minimum velocity, mean velocity, pulsatility index, and resistive index were determined from the Doppler spectra from the proper hepatic artery, celiac artery, and superior mesenteric artery. We also examined 15 healthy subjects (age, 59.3 +/- 4.60 years; 10 men, five women) as controls. RESULTS: The maximum velocity of the proper hepatic artery in patients with severe acute pancreatitis was significantly higher than that in patients with mild to moderate acute pancreatitis (p = 0.011) and in control subjects (p = 0.0047). Similarly, significant increases in both the minimum velocity and the mean velocity of the proper hepatic artery were observed in patients with severe acute pancreatitis. Neither pulsatility index nor resistive index of the proper hepatic artery showed a significant difference among the three groups. There were no significant differences among the three groups with respect to the flow velocity of the superior mesenteric artery. In contrast, the pulsatility index of the superior mesenteric artery in patients with severe acute pancreatitis was significantly lower than that in patients with mild to moderate acute pancreatitis (p = 0.0058) or in control subjects (p = 0.0024). For patients with acute pancreatitis, a significant inverse correlation was obtained between the maximum velocity of the proper hepatic artery and the pulsatility index of the superior mesenteric artery (r = -0.658, p = 0.0145). CONCLUSION: The increase in the hepatic arterial flow velocity and the decrease in the superior mesenteric arterial pulsatility index may represent early events of the severe type of acute pancreatitis.     

Hepatic arterial pulsatility index in cirrhosis: correlation with portal pressure.

BACKGROUND/AIMS: Determination of the pulsatility index by means of duplex sonography provides the opportunity to evaluate the vascular resistance of the hepatic artery noninvasively. The aim of this study was to investigate the relationship between the hepatic arterial pulsatility index and the hepatic venous pressure gradient in cirrhosis. METHODS: In 50 patients with cirrhosis, hepatic venous pressure gradient was determined in the fasting state. Immediately thereafter, hepatic arterial pulsatility index and portal blood flow velocity were measured by duplex sonography with no knowledge of hepatic venous pressure values. In addition, the duplex parameters were determined in 20 controls. RESULTS: Hepatic arterial pulsatility index was significantly higher in patients with cirrhosis than in controls (0.92+/-0.1 vs. 1.14+/-0.18; p<0.001) and directly correlated with the hepatic venous pressure gradient (r = 0.7; p<0.001). Furthermore, weak correlations were found between hepatic arterial pulsatility index and Child-Pugh score (r = 0.49; p<0.01) and between portal blood flow velocity and hepatic venous pressure gradient (r = -0.48; p<0.01). CONCLUSION: In cirrhosis the hepatic arterial vascular resistance seems to increase parallel to the rise of the portal pressure. Therefore, duplex sonographic determination of the hepatic arterial pulsatility index may contribute to the noninvasive evaluation of portal hypertension.     

Effect of secretin on portal venous flow.

In this study we evaluated the effect of two different doses of secretin on portal haemodynamics (by pulsed Doppler associated with real time ultrasound) in 24 healthy humans. In 12 subjects (group A) we administered an intravenous dose of 75 clinical units of secretin and in the remaining 12 (group B) a dose of 20 CU. In all subjects the following parameters were studied before, during, and for 10 minutes after secretin administration: (a) calibre of the portal vein, (b) mean velocity of portal venous flow, and (c) volume of portal venous flow. In three subjects in each group we also evaluated the changes in flow in the superior mesenteric artery. Secretin injection induced a slight increase in both groups in comparison to basal values of portal vein calibre (mean of maximal per cent increase +25% in group A, not significant, and +16.7% in group B, not significant) and a noticeable increase of mean velocity (mean of maximal per cent increases +61.4% in group A, p less than 0.005, and +65.4% in group B, p less than 0.01) and flow volume (mean of maximal per cent increase +127% group A, p less than 0.005, and +114% group B, p less than 0.005). The magnitude of the haemodynamic changes did not differ significantly between the two groups. Doppler investigation of the superior mesenteric artery showed a marked increase of flow velocity (mean of maximal per cent increase +218% in group A and +246% in group B) and flow volume (mean of maximal per cent increase +276% in group A and +311% in group B). These data suggest that secretin has an appreciable vasoactive effect and induces a significant increase in portal venous flow even at doses much lower than those necessary for a maximal stimulation of exocrine pancreatic secretion.     

Effects of terlipressin on systemic, hepatic and renal hemodynamics in patients with cirrhosis

Background and Aim: Terlipressin has been shown to be effective in the management of hepatorenal syndrome. However, how terlipressin exerts its effect on the renal artery is unknown. The aim of the present study was to assess the effects of terlipressin on systemic, hepatic and renal hemodynamics in cirrhosis. Methods: Twenty‐eight patients with cirrhosis and portal hypertension were studied. Systemic and hepatic hemodynamics, hepatic and renal arterial resistive indices and neurohumoral factors were measured prior to and 30 min after intravenous administration of 1 mg terlipressin (n = 19) or placebo (n = 9). Results: After terlipressin, there were significant increases in both mean arterial pressure (P < 0.001) and systemic vascular resistance (P < 0.001), whereas heart rate (P < 0.001) and cardiac output (P < 0.001) decreased significantly. There was a significant decrease in the hepatic venous pressure gradient (P < 0.001). Portal venous blood flow also decreased significantly (P < 0.001). The mean hepatic arterial velocity increased significantly (P < 0.001). Although there was a significant decrease in the hepatic arterial resistive index (0.72 ± 0.08 to 0.69 ± 0.08, P < 0.001) and renal arterial resistive index (0.74 ± 0.07 to 0.68 ± 0.07, P < 0.001), portal vascular resistance was unchanged (P = 0.231). Plasma renin activity decreased significantly (P < 0.005), and there was a significant correlation between this decline and the decrease in renal arterial resistive index (r = 0.764, P < 0.005). The effects of terlipressin on systemic, hepatic and renal hemodynamics were observed similarly in patients with and without ascites. Placebo caused no significant effects. Conclusion: Terlipressin decreases hepatic and renal arterial resistance in patients with cirrhosis.     

Effects of glypressin on the splanchnic and systemic circulation in patients with cirrhosis

Although not demonstrated in patients with cirrhosis, it is generally claimed that administration of vasopressin in the form of triglycyl-lysine-vasopressin (glypressin) may prevent untoward systemic effects of this former hormone. The aim of this study was to assess the effects of intravenous administration of 2 mg of glypressin on splanchnic and systemic hemodynamics in 9 patients with cirrhosis under stable circulatory conditions. One hour after the injection, the following statistically significant changes were observed as compared to the baseline values (m +/- SEM): wedged hepatic venous pressure, -9 +/- 2 p. 100; hepatic venous pressure gradient, -16 +/- 3 p. 100; azygos blood flow, -24 +/- 6 p. 100; heart rate, -16 +/- 3 p. 100; cardiac index, -23 +/- 2 p. 100; systemic vascular resistances, +47 +/- 11 p. 100; wedged pulmonary arterial pressure, +44 +/- 15 p. 100. In conclusion, in patients with cirrhosis in a stable hemodynamic condition, intravenous administration of glypressin decreased portal venous pressure and blood flow into the superior portal systemic collateral circulation but did not prevent the untoward systemic hemodynamic effects of vasopressin.     

Octreotide inhibits the meal-induced increases in the portal venous pressure of cirrhotic patients with portal hypertension: a double-blind, placebo-controlled study.

The aim of this study was to determine the effects of the long-acting somatostatin analog, octreotide, on portal venous pressure and collateral blood flow in cirrhotic patients with portal hypertension during fasting and postprandial states. In a double-blind, placebo-controlled study, we investigated the effects of octreotide on the hepatic venous pressures and azygos blood flow of 21 patients before and after a standard liquid meal containing 40 gm of protein in 250 ml. Octreotide significantly reduced azygos blood flow from a mean of 499 +/- 65 ml/min to a mean of 355 +/- 47 ml/min (p < 0.01), but it had no effect on the hepatic venous pressure gradient. The hepatic venous pressure gradient of patients in the placebo group increased significantly, from a fasting mean of 16.4 +/- 1.6 mm Hg to a mean of 20.0 +/- 1.7 mm Hg 30 min after the meal (p < 0.01). In a second protocol hepatic venous pressures were measured in 20 patients at 30-min intervals for 2 hr after ingestion of the mixed meal. Again the placebo group showed a significant increase in the hepatic venous pressure gradient 30 min after the meal (20.4 +/- 1.5 mm Hg vs. 18.2 +/- 1.2 mm Hg; p < 0.05), but the group receiving octreotide showed no significant changes during the 2 hr of observation. We conclude that octreotide significantly reduces azygos blood flow, with little effect on portal venous pressure, and that it appears to inhibit postprandial increases in portal pressure in cirrhotic patients with portal hypertension.     

Combination of ketanserin and verapamil or propranolol in patients with alcoholic cirrhosis: search for an additive effect

Drugs reported to reduce portal pressure through different mechanisms were combined in the hope of either additive portal hypotensive effects in "responders," or inducing a portal hypotensive effect in "nonresponders" to the initial drug. Seven patients with alcoholic cirrhosis received verapamil, 10 mg i.v., and, 60 min later, ketanserin, 5 mg i.v. Verapamil decreased heart rate and increased free hepatic venous pressure but had no effect on hepatic venous pressure gradient or azygos blood flow. When combined with verapamil, ketanserin significantly diminished wedged hepatic venous pressure and hepatic venous pressure gradient. Ten other patients with alcoholic cirrhosis received propranolol, 15 mg i.v., and 45 min later, ketanserin, 5 mg i.v. In all patients, heart rate, cardiac index and azygos blood flow significantly decreased after propranolol. After propranolol alone, however, wedged hepatic venous pressure decreased in only five patients, responders. In five other patients, defined as nonresponders, propranolol did not decrease this pressure. The addition of ketanserin to propranolol induced further significant reduction in wedged hepatic venous pressure, hepatic venous pressure gradient and azygos blood flow. Among the five nonresponders, three had a reduced wedged hepatic venous pressure after ketanserin was combined. We conclude that verapamil does not reduce portal pressure or collateral blood flow in patients with alcoholic cirrhosis. The splanchnic hemodynamic effects of propranolol and ketanserin appear to be independent and additive, without significant systemic alteration.     

Effect of propranolol on hepatic and systemic hemodynamics in dogs with chronic bile duct ligation

Propranolol has been reported to reduce portal and wedged hepatic vein pressures in man and may be useful for the prevention of variceal bleeding. However, its mechanism of action remains unclear. We have examined the effect of propranolol on the systemic and hepatic circulations in dogs with chronic bile duct ligation and secondary biliary cirrhosis. Under anesthesia, eight dogs received four increasing doses of propranolol as an i.v. bolus followed by continuous infusion. Systemic and hepatic hemodynamic parameters were measured in basal conditions and after a 30 min infusion for each dose. Portal vein and hepatic artery blood flows were measured with electromagnetic flow meters. All dogs had portal hypertension (portal venous pressure 15.3 +/- 0.8 mm Hg), a hyperdynamic circulation and severe liver disease resulting in a marked decrease of propranolol systemic clearance (8.75 ml per min per kg) and extraction (40%). The first dose of propranolol induced a decrease in heart rate (-27%) and in cardiac index (-21%), and an increase in systemic vascular resistance (+20%). With increasing doses, the systemic vascular resistance decreased with an increase in the cardiac index. Propranolol was not associated with significant modifications of hepatic hemodynamics: portal, wedged and free hepatic venous pressures and hepatic artery blood flow were stable, and portal blood flow decreased slightly at very high propranolol levels. In seven dogs studied without dissection of the hepatic vessels, there was a small decrease in portal pressure, but not in wedged and free hepatic venous pressures with increasing doses of propranolol. Thus, in dogs with intrahepatic portal hypertension, propranolol has significant effects on systemic hemodynamics, but only minimal effects on the hepatic circulation.     

The effects of arterialisation of the portal stump on liver function and hepatic haemodynamics in cirrhotic rats with a portacaval shunt

Liver blood flow (xenon-133 clearance method) and wedged hepatic venous pressure were studied in cirrhotic rats immediately after and 3 weeks following portacaval shunting (PCS), PCS and arterialisation of the portal stump with the left gastric artery (PCS-ART) or sham operation. Liver weight and function were compared 3 weeks after operation. Liver blood flow and wedged hepatic venous pressure were significantly reduced immediately after and 3 weeks following PCS. PCS-ART maintained liver blood flow and wedged hepatic venous pressure within the pre-operative range and prevented the liver atrophy and deterioration in liver function observed in rats with PCS. The results suggest that arterialisation of the portal vein with an artery which does not significantly increase sinusoidal pressure may be of benefit in preventing the early undersirable sequelae of PCS in man.     

Hepatic arterial and portal flow in cardiogenic and hemorrhagic shock in awake dogs

The changes in liver blood flow produced by experimental cardiogenic and hemorrhagic shock are relatively unexplored. Fifteen unanesthetized dogs in which electromagnetic blood flow transducers had been implanted on the common hepatic artery and portal vein were subjected to acute myocardial infarction by mercury embolization of the circumflex coronary artery. Another group of ten dogs were bled to an arterial pressure of 40 mmHg and maintained at that level for 2 hours before reinfusion. Six additional dogs in which blood flow transducers had been implanted on the superior mesenteric artery and portal vein also were subjected to hemorrhage. In three of the six, phenoxybenzamine was infused directly into the superior mesenteric artery 45 minutes prior to bleed-out. During cardiogenic shock, both hepatic arterial and protal venous flow fell. However, whereas protal flow continued to fall, eventually stabilizing at values 36 +/- 3% of control, hepatic arterial flow subsequently rose, reaching values 93 +/- 9% above control. Total liver blood flow, after an initial decline to 53 +/- 4% of control levels rose as a result of the increased hepatic arterial flow to 73 +/- 4% of control values. During hemorrhage, both hepatic arterial and protal venous flows decreased as aortic pressure fell. Within 5 minutes of reinfusion, hepatic arterial flow surpassed its control values. Portal flow also increased but, on a percentage basis, not to so great an extent. Flow in hepatic artery remained high for 40 minutes after reinfusion, whereas portal flow rapidly decreased to levels seen at the end of hemorrhage. In hemorrhage without alpha-adrenergic receptor blockade the superior mesenteric bed constricted, thereby supporting systemic pressure. With alpha-adrenergic blockade, however, mesenteric flow became pressure-dependent and no longer acted as a homeostatic mechanism.     

Portal Hemodynamic Responses after Oral Intake of Glucose in Patients with Cirrhosis

Changes of portal, superior mesenteric, and splenic venous flows, and portohepatic gradient (portal vein pressure minus free hepatic vein pressure) after a meal were studied in patients with cirrhosis using the duplex ultrasonic Doppler flowmeter, and portal and hepatic vein catheterizations after ingestion of 227 ml of 33% glucose solution (300 kcal). As a control, changes of portal venous flow and portohepatic gradient after drinking 227 ml of water, were studied. Portal and superior mesenteric venous flows increased significantly at 30 min after glucose intake, and they returned gradually to the basal values, whereas no significant postprandial change occurred in splenic venous flow. The sum of superior mesenteric and splenic venous flows was greater than the estimated portal venous flow before glucose intake, and the difference widened during post-prandial mesenteric hyperemia, indicating an increase of blood flow into the portal-systemic shunts. After glucose intake, portohepatic gradient elevated immediately, in parallel with an increase of portal venous flow, and these changes persisted for the 30 min studied; however, no significant change occurred in these parameters after drinking water. In conclusion: 1) In patients with cirrhosis, hyperemia occurs in the intestine but not in the spleen after glucose intake, and 2) postprandial mesenteric hyperemia causes an increase of portal venous inflow, portal-systemic collateral flow, portal venous flow, and an elevation of portohepatic gradient.     

Doppler ultrasonographic evaluation of splanchnic blood flow in coeliac disease.

BACKGROUND: Current knowledge on splanchnic haemodynamics in coeliac disease is limited and incomplete. AIM: To evaluate splanchnic arterial and venous blood flow in coeliac disease. METHODS: In 22 coeliac (13 untreated, nine treated) patients and in nine healthy subjects the following variables were assessed: vessel diameter and mean flow velocity in portal vein, splenic vein, superior mesenteric vein, and superior mesenteric artery. Peak systolic velocity, end diastolic velocity and pulsatility index were also determined in the superior mesenteric artery. Five patients of the untreated group were re-evaluated after nine months on a gluten free diet. RESULTS: Significant differences in haemodynamic variables between the three groups were shown only in the superior mesenteric artery. An increase in both mean flow velocity and end diastolic velocity and a reduction in pulsatility index occurred in untreated patients compared with treated patients (p < 0.002; p < 0.04; p < 0.035) and with healthy controls (p < 0.001; p < 0.025; p < 0.0003). Similar results were obtained for the five patients evaluated before and after treatment (p < 0.03; p < 0.02; p < 0.03), in whom the mean flow velocity in the superior mesenteric vein also decreased after treatment (p < 0.05). No significant differences were noted between treated coeliac patients and healthy controls. CONCLUSIONS: In untreated coeliac disease there is a hyperdynamic mesenteric circulation that decreases after treatment.     

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.     

Increased urotensin II plasma levels in patients with cirrhosis and portal hypertension

BACKGROUND/AIMS: Vasodilatation--despite activation of endogenous vasoconstrictors--is pronounced in portal hypertension. We therefore investigated the role of Urotensin II (U II), a newly described peptide reported to be a vasoconstrictor in the central arterial compartment and a vasodilator in the splanchnic vasculature. METHODS: U II immunoreactivity was measured in 50 patients with cirrhosis and in 15 healthy controls. U II levels were compared in portal venous and central venous blood of 30 patients immediately before transjugular intrahepatic porto-systemic stent shunt implantation. RESULTS: U II levels (median, range, ng/ml) were significantly increased in cirrhotics (12.3, 1.6-41.4) compared to controls (3.6, 0.1-12.0; P<0.001). In patients with cirrhosis, U II levels were significantly higher in central venous (12.9, 2.5-41.4) than in portal venous blood (11.0, 0.6-31.9; P<0.005). U II levels were higher in ascitic than in non-ascitic patients (P<0.02). They correlated positively with the wedged hepatic venous pressure gradient (rho=0.34, P<0.005) and negatively with the mean arterial pressure (rho=-0.41; P<0.001). CONCLUSIONS: Urotensin II formation is upregulated in patients with cirrhosis and portal hypertension. The transhepatic gradient suggests a hepatic production of this peptide.     

The effect of isradipine in acute altitude hypoxia on cerebral,renal, and splanchnic blood flow evaluated by Doppler measurements

Recent studies have suggested that calcium antagonists may have a beneficial effect on high altitude pulmonary edema, but the effect on regional blood flow distribution is unknown. This study by transcranial and duplex Doppler evaluated the effect of the calcium antagonist isradipine on cerebral, renal, and splanchnic blood flows in acute altitude hypoxia. Twelve healthy subjects were investigated at sea level and repeatedly after 3–56 hours at high altitude (4350 m). Before the ascent, the subjects were randomized to treatment with isradipine 5 mg/day (n=6) or placebo (n=6). We measured flow velocities in middle cerebral arteries; flow rates in internal carotid arteries, portal vein, and right renal artery; and resistance indices in middle cerebral, internal carotid, renal, superior mesenteric, and hepatic arteries. Hypoxia increased middle cerebral artery flow velocity by 30% (placebo,p<0.05) and 39% (isradipine,p<0.01); increased internal carotid artery flow rate by 57% (placebo,p<0.01) and 55% (isradipine,p<0.05); and decreased middle cerebral and internal carotid artery resistance indices without differences between placebo and isradipine groups. Superior mesenteric artery resistance index was lower in hypoxia with isradipine compared with placebo (p<0.05), suggesting a higher splanchnic blood flow. In conclusion, acute hypoxia induced an increase in cerebral blood flow. Besides decreasing superior mesenteric artery resistance index, prophylactic isradipine did not modulate the circulatory responses to acute hypoxia. The clinical significance of this increased splanchnic blood flow remains unclear.This study was supported by the Danish Society of Diagnostic Ultrasound, Denmark; B & K Medical, France; Laboratoires Sandoz, FrancePresented at the 35th Annual World Congress, International College of Angiology, Copenhagen, Denmark, July 1993     

Effects of somatostatin on hepatic and systemic hemodynamics in patients with cirrhosis of the liver: comparison with vasopressin

The effects of somatostatin on hepatic and systemic hemodynamics were investigated in 17 patients with chronic liver disease and severe portal hypertension during the hemodynamic assessment before elective portal-systemic shunt surgery. The injection of somatostatin (1.0 microgram/kg) caused a decrease of the wedged hepatic venous pressure, from 19.5 +/- SE 1.3 mmHg to 14.0 +/- 1.0 mmHg (p < 0.001). Injections of 0.5 and 2.0 microgram/kg had similar effects. During somatostatin infusion at a constant rate (7.5 microgram/min) there was a reduction of the wedged hepatic venous pressure (-17.0%, p < 0.001) and estimated hepatic blood flow (-17.5%, p < 0.01) but no significant changes in hepatic vascular resistance, cardiac output, systemic blood pressure, peripheral resistance, or cardiopulmonary pressures. In marked contrast to the selective action of somatostatin on splanchnic hemodynamics, vasopressin infusion (0.3 U/min) in 6 patients caused not only significant falls in the wedged hepatic venous pressure and estimated hepatic blood flow (-28.6% and -31.8%, respectively), but also significant changes in the systemic circulation, including a reduction of the cardiac output (-19.7%, p < 0.01) and heart rate (-12.6%, p < 0.01) and an increase of the arterial pressure (+18.8%, p < 0.01) and peripheral resistance (+46.8%, p < 0.01). These results show that somatostatin effectively reduces hepatic blood flow and portal pressure in patients with cirrhosis and severe portal hypertension, without altering the systemic circulation.     

Role of echo Doppler ultrasonography in the evaluation of postprandial hyperemia in cirrhotic patients

AIM： TO assess the role of echo-Doppler ultrasonography in postprandial hyperemia in cirrhotic patients by comparing the results with the hepatic vein catheterization technique.
METHODS： Patients with cirrhosis, admitted to the portal hemodynamic laboratory were included into the study. After an overnight fast, echo-Doppler ultrasonography （basal and 30 min after a standard meal） and hemodynamic studies by hepatic vein catheterization （basal, 15 min and 30 min after a standard meal） were performed. Ensure Plus （Abbot Laboratories, North Chicago, IL） was used as the standard liquid meal. Correlation analysis of the echo- Doppler and hepatic vein catheterization measurements were done for the basal and postprandial periods.
RESULTS： Eleven patients with cirrhosis （5 Child A, 4 Child B, 2 Child C） were enrolled into the study. After the standard meal, 8 of the 11 patients showed postprandial hyperemia with increase in portal blood flow, portal blood velocity and hepatic venous pressure gradient. Hepatic venous pressure gradient in the postprandial period correlated positively with postprandial portal blood velocity （r = 0.8, P 〈 0.05） and correlated inversely with postprandial superior mesenteric artery pulsatility index （r = -1, P 〈 0.01）.
CONCLUSION： Postprandial hyperemia can be efficiently measured by echo-Doppler ultrasonography and the results are comparable to those obtained with the hemodynamic studies.     

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.     

Nitroglycerin improves the hemodynamic response to vasopressin in portal hypertension

This study was designed to investigate whether the addition of nitroglycerin to vasopressin infusion could avoid the deleterious systemic effects of vasopressin while maintaining or enhancing the therapeutic benefits of portal pressure reduction. The effect of nitroglycerin on splanchnic and systemic hemodynamics was studied in cirrhotic patients and portal hypertensive dogs receiving i.v. vasopressin. During i.v vasopressin infusion (0.4 units per min), the cardiac output decreased in patients by 14% from 7.6 +/- 0.9 (mean +/- S.E.) to 6.5 +/- 0.7 liters per min, p less than 0.01, the mean arterial pressure increased 21% from 87 +/- 2 to 105 +/- 4, p less than 0.01, and the heart rate decreased 11% from 79 +/- 3 to 71 +/- 3, p less than 0.01. The administration of sublingual nitroglycerin (0.4 mg) returned all the systemic hemodynamic parameters to baseline values. In dogs, vasopressin infusion significantly reduced portal pressure and flow while increasing portal venous resistance. Nitroglycerin when added to the vasopressin infusion reduced portal venous resistance and further decreased portal pressure in dogs. In patients, vasopressin reduced the hepatic blood flow (44%), wedged hepatic venous pressure (11%), and the gradient between wedged and free hepatic venous pressures (23%). Nitroglycerin administration caused a further reduction of the wedged hepatic venous pressure (23.6 +/- 2.3 to 21.1 +/- 2.0, 11%, p less than 0.01). There was a small but not significant further decline (7%) in the hepatic venous pressure gradient. These results provide evidence that the addition of nitroglycerin to an i.v. infusion of vasopressin reversed the detrimental effects of vasopressin while preserving the beneficial effects.     

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.