Changes In Hepatic Hemodynamics Research Articles

Effects of a somatostatin analogue SMS 201-995 on hepatic haemodynamics in the pig and on intravariceal pressure in man.

The effects of a somatostatin analogue, SMS 201-995, on hepatic haemodynamics in the pig and on intravariceal pressure in man were studied. An infusion of 250 micrograms/h SMS 201-995 significantly reduced portal pressure, portal venous flow and hepatic artery flow in the pig. These changes in hepatic haemodynamics were accompanied by a reduction in cardiac output, a reflex slowing of the heart and an increase in arterial blood pressure. Splanchnic vascular resistance was increased following SMS 201-995 administration but hepatic vascular resistance remained unchanged. Administration of 50 micrograms SMS 201-995 reduced the intravariceal pressure from 27.4 +/- 2.5 to 15.8 +/- 2.1 mmHg in 9 patients with cirrhosis and portal hypertension. Administration of 50 micrograms SMS 201-995 also reduced portal pressure from 29 to 22 mmHg in a patient undergoing an elective portacaval shunt. These results suggest that SMS 201-995 may be of value in the control of bleeding oesophageal varices. Furthermore, because of its prolonged duration of action SMS 201-995 may be useful in the long term management of portal hypertension in patients with cirrhosis.

Hepatic outflow obstruction created by balloon occlusion of the hepatic vein: induced hepatic hemodynamic changes and the therapeutic applications of hepatic venous occlusion with a balloon catheter in interventional radiology.

Hepatic outflow obstruction created by balloon occlusion of the hepatic vein induces characteristic angiographic findings in the occluded area: prolonged enhancement on hepatogram followed by reversed portal opacification on the hepatic arteriogram and perfusion defect on the arterial portogram. The following induced hepatic hemodynamic changes are suggested: hepatic arterial flow increases, and the portal vein acts as a draining vein with slow reversed flow. These unique hemodynamic changes enhance the effect of hepatic interventional therapies. In transcatheter arterial infusion, increasing hepatic arterial flow and absence of portal inflow can bring about a high concentration of drugs, the presence of which is greatly protracted due to outflow blockage. In transcatheter arterial chemoembolization, reversed portal flow can allow portal embolization in addition to arterial embolization. In microwave coagulation therapy and radiofrequency ablation therapy, decreasing portal flow can cause larger areas of coagulation. Further, the technique of hepatic venous occlusion has potential therapeutic applications.

Investigation of Liver Parenchymal Flow Using Contrast‐Enhanced Ultrasound in Patients With Alcoholic Liver Disease

Background: Peripheral hepatic blood flow has not been investigated using contrast‐enhanced ultrasound. The aim of this study was to assess the characteristics of peripheral blood flow within the liver parenchyma using Levovist in patients with alcoholic liver disease (ALD).Methods: The study population comprised 160 patients: 7 normal control subjects (NC), 89 with chronic viral hepatitis (CVH), 8 with alcoholic liver injury (ALI), 18 with viral liver cirrhosis without portosystemic shunting (VLCwoPSS) plus 11 with PSS (VLCwPSS), and 12 with alcoholic liver cirrhosis without PSS (ALCwoPSS) plus 15 with PSS (ALCwPSS). First, continuous spectral Doppler ultrasound was performed to assess peripheral blood flow within the liver parenchyma. We defined the arrival time (AT) as the time when signals began to increase in the region of interest after the injection of Levovist, whereas the peak time (PT) was the time between the AT and the maximum signal. Second, stimulated acoustic emission imaging was compared between the liver parenchyma and the right kidney at 20 sec, 90 sec, and 5 min after injection of Levovist.Results: The average AT was as follows: NC, 18.4 sec; CVH, 18.7 sec; ALI, 15.5 sec; VLCwoPSS, 18.2 sec; VLCwPSS, 12.5 sec; ALCwoPSS, 13.5 sec; and ALCwPSS, 12.7 sec. In patients with ALI and cirrhosis (excluding VLCwoPSS), the AT was earlier than in NC and CVH. The average PT was as follows: NC, 18.3 sec; CVH, 19.4 sec; ALI, 20.3 sec; VLCwoPSS, 19.3 sec; VLCwPSS, 9.0 sec; ALCwoPSS, 10.7 sec; and ALCwPSS, 4.9 sec. In patients with cirrhosis (excluding VLCwoPSS), the PT was earlier than in the other groups. As PSS developed, the PT of ALC became much earlier. In NC, the stimulated acoustic emission study showed no enhancement of the liver parenchyma at 20 sec. However, most of the patients with ALD showed marked enhancement of the liver at 20 sec. It is interesting that only slight enhancement of the liver was seen in ALCwPSS, although NC showed marked liver enhancement at 5 min.Conclusions: Our results suggest that ALD is accompanied by regional hepatic and systemic hemodynamic changes, such as hyperdynamic circulation and arterialization of the liver, before progression to cirrhosis.

Hepatic arterioportal shunts: dynamic CT and MR features.

With the increased temporal resolution available in dynamic computed tomography (CT) and magnetic resonance imaging (MRI), hepatic arterioportal shunts are now more frequently encountered than in the past. The condition occurs in various hepatic diseases in which portal or hepatic venous flow is compromised. The underlying mechanism and the degree of shunt affect its appearance at dynamic imaging. The dynamic CT and MRI findings have been summarized as early enhancement of peripheral portal veins, and wedge-shaped transient parenchymal enhancement during the hepatic arterial phase. Recognition of arterioportal shunt can suggest the presence of a previously unsuspected disorder and avoids false-positive diagnosis or overestimation of a hepatic disease. Familiarity with the pathophysiology of arterioportal shunt also allows investigation of the hepatic hemodynamic changes occurring in various hepatic diseases.

Outcome and Hepatic Hemodynamics in Liver Transplant Patients with Portal Vein Arterialization

Few cases of successful portal vein arterialization in orthotopic and auxiliary liver transplantation have been reported.Aim: To evaluate the effect of portal vein arterialization on hepatic hemodynamics and long-term clinical outcome in three patients undergoing liver transplantation.Methods: Two patients with extensive splanchnic venous thrombosis received an orthotopic liver transplant and one with fulminant hepatic failure received an auxiliary heterotopic graft. Portal vein arterialization was performed in all cases.Results: One patient died 4 months after transplant and two are still alive. Auxiliary liver graft was removed 3 months post-transplant when complete native liver regeneration was achieved. Immediate post-transplant liver function was excellent in all cases. Only one patient developed encephalopathy and variceal bleeding owing to prehepatic portal hypertension secondary to arterioportal fistula 14 months after transplant. He was successfully treated by embolization of the hepatic artery. Hepatic hemodynamic measurements demonstrated a normal pressure gradient between wedged and free hepatic venous pressures in all cases. Liver biopsy showed acceptable graft architecture in two cases and microsteatosis in one.Conclusions: Liver transplantation with portal vein arterialization is an acceptable salvage alternative when insufficient portal venous flow to the graft is present. The double arterial supply does not imply changes in hepatic hemodynamics, at least in the early months post-transplant.

Changes in hepatic hemodynamics after orthotopic liver transplantation: color Doppler sonography.

Liver perfusion has an influence on therapy results in patients undergoing orthotopic liver transplantation (OLT). The objective of the present study was to investigate changes in hepatic hemodynamics in patients after OLT with color-coded Doppler sonography (CCDS). Forty-five consecutive patients were included. The examinations were done before, on postoperative day 1, and then weekly until the patients were discharged. Mean velocity of the portal (PV-V) and splenic (SV-V) veins and the maximum velocity and resistance index of the hepatic artery were determined. After OLT a significant increase in PV-V and SV-V was observed. Twenty-five patients had normal perfusion of the hepatic artery, whereas 16 patients had abnormal flow patterns. In these patients prostaglandin I(2) was used until flow rates normalized. In four patients, CCDS could not detect perfusion of the hepatic artery. CCDS is a suitable method for evaluating hepatic hemodynamics before and after OLT. Changes in blood flow velocities in the liver-supplying vessels are detectable, but perfusion of the hepatic artery is seldom detectable. These observations are of special interest after OLT, where liver circulation has an influence on therapy results.

Changes in hepatic hemodynamics after orthotopic liver transplantation: color Doppler sonography.

Changes in hepatic hemodynamics after orthotopic liver transplantation: color Doppler sonography.

Changes in prostaglandin and nitric oxide levels in the hyperdynamic circulation following liver resection.

Significant changes in hepatic haemodynamics occur after major hepatectomy, but the pathogenesis of this phenomenon is unclear. This study investigates the serum profile of prostaglandin and nitric oxide in the hepatic and systemic circulation before and after hepatectomy and the temporal relationship of these to changes in the hepatic blood flow. Blood samples were collected from the internal jugular, portal and hepatic veins of six Yorkshire pigs (17-25 kg) before, immediately after and 48 h after partial hepatectomy. Serum levels of prostacyclin I2 (PGI2) and prostaglandin E2 (PGE2) from the systemic circulation, the portal circulation and from the hepatic veins were found to differ considerably even before hepatectomy. After the hepatectomy was performed, there was a significant rise in PGI2 levels in the systemic circulation (P=0.027). Hepatic blood flow and cardiac output were measured before hepatectomy, 24 and 48 h after hepatectomy in another six pigs. A significant increase in hepatic blood flow (P=0.029) occurred after the hepatectomy and this was accompanied by a concomitant increase in the cardiac output (P=0.042). The increase in PGI2 concentration in the systemic circulation after hepatectomy appears to accompany the development of hyperdynamic hepatic and systemic circulations. No significant change was found in circulating PGE2 levels in the systemic, portal and hepatic veins at the three collection intervals (i.e. pre, post and 48 h after hepatectomy). The PGE2 levels in the hepatic vein, however, were significantly higher from than in the portal vein (P=0.028). No significant changes were observed in the level of nitric oxide. This study demonstrates an increase in the total hepatic blood flow after hepatectomy together with a threefold increase in prostacyclin in the systemic circulation. The liver was identified as the main source of circulatory prostaglandin.

A non-invasive isotope dilution technique for quantifying hepatic blood flow using radiolabelled red blood cells.

Clinically significant changes in hepatic haemodynamics accompany the development of portal hypertension, hepatocellular carcinoma, liver metastases and liver cirrhoses, and after major liver resection. Hepatic blood flow parameters, such as hepatic arterial flow (HAF), hepatic portal flow (HPF), total hepatic blood flow (THBF) and hepatic perfusion index (HPI), are useful adjuncts to the diagnosis of liver pathology, the evaluation of disease progress and prognostication. Here, we describe a non-invasive method that combines the measurement of these parameters in a single study in real time. Red blood cells from eight pigs were labelled with 99Tc(m) using an in-vitro method and re-injected into the pigs. Data acquisition over the heart, lungs, liver and kidneys was started immediately and a blood sample was obtained 15 min post-injection. Hepatic arterial flow was determined from the ratio of the maximum gradients between the integrated time-activity curve of the left ventricle and the first-pass time-activity curve of the liver before the peak of the kidneys time-activity curve. The hepatic perfusion index was determined by comparing the slope of the liver time-activity curve before and after the kidney peak. Hepatic portal flow was determined from the hepatic arterial flow and the hepatic perfusion index, and total hepatic blood flow was determined as the sum of arterial and portal flow. The results were compared against those obtained from a clearance method using 99Tc(m)-DISIDA. The average hepatic perfusion index was 0.38, and the average hepatic arterial flow and hepatic portal flow were 168.3 +/- 52.9 and 274.6 +/- 60.1 ml x min(-1) respectively. The average total hepatic blood flow was 442.8 +/- 53.5 ml x min(-1), while the total hepatic flow determined by 99Tc(m)-DISIDA clearance was 419.7 +/- 62.6 ml x min(-1). No significant difference in total hepatic blood flow was found between the two methods. The results of this study show that it is possible to obtain all hepatic haemodynamics data in a single study using a non-invasive method.

Paracentesis-induced circulatory dysfunction: Mechanism and effect on hepatic hemodynamics in cirrhosis

BACKGROUND & AIMS: Therapeutic paracentesis may be associated with a circulatory dysfunction, manifested by a marked increase of the plasma renin activity and plasma norepinephrine. The aim of the study was to characterize the systemic and hepatic hemodynamic changes associated with paracentesis-induced circulatory dysfunction.METHODS: Changes in plasma renin, aldosterone, and norepinephrine, and in systemic and hepatic hemodynamics were assessed 1 hour and 6 days after complete mobilization of ascites in 37 patients treated by total paracentesis plus intravenous dextran-70 infusion.RESULTS: Paracentesis-induced circulatory dysfunction occurred in 10 patients (renin and norepinephrine increased from 9.0 +/- 10.5 to 28.8 +/- 19.0 ng.mL-1.h-1 and from 752.0 +/- 364.0 to 1223.0 +/- 294.0 pg/mL, respectively) and was associated with significant reduction in systemic vascular resistance (-13.0% +/- 2.6%; P < 0.05) and increase in hepatic venous pressure gradient (from 19.5 +/- 1.5 to 22.5 +/- 2.4 mm Hg; P < 0.01). In the remaining 27 patients, mobilization of ascites also induced a significant but smaller reduction in systemic vascular resistance (- 5.0% +/- 1.6%; P < 0.05) without significant changes in renin, norepinephrine, and hepatic venous pressure gradient.CONCLUSIONS: Paracentesis-induced circulatory dysfunction is predominantly caused by an accentuation of the arteriolar vasodilation already present in untreated cirrhotic patients with ascites. The homeostatic activation of endogenous vasoactive systems may account for the increased intrahepatic vascular resistance associated with this condition.(Gastroenterology 1997 Aug;113(2):579-86)

Systemic and hepatic hemodynamic changes in acute liver injury.

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

Changes in hepatic hemodynamics due to primary liver tumours.

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls. The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change. The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01). On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

Duplex sonography after transjugular intrahepatic portosystemic shunts (TIPS): normal hemodynamic findings and efficacy in predicting shunt patency and stenosis.

Portal hemodynamics are altered by placement of a transjugular intrahepatic portosystemic shunt (TIPS). Normal duplex sonographic findings after TIPS placement and hemodynamic alterations indicating shunt failure have not yet been well described. The purposes of this study were to determine normal hemodynamic changes on duplex sonography after TIPS placement and to assess the efficacy of duplex sonography in detecting shunt dysfunction. Forty patients underwent TIPS placement and were entered into a study that included routine sonographic evaluation and portal venography at regular intervals. Portal venography was also performed if shunt velocities on duplex sonography changed from the baseline, which raised the question of shunt stenosis or occlusion. The pre-TIPS duplex sonographic study included determination of patency, velocity, and flow direction in the main, right, and left portal veins and in the hepatic artery. Follow-up sonography included the pre-TIPS examination in addition to velocity determinations in three segments of the shunt. Correlation was made between 82 concurrent sonographic and portal venographic studies. High-velocity blood flow (mean peak velocity, 135-200 cm/sec) was consistently seen within patent, well-functioning shunts. Hepatic artery peak systolic velocities increased from 79 cm/sec before TIPS placement to 131 cm/sec after TIPS placement (p < .001). Main portal vein velocities increased from 21.8 cm/sec before TIPS placement to 41.5 cm/sec after TIPS placement (p < .001). When compared with portal venography, duplex sonography was 98% sensitive and 100% specific in predicting the presence of blood flow within the stent. Sonography was highly sensitive and specific for detecting stent stenosis. Final sonographic criteria for shunt stenosis in angiographically documented cases were low-velocity shunt flow (< or = 60 cm/sec) in the entire stent, or low-velocity shunt flow with an associated focal velocity elevation. Consistent changes in portal venous and hepatic arterial hemodynamics are normally seen on duplex sonography after placement of a TIPS. Duplex sonography accurately predicts shunt patency and dysfunction when compared with portal venography. Duplex sonography is an effective, noninvasive method of evaluating shunt function and should be considered for use as the primary imaging technique in routine follow-up after TIPS placement.

Sonography of transjugular intrahepatic portosystemic shunts

Transjugular intrahepatic portosystemic shunting (TIPS) is an effective procedure for relieving portal hypertension. Sonography can usefully assist portal vein puncture. Color and duplex sonography after TIPS demonstrates changes in hepatic vascular hemodynamics, detects complications, and confirms shunt patency. A large proportion of shunts will develop progressive stenosis over 12 months. Stenosis occurs because of pseudointimal hyperplasia in the stent or in the hepatic vein. Patent shunts are characterized by velocities in excess of 70 cm/s and hepatofugal flow in the portal circulation distal to the shunt. Although the cause of the stenosis can rarely be seen, velocities of less than 50 cm/s indicate shunt stenosis. Loss of cardiac pulsatility is another useful sign of shunt stenosis. Regular sonographic monitoring reliably detects stenosis, allowing stent revision and preventing recurrence of bleeding.

Noninvasive measurement of femoral blood flow and portal pressure response to propranolol in patients with cirrhosis

This study investigated the correlation between changes in hepatic and systemic hemodynamics and femoral blood flow (FBF), measured by dual-beam pulsed wave Doppler, in 58 portal hypertensive patients receiving propranolol (0.15 mg/Kg intravenously; n = 44) or placebo (n = 14) under double-blind conditions. Placebo administration had no effects. Propranolol caused significant reductions (P < .0001) in hepatic venous pressure gradient (HVPG; from 19.1 +/- 4.1 to 16.2 +/- 4.2 mm Hg), azygos blood flow (from 563 +/- 204 to 387 +/- 176 mL/min), cardiac index (CI; from 4.4 +/- 1.0 to 3.3 +/- 0.8 L/m2/min), and FBF (from 237 +/- 79 to 176 +/- 58 mL/m2/min). In 17 patients HVPG decreased below 12 mm Hg and/or more than 20% of the baseline value (good response; mean change, -26 +/- 8%); in the remaining 27 patients (poor response) the mean change in HVPG was less: -9 +/- 6%. Patients with a good response had bled less often from varices, had significantly higher FBF (272 +/- 73 vs. 215 +/- 76 mL/m2/min) and lower baseline HVPG (16.8 +/- 3.9 vs. 20.6 +/- 3.6 mm Hg) than those with poor response in HVPG. The good response was also associated with greater decreases in FBF (-33 +/- 12 vs. -19 +/- 13% in poor responders), CI (-30 +/- 9 vs. -19 +/- 12%), and heart rate (-19 +/- 5 vs. -16 +/- 6%). A decrease in FBF of > 20% predicted a good response in 16 of 28 patients (positive predictive value, 57%).(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive measurement of femoral blood flow and portal pressure response to propranolol in patients with cirrhosis

This study investigated the correlation between changes in hepatic and systemic hemodynamics and femoral blood flow (FBF), measured by dual-beam pulsed wave Doppler, in 58 portal hypertensive patients receiving propranolol (0.15 mg/Kg intravenously; n = 44) or placebo (n = 14) under double-blind conditions. Placebo administration had no effects. Propranolol caused significant reductions ( P < .0001) in hepatic venous pressure gradient (HVPG; from 19.1 ± 4.1 to 16.2 ± 4.2 mm Hg), azygos blood flow (from 563 ± 204 to 387 ± 176 mL/ min), cardiac index (CI; from 4.4 ± 1.0 to 3.3 ± 0.8 L/m 2/min), and FBF (from 237 ± 79 to 176 ± 58 mL/m 2/min). In 17 patients HVPG decreased below 12 mm Hg and/or more than 20% of the baseline value (good response; mean change, −26 ± 8%); in the remaining 27 patients (poor response) the mean change in HVPG was less: −9 ± 6%. Patients with a good response had bled less often from varices, had significantly higher FBF (272 ± 73 vs. 215 ± 76 mL/m 2/min) and lower baseline HVPG (16.8 ± 3.9 vs. 20.6 ± 3.6 mm Hg) than those with poor response in HVPG. The good response was also associated with greater decreases in FBF (−33 ± 12 vs. −19 ± 13% in poor responders), CI (−30 ± 9 vs. −19 ± 12%), and heart rate (−19 ± 5 vs. −16 ± 6%). A decrease in FBF of >20% predicted a good response in 16 of 28 patients (positive predictive value, 57%). A negative test (decrease in femoral blood flow of <20%) predicted a lack of response in HVPG in 15 of 16 patients (negative predictive value, 94%). This study suggests that the noninvasive measurements of FBF allow the identification of patients with a poor response of HVPG to propranolol. However, measurements of HVPG would still be needed for patients whose FBF decreased >20%, half of whom have an insufficient decrease in HVPG.

ET-1 induced alterations of hepatic microcirculation: sinusoidal and extrasinusoidal sites of action.

Using epifluorescence microscopy, we investigated the dynamic changes in hepatic sinusoidal hemodynamics in vivo during continuous infusion of endothelin-1 (ET-1) in pentobarbital-anesthetized rats. ET-1 was infused for 20 min at rates of 2 or 10 pmol/min either systemically or into the portal vein, followed by a 90-min recovery period. In contrast to systemic application of ET-1 that did not cause a consistent hepatic microvascular effect, we observed two different patterns of microcirculatory alterations during portal application. Infusion of 2 pmol/min elicited a rapid, reversible decrease in sinusoidal diameter that was paralleled by a slight increase in red cell velocity, resulting in conservation of volumetric flow and sinusoid density. Infusion of 10 pmol/min resulted in a biphasic narrowing followed by transient increase in sinusoidal diameter and a profound and lasting decrease in red cell velocity, leading to an almost complete cessation of hepatic microvascular blood flow. These results indicate that ET-1 is a potent constrictor in the liver microcirculation in vivo and acts at both extrasinusoidal and sinusoidal sites, although the sinusoidal sites appear to be more sensitive to lower concentrations.

Nicardipine increases hepatic blood flow and the hepatic clearance of indocyanine green in patients with cirrhosis

The present study investigated the hemodynamic effects of nicardipine, a new calcium channel blocker, and placebo in 14 patients with cirrhosis. Sixty minutes after nicardipine administration (20 mg orally; n = 8), there was a significant increase in hepatic blood flow (25 +/- 21%; p < 0.05) and azygos blood flow (33 +/- 40%; p < 0.05) but no significant change in the hepatic venous pressure gradient. As a result of the increase in hepatic blood flow and the lack of change in the hepatic venous pressure gradient, nicardipine significantly reduced hepatic sinusoidal resistance (-14 +/- 15%; p < 0.05). Enhanced liver perfusion was associated with a significant increase in the hepatic clearance of indocyanine green (from 241 +/- 81 to 265 +/- 92 ml/min, p < 0.05). A mild, well-tolerated decrease in mean arterial pressure (-10 +/- 6%, p < 0.05), without significant changes in cardiac output, systemic vascular resistance and heart rate, was also observed. Placebo administration (n = 6) did not cause significant changes in systemic or hepatic hemodynamics. The results of the present study show that nicardipine, unlike other calcium channel blockers, effectively increases hepatic blood flow and the hepatic clearance of indocyanine green in patients with cirrhosis. The acute beneficial effects of nicardipine should be confirmed in chronic studies.

Reduction of variceal pressure by propranolol: Comparison of the effects on portal pressure and azygos blood flow in patients with cirrhosis

This study investigated the correlation between changes in hepatic hemodynamics and esophageal variceal pressure--measured with a noninvasive, pressure-sensitive endoscopic gauge--in 37 portal-hypertensive cirrhotic patients receiving propranolol (0.15 mg/kg, intravenously; n = 21) or placebo (n = 16) under strict double-blind conditions. Placebo administration had no effect on hepatic venous pressure gradient, azygos blood flow or variceal pressure. Propranolol caused a significant reduction in hepatic venous pressure gradient (from 19.6 +/- 1 to 17.3 +/- 1 mm Hg, p < 0.001), azygos blood flow (from 0.61 +/- 0.06 to 0.39 +/- 0.03 L/min, p < 0.001) and variceal pressure (from 13.1 +/- 0.9 to 10.2 +/- 0.9 mm Hg, p < 0.001). In eight patients (propranolol nonresponders) hepatic venous pressure gradient was not modified or decreased by less than 10% after propranolol (mean change, -4.1 +/- 1.6%). However, we found no significant differences between propranolol responders and nonresponders with regard to the decrease in variceal pressure (3.3 +/- 0.7 vs. 2.3 +/- 1.4 mm Hg) and azygos blood flow (0.23 +/- 0.07 vs. 0.21 +/- 0.07 L/min). As expected, in most propranolol responders (11 of 13), reduction in hepatic venous pressure gradient was accompanied by a similar response in variceal pressure (> 10% decrease). However, among propranolol nonresponders, in terms of reduction in hepatic venous pressure gradient, four out of eight patients had decreases greater than 10% in variceal pressure. The results of this study confirm that reduction in hepatic venous pressure gradient by propranolol is associated with a significant decrease in variceal pressure and azygos blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Transjugular intrahepatic portosystemic shunt: evaluation with Doppler sonography.

To assess the potential role of ultrasound (US) in evaluating transjugularly inserted intrahepatic portosystemic shunts, the authors performed sonographic, including duplex and color Doppler, studies in 23 patients. Imaging was performed before, during the first week after, and 2-3 months after shunt placement. The prostheses were readily visualized and shunt patency was easily determined with Doppler US in all patients. The mean of the maximum blood flow velocity in the main portal vein increased from 7 (range, 3-16) cm/sec before shunting to 24 (range, 18-47) cm/sec 2-3 months after shunting. Flow reversal was detected in the intrahepatic portal branches in 16 (69%) of the 23 patients. US allowed prompt detection and management of two cases of incomplete stent expansion and one case of shunt stenosis due to pseudo-intimal hyperplasia. Sonography is a valuable tool for evaluation of changes in hepatic hemodynamics after transjugular intrahepatic shunt placement.