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Biomedical subjects

J Bosch

Publications and source records attributed to J Bosch.

At least 217 records · Page 12Linked to original sources
PubMed1993

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)

Adult↗
PubMed1993

Effects of ritanserin, a selective and specific S2-serotonergic antagonist, on portal pressure and splanchnic hemodynamics in rats with long-term bile duct ligation.

This study investigated the short-term effects of ritanserin, a selective and specific S2-serotonergic antagonist, in an experimental model of cirrhosis and intrahepatic portal hypertension caused by long-term bile duct ligation and division and in normal control rats. The rats subjected to bile duct ligation were randomized under blind conditions into two groups to receive ritanserin (0.7 mg/kg body wt, intravenously; n = 10) or the same volume of placebo (isotonic saline solution; n = 10). We performed hemodynamic studies with radiolabeled microspheres 60 min after drug administration. Two groups of normal rats (n = 6) were studied after they received ritanserin or placebo. Ritanserin administration to rats subjected to bile duct ligation significantly reduced portal pressure (from 16.2 +/- 1.3 mm Hg to 12.3 +/- 0.7 mm Hg; mean decrease, 22% +/- 5%; p < 0.05). This reduction was associated with lower portal venous resistance (4.3 +/- 0.5 mm Hg.min.100gm/ml in the placebo group vs. 3.1 +/- 0.3 mm Hg.min.100 gm/ml in rats given ritanserin; mean decrease, 28%; p = 0.069), but we saw no changes in portal vein inflow (3.9 +/- 0.5 ml/min.100 gm vs. 4.4 +/- 0.4 ml/min.100 gm), mean arterial pressure (110 +/- 9 mm Hg vs. 102 +/- 9 mm Hg) and cardiac index (32.9 +/- 2.7 ml/min.100 gm vs. 40.5 +/- 6.7 ml/min.100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. Ritanserin had no systemic or splanchnic effects in normal rats. Our results demonstrate that ritanserin infusion decreases portal pressure without any systemic hemodynamic change in rats with secondary biliary cirrhosis and portal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal-hypertensive anesthetized rats.

This study investigates the effects of inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine-anesthetized rats with portal hypertension induced by partial portal vein ligation. The hydrogen gas-clearance technique was used for measurement of gastric mucosal blood flow. Blood pressure increased with L-NAME administration in a similar manner in portal-hypertensive and sham-operated rats. Low doses of L-NAME (1 and 3 mg/kg, intravenously) caused a significant and dose-dependent reduction in gastric mucosal blood flow in portal-hypertensive rats but had no effect on sham-operated animals. With a higher dose of L-NAME (13 mg/kg, intravenously), a significant decrease in gastric mucosal blood flow was observed in both portal-hypertensive and sham-operated rats. Indomethacin pretreatment (5 mg/kg, subcutaneously) caused a significant decrease in basal gastric mucosal blood flow of portal-hypertensive rats but did not modify this parameter in sham-operated animals. In sham-operated rats pretreated with indomethacin, the lower dose of L-NAME (3 mg/kg) did not significantly modify basal gastric mucosal blood flow. Likewise, pretreatment with indomethacin in sham-operated rats did not augment the significant reduction in gastric mucosal blood flow produced by the higher dose of L-NAME. In portal-hypertensive rats the significant dose-dependent reduction in gastric mucosal blood flow induced by L-NAME (3 and 13 mg/kg) was not significantly altered by pretreatment with indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1993

Transjugular liver biopsy in BMT.

With the aim of evaluating liver disturbances after BMT in 76 patients, the hepatic venous pressure gradient was measured and a transvenous liver biopsy was performed through the jugular vein. Catheterization was successful in 71 patients (93%). In 11 cases the procedure was performed twice, yielding a total number of 82 studies. In five (6%) liver biopsies were non-evaluable. Complications were rare (7%), minor and reversible. As a result of this procedure, the diagnosis was modified in 45%, with both the diagnosis and treatment being modified in 30% of patients. Veno-occlusive disease (VOD) was histologically demonstrated in 15 out of 26 patients (58%) in whom this complication was suspected and in two out of 33 (6%) in whom it was not. Acute GVHD of the liver was confirmed in 15 out of the 35 patients (43%) in whom this complication was suspected and in four of 24 (17%) in whom it was not. The hepatic venous pressure gradient was significantly higher in VOD than in liver GVHD. Whereas 14/17 (82%) patients with VOD had a gradient pressure higher than 9 mmHg, no patient with GVHD had a gradient above this value. We conclude that transjugular liver biopsy is an effective, safe, and useful technique to evaluate BMT related liver dysfunction.

Biopsy↗
PubMed1993

Hemodynamic and humoral changes after liver transplantation in patients with cirrhosis.

Splanchnic and systemic hemodynamics and plasma levels of aldosterone, glucagon and plasma renin were investigated in 12 patients with advanced cirrhosis before and 2 wk (14.6 +/- 2.8 days) and 2 mo (60.8 +/- 10.5 days) after orthotopic liver transplantation. Liver transplant was followed by significant (p < 0.01) changes in systemic hemodynamics at 2 wk, with a marked reduction in cardiac index (4.9 +/- 0.8 vs. 3.7 +/- 0.7 L/min.m2) and increases in mean arterial pressure (79 +/- 8 vs. 101 +/- 11 mm Hg) and peripheral vascular resistance (721 +/- 149 vs. 1,274 +/- 253 dyn.sec.cm-5). Two months after liver transplant, we saw further significant increases in peripheral vascular resistance (1,700 +/- 341 dyn.sec.cm-5; p < 0.05) without changes in cardiac index. Hepatic venous pressure gradient, very high before transplantation, was normal 2 wk after liver transplant (18.7 +/- 3.0 vs. 2.1 +/- 0.8 mm Hg; p < 0.01). Hepatic blood flow rose markedly from 1.03 +/- 0.46 to 2.25 +/- 0.79 L/min (p < 0.01) and was still elevated at 2 mo (1.84 +/- 0.74 L/min). Azygos blood flow had not changed after 2 wk with respect to pretransplant values (0.65 +/- 0.26 vs. 0.69 +/- 0.39 L/min) but had decreased significantly at 2 mo (0.39 +/- 0.16 L/min; p < 0.05). The elevated aldosterone, plasma renin and glucagon levels found in our cirrhotic patients before transplantation decreased to near-normal values 2 wk after the procedure. These results suggest that most of the hemodynamic and humoral abnormalities characteristic of advanced cirrhosis are reversed after liver transplant.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamics↗
PubMed1993

[Severe craniocerebral injuries with a lucid interval].

Some variables were analyzed in 35 patients with severe cranioencephalic injuries following a lucid interval according to mortality. The variables analyzed were: age of less than 40 years, interval of time accident-admission (TAA), admission-operation (TAO), level of consciousness (Glasgow scale), associated extracranial lesions, type of intracranial lesion, and tomodensitometric signs of intracranial hypertension. The only variables demonstrating significant statistical differences (p < 0.05) were the level of consciousness (Glasgow scale < 6 points) and the presence of subdural hematoma. Twelve (70.5%) patients who died had less than 6 on the Glasgow scale and in contrast only 5 (27.7%) of the living. Eleven (64.7%) of the group who died and 4 (22.2%) of the living had subdural hematoma. These data suggest that the level of consciousness and the type of lesion are determining factors of the mortality in this type of patients. Early detection and energic treatment of secondary lesions contribute to prognostic improvement of cranioencephalic injuries.

Adult↗
PubMed1993

[Perinatal Streptococcus agalactiae infections. Clinical epidemiological study and evaluation of a prevention program].

BACKGROUND: To prove both the importance of SGB (group B streptococci) as a cause of perinatal infection and the efficacy of a prophylactic treatment in pregnant women with cervicovaginal colonization by SGB. METHODS: Retrospective study of 197 third trimester pregnant women who were carriers of SGB (155 received intrapartum prophylaxis) and of 44 patients with SGB infections during pregnancy, post-partum and neonatal periods. RESULTS: No neonatal sepsis was detected in the group of SGB carrier mothers who received antibiotic prophylaxis. In carrier pregnant women who did not receive prophylaxis, one case of neonatal sepsis by SGB was detected and a greater prevalence of intrapartum fever, and neonatal infection with negative cultures was observed. SGB was frequently isolated as a cause of early sepsis and neonatal meningitis (13 cases), intraamniotic infection (12 cases) and puerperal endometritis (8 cases). In 45% of the patients with perinatal infections by SGB, the cervicovaginal culture performed in the third trimester of pregnancy did not detect the presence of SGB. CONCLUSIONS: The administration of intrapartum ampicillin to pregnant SGB carriers permits the prevention of perinatal infections by this microorganism in a great number of patients, although the possibility of late colonization, which may not be detected during pregnancy, stil remains.

Ampicillin↗
PubMed1993

Renal effects of acute isosorbide-5-mononitrate administration in cirrhosis.

The aim of this study was to assess the effects of an oral dose (20 mg) of isosorbide-5-mononitrate on systemic hemodynamics, kidney function, plasma renin activity and plasma aldosterone and atrial natriuretic peptide concentrations in 16 nonazotemic cirrhotic patients. Isosorbide-5-mononitrate significantly reduced cardiopulmonary pressures, cardiac output, peripheral vascular resistance, mean arterial pressure, renal plasma flow, glomerular filtration rate, free water clearance, sodium excretion and atrial natriuretic peptide concentration and significantly increased renin and aldosterone values. Cardiopulmonary pressures, atrial natriuretic peptide, cardiac output and mean arterial pressure decreased to a similar extent in patients with (n = 9) and without ascites (n = 7). In patients with ascites we noted marked increases in plasma renin activity (3.7 +/- 1.1 ng/ml/hr to 6.4 +/- 1.8 ng/ml/hr; p = 0.01) and aldosterone level (61.1 +/- 17.5 ng/dl to 108.4 +/- 36.1 ng/dl; p = 0.01). In contrast, in patients without ascites the elevation of plasma renin activity (0.5 +/- 0.16 ng/ml/hr to 0.95 +/- 0.27 ng/ml/hr; p = 0.02) and aldosterone level (5.9 +/- 1.3 ng/dl to 12.3 +/- 3.8 ng/dl; p = 0.02) was mild, and in no case did these parameters increase over the upper normal limit. Isosorbide-5-mononitrate produced a significantly greater reduction of glomerular filtration rate (-21.4% +/- 3.3% vs. -8.9% +/- 4.2%; p = 0.03) and free water clearance (-82.4% +/- 16.1% vs. -34.5% +/- 12.3%; p = 0.03) in patients with ascites than in those without.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1992

[Prognostic value of hepatic clearance of indocyanine green in patients with liver cirrhosis and hemorrhage of esophageal varices].

BACKGROUND: The prognostic value of the quantitative tests of hepatocellular function are not clearly established. Although these tests have significantly correlated with the Child-Pugh classification, it has not been demonstrated that they are better than the same in regards to prognosis. METHODS: The present study was aimed at investigating the prognostic values of hepatic clearance and the intrinsic clearance of indocyanine green (ICG) in 91 cirrhotic patients who had presented hemorrhage due to rupture of the esophageal varices. The clinical and biochemical data, portal pressure determined during suprahepatic vein catheterization, and the clearance, intrinsic clearance, extraction and hepatic blood flow measured during continual infusion of ICG were included in the analysis. All these data were obtained following the stabilization of the patients once over the hemorrhagic episode. RESULTS: The mean survival of the series was 48 months. During follow up (25 +/- 17, interval 1-58 months) 3 of the 32 patients died (9%) of group A of the Child-Pugh classification, 17 of the 52 patients of group B (33%) and 6 of the 7 patients of group C (85%). The Child-Pugh classification was the only variable with an independent predictive value in the multivariate analysis in the Cox model. On exclusion of the 7 patients pertaining to group C, whose survival was clearly inferior to that of the rest of the series, the variables with independent predictive value were, hepatic clearance of less than 240 ml/min and the presence of ascites, while the Child-Pugh classification had no independent predictive value on survival. CONCLUSIONS: The results of the present study indicate that hepatic clearance of ICG and the presence of ascites may have prognostic value in patients of Child-Pugh classification A and B who have recovered from a hemorrhagic episode due to rupture of esophageal varices.

Adult↗
PubMed1992

Frequency domain models of the EEG.

The structure of the normal resting EEG crosspectrum SVV(omega) is analyzed using complex multivariate statistics. Exploratory data analysis with Principal Component Analysis (PCA) is followed by hypothesis testing and computer simulations related to possible neural generators. The SVV(omega) of 211 normal individuals (ages 5 to 97) may be decomposed into two types of processes: the xi process with spatial isotropicity reflecting diffuse, correlated cortical generators with radial symmetry, and processes that seem to be generated by more spatially concentrated, correlated sources. The latter are reflected as spectral peaks such as the process. The eigenvectors of the xi process are the Spherical Harmonic Functions which explains the recurring pattern of maps characteristic of the spatial PCA of qEEG data. A new method for estimating sources in the frequency domain which fits dipoles to the whole crosspectrum is applied to explain the characteristics of the localized sources.

Age Factors↗
PubMed1992

Lymphocyte beta 2-adrenoceptors and plasma catecholamines in patients with cirrhosis.

The hemodynamic response to propranolol in patients with cirrhosis is heterogeneous. In some patients, there is an expected decrease in portal pressure, whereas in others, portal pressure fails to decrease despite adequate beta-blockade. It has been suggested that this lack of response could be related to down-regulation of beta 2-adrenoceptors, promoted by the increased adrenergic activity frequently found in decompensated cirrhosis. The present study investigated this hypothesis by measuring the density and affinity of lymphocyte beta 2-adrenoceptors (L-beta 2-AR), an established index of beta 2-adrenoceptors in target organs, and the plasma levels of norepinephrine and epinephrine in a group of 32 patients with cirrhosis and portal hypertension. The portal pressure response to propranolol administration (0.1 mg/kg + 2 mg/h) was also investigated (n = 27). Patients with cirrhosis had increased norepinephrine levels (605 +/- 360 vs. 224 +/- 110 pg/mL in controls; P less than 0.001), but plasma epinephrine level was not increased (136 +/- 72 vs. 111 +/- 22 pg/mL in controls; NS). There were no differences between cirrhotic patients and controls in the density of L-beta 2-AR (1398 +/- 489 vs. 1278 +/- 356 receptors/cell; NS). Portal pressure decreased greater than 10% in 12 patients (responders) and less than 10% in the remaining 15 (nonresponders). Contrary to previous suggestions, there were no significant differences between responders and nonresponders in relation to the density of L-beta 2-AR (1362 +/- 527 vs. 1487 +/- 419 receptors/cell; NS), to the affinity of these receptors (0.15 +/- 0.27 vs. 0.13 +/- 0.12 nmol/L; NS), to the plasma levels of norepinephrine (661 +/- 508 vs. 621 +/- 256 pg/mL; NS), and to plasma epinephrine concentration (141 +/- 90 vs. 140 +/- 75 pg/mL; NS). These results show that the response of portal pressure to propranolol administration is neither related to the density and affinity of L-beta 2-AR nor to the plasma levels of norepinephrine and epinephrine. Thus, the determination of these parameters cannot substitute measurements of portal pressure to identify those patients with an adequate portal pressure response to propranolol treatment.

Aged↗
PubMed1992

Mineralocorticoid escape in patients with compensated cirrhosis and portal hypertension.

Failure to escape from mineralocorticoids in compensated cirrhosis is considered a major argument supporting the overflow theory of ascites. To assess the frequency and mechanism of mineralocorticoid escape in cirrhosis, 9-alpha-fluorohydrocortisone (0.6 mg/day) was administered to 19 patients with compensated cirrhosis, portal hypertension, and no history of ascites who were able to maintain sodium balance on a 250 mmol Na+ diet. Fifteen patients (78.9%) escaped from mineralocorticoids, while 4 patients (21.1%) did not escape and developed ascites. Patients who did not escape had significantly higher cardiac index (4.97 +/- 0.42 vs 3.46 +/- 0.21 L.min-1.m-2) and lower peripheral vascular resistance (485.9 +/- 37.5 vs. 665.8 +/- 32.9 dyne.s.cm-5/m2) than those who escaped. Hepatic venous pressure gradient was not significantly different. The escape phenomenon was associated with a significant increase in mean arterial pressure, creatinine clearance, and atrial natriuretic factor and suppression of plasma renin activity. All of these parameters showed minimal or no changes in patients who did not escape. These results indicate that failure to escape from mineralocorticoids is uncommon in patients with compensated cirrhosis, is related to an inadequate expansion of effective plasma volume due to the accumulation of ascites, and occurs in patients with marked peripheral arteriolar vasodilation.

Adult↗
PubMed1992

Effects of acute normovolemic anemia on gastric mucosal blood flow in rats: role of nitric oxide.

The present study investigates the effects of acute normovolemic anemia induced by isovolemic hemodilution on gastric mucosal blood flow (GMBF), measured by hydrogen gas clearance, and on the oxygen and hemoglobin content in the gastric mucosa, estimated by reflectance spectrophotometry. GMBF significantly increased after 3 and 6 mL of isovolemic hemodilution (from 50 +/- 5 to 70 +/- 7 and 77 +/- 6 mL.min-1.100 g-1, respectively; P less than 0.05) compared with basal values (50 +/- 5.mL-1.min-1.100 g-1; P less than 0.05). Oxygen content remained unchanged, whereas hemoglobin concentration decreased in parallel with the decrease in hematocrit. In a second set of experiments, the role of endogenous nitric oxide (NO) as a possible mediator of the gastric vascular changes induced by hemodilution was investigated by using the specific inhibitor of NO biosynthesis, NG-monomethyl-L-arginine (L-NMMA). The increase in GMBF induced by 3 mL of isovolemic hemodilution (delta 23 +/- 7 mL.min-1.100 g-1) was attenuated in a dose-related manner with L-NMMA, 6.25 mg/kg IV (delta 15 +/- 4 mL.min-1.100 g-1) or 50 mg/kg IV (delta 5 +/- 2 mL.min-1.100 g-1 g; P less than 0.05). The concurrent administration of L-arginine (the precursor of NO biosynthesis) abolished the effects of L-NMMA on GMBF changes. The current findings show that acute normovolemic anemia causes an increase in GMBF that is dependent on the endogenous formation of NO.

Acute Disease↗
PubMed1992

Increased gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy.

To characterize gastric mucosal perfusion in cirrhotic patients with portal hypertensive gastropathy, 34 cirrhotics with this lesion and 24 noncirrhotics were studied by reflectance spectrophotometry and laser-Doppler flowmetry during endoscopy. A significant correlation was observed between the hemoglobin content of the gastric mucosa, measured by reflectance spectrophotometry, and the serum hemoglobin concentration both in cirrhotics (r = 0.72) and in noncirrhotics (r = 0.87). IHb ratio (hemoglobin content of gastric mucosa divided by blood hemoglobin concentration) was higher in cirrhotics with portal hypertensive gastropathy than in noncirrhotics (P < 0.001), whereas the oxygen content of the gastric mucosa was similar in both groups. This pattern indicates that cirrhotics with portal hypertensive gastropathy have increased gastric perfusion without congestion. Gastric blood flow estimated by laser-Doppler was significantly higher in cirrhotics with portal hypertensive gastropathy than in noncirrhotics (P < 0.001). In cirrhotic patients, gastric areas with cherry red spots showed a significantly higher IHb ratio than areas with a mosaic or scarlatina pattern (P < 0.05). The magnitude of changes in gastric perfusion and the endoscopic severity of portal hypertensive gastropathy had no relationship with the degree of portal hypertension or the azygos blood flow.

Female↗
PubMed1992

Modulation of the hyperdynamic circulation of cirrhotic rats by nitric oxide inhibition.

The effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) biosynthesis on the splanchnic and systemic circulation, were investigated in rats with cirrhosis induced by carbon tetrachloride. Portal hypertension in these rats was accompanied by decreased arterial blood pressure and peripheral vascular resistance as well as by splanchnic vasodilation with increased portal venous inflow and decreased splanchnic resistance. Intravenous bolus administration of L-NMMA (25 mg/kg) significantly increased systemic blood pressure and decreased cardiac output. L-NMMA also significantly increased systemic and splanchnic vascular resistance; whereas blood flow to the stomach, small intestine, colon, pancreas, mesentery, spleen, and kidney was decreased significantly. L-NMMA did not alter the portal pressure or portosystemic shunting in these cirrhotic rats, yet portal vascular resistance increased, suggesting effects on the intrahepatic and collateral circulation. Pretreatment with L-arginine (300 mg/kg) prevented the hemodynamic changes induced by L-NMMA. These findings support the concept that local excess formation of NO contributes to changes in splanchnic circulation associated with portal hypertension in cirrhosis.

Animals↗
PubMed1992

Oral administration of clonidine in patients with alcoholic cirrhosis. Hemodynamic and liver function effects.

The effects of long-term oral clonidine treatment on hepatic and systemic hemodynamics and on quantitative liver function tests were investigated in 15 patients with alcoholic cirrhosis. Clonidine was administered at a mean dose of 0.33 +/- 0.1 mg/day (mean +/- SD) for a mean period of 64 +/- 10 days. Oral clonidine induced a significant reduction in the hepatic venous pressure gradient from 18.8 +/- 3.0 mm Hg to 15.9 +/- 3.4 mm Hg (P less than 0.001), which was the result of an increase in the free hepatic venous pressure from 5.1 +/- 4.2 mm Hg to 8.7 +/- 3.8 mm Hg (P less than 0.05). In 10 of the 15 patients (67%), the reduction in the hepatic venous pressure gradient was greater than 10% of baseline values. Hepatic blood flow did not change significantly after clonidine treatment. Additionally, treatment with clonidine decreased mean arterial pressure by 15.5% +/- 6% (P less than 0.001), heart rate by 17.7% +/- 7% (P less than 0.001), and cardiac output by 14.6% +/- 7% (P less than 0.001). However, systemic vascular resistance did not change significantly. There were no adverse effects on liver function, as shown by the nonsignificant changes in galactose-elimination capacity (149 +/- 59 vs. 170 +/- 58 mg/min), hepatic clearance of indocyanine green (0.19 +/- 0.10 vs. 0.17 +/- 0.07 L/min), and hepatic intrinsic clearance of indocyanine green (0.23 +/- 0.14 vs. 0.21 +/- 0.1 L/min) before and after clonidine treatment, respectively. In none of the patients was the drug withdrawn because of side effects, although 12 subjects complained of dry mouths. This study suggests that in patients with alcoholic cirrhosis, long-term oral clonidine administration achieves a reduction in the hepatic venous pressure gradient without adverse effects on hepatic blood flow and liver function.

Administration, Oral↗