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D Lebrec

Publications and source records attributed to D Lebrec.

At least 163 records · Page 9Linked to original sources
PubMed1992

[Effect of the severity of liver disease on renal hemodynamics and renal oxygen consumption in patients with cirrhosis].

In patients with cirrhosis, it has been shown that abnormal systemic and splanchnic hemodynamics and systemic oxygen (O2) consumption are related to the severity of liver disease. Little is known on the relationship between the severity of cirrhosis, on one hand, and renal hemodynamics and O2 consumption, on the other. We measured renal hemodynamics and renal O2 consumption in 31 patients Pugh's grade A and B and in 13 patients grade C. Systemic and splanchnic hemodynamics as well as systemic O2 consumption were studied. Renal blood flow, glomerular filtration rate, and renal O2 consumption were not significantly different between grades A and B and grade C patients. The renal fraction of systemic O2 consumption was higher (11.4 +/- 5.9 vs 7.9 +/- 4.1 percent respectively; P less than 0.05) and the systemic O2 consumption (111 +/- 23 vs 128 +/- 26 ml.min-1.m-2 respectively; P less than 0.05) lower in patients with grade C than in grades A and B patients. The degree of systemic hyperkineticism and portal hypertension was related to the severity of cirrhosis. In our patients, renal hemodynamics and renal O2 consumption were not related to the severity of cirrhosis. However, liver failure was associated with an increased renal fraction of systemic O2 consumption due to unchanged renal O2 consumption and decreased systemic O2 consumption.

Adult↗
PubMed1992

[Hemodynamic effects of the administration of terlipressin alone or combined with nitroglycerin in patients with cirrhosis].

Terlipressin (Glypressin), a synthetic analog of vasopressin, induces arteriolar vasoconstriction which causes both a portal hypotensive effect and certain side-effects on the systemic circulation (elevated arterial pressure and reduced cardiac output). The combination of nitroglycerin with terlipressin might accentuate the portal hypotensive effect and prevent the side-effects on the systemic circulation. The aim of this study was to examine the systemic and splanchnic hemodynamic responses to terlipressin administered alone or combined with nitroglycerin in patients with cirrhosis. Systemic and splanchnic hemodynamics were measured before and 1 h after a bolus of terlipressin (1 to 2 mg IV) given alone (n = 10) or in association with nitroglycerin infusion (25 micrograms/min, n = 9). Terlipressin alone significantly increased the arterial pressure by 21%, systemic vascular resistance by 60%, and significantly decreased cardiac output by 23%. The right atrial and pulmonary pressures significantly increased and the wedged hepatic venous pressure and hepatic venous pressure gradient significantly decreased by 8% and 16%, respectively. The combined therapy decreased the cardiac output by 20%, but did not significantly modify the other systemic and splanchnic hemodynamic values. No significant differences were found between terlipressin and the combined therapy concerning changes in wedged hepatic venous pressure or hepatic venous pressure gradient. We conclude that in patients with cirrhosis, nitroglycerin prevents the deleterious vasoconstrictor and vasopressor effects of terlipressin. However, the combined therapy, as terlipressin alone, decreases the cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1992

[Renal sympathetic nervous activity in patients with cirrhosis].

This study was designed to evaluate the renal contribution to overall sympathetic nerve hyperactivity and the relationships between renal sympathetic activity and systemic, splanchnic or renal hemodynamics in a series of 55 cirrhotic patients. Plasma noradrenaline concentrations were significantly higher in the renal vein than in the pulmonary artery (803 +/- 54 vs 608 +/- 47 pg/ml, P less than 0.01). These two concentrations were significantly correlated, which suggests that renal sympathetic activity and overall sympathetic activity increase in parallel in patients with cirrhosis. However, the estimated renal net release of noradrenaline was not correlated with plasma noradrenaline concentration in the pulmonary artery, suggesting that overall sympathetic nerve activity is not directly dependent on renal contribution in patients with cirrhosis. Neither plasma noradrenaline concentration in the renal vein nor renal net release of noradrenaline were correlated with systemic. splanchnic or renal hemodynamics. Thus, this study did not show a major role of renal sympathetic activity in the hemodynamic changes in cirrhosis.

Adult↗
PubMed1992

Long-term sympathetic and hemodynamic responses to clonidine in patients with cirrhosis and ascites.

The aim of the present study was to examine the short- and long-term effects of the alpha 2-agonist clonidine on sympathetic overactivity, systemic, splanchnic, and renal circulation changes, and abnormal renal sodium excretion in cirrhotic patients with ascites. Of 17 patients, 8 received clonidine and 9 a placebo. Measurements were taken before and after either a single dose of clonidine (150 micrograms) and placebo or a 1-week treatment with clonidine (150 micrograms/day) and placebo. Clonidine but not placebo induced significant short- and long-term decreases in plasma norepinephrine concentrations in the pulmonary artery and the right renal vein. Acute clonidine administration induced a significant reduction in cardiac output, heart rate, arterial pressure, and hepatic venous pressure gradient but had no effect on renal hemodynamics. Long-term clonidine administration induced a significant decrease in the hepatic venous pressure gradient from 20.1 +/- 1.9 to 17.6 +/- 2.0 mm Hg (mean +/- SEM) but had no significant effects on systemic or renal hemodynamics or renal excretion of sodium. It is concluded that long-term clonidine administration in cirrhotic patients induced a sustained decrease in sympathetic nervous activity and portal pressure. In contrast, clonidine had no prolonged effect on systemic hemodynamics. In addition, short- and long-term clonidine administration did not modify renal hemodynamics or induce a natriuretic response in patients with ascites.

Ascites↗
PubMed1992

Methods to evaluate portal hypertension.

There are a variety of clinical investigations available to evaluate the development of portal hypertension and its complications. Although portal pressure or hepatic venous pressure gradient measurements are the most appropriate methods, clinical findings and other hemodynamic measurements should also be evaluated in patients with portal hypertension. Noninvasive techniques such as variceal pressure and echo Doppler flowmetry have not yet been entirely validated, and new techniques are being investigated. Finally, experimental hemodynamic studies of different models of portal hypertension give additional information for the study of this syndrome.

Animals↗
PubMed1991

Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clinical trials. Franco-Italian Multicenter Study Group.

BACKGROUND: The value of beta-adrenergic-antagonist drug therapy for the prevention of initial episodes of gastrointestinal bleeding in patients with cirrhosis and esophageal varices is uncertain, both positive and negative study results having been reported. METHODS: In this study, we analyzed data on individual patients from four randomized, controlled trials to assess the efficacy of this treatment. Of the 589 patients studied, 286 received a beta-adrenergic-antagonist drug (propranolol in 203 and nadolol in 83) and 303 received placebo. RESULTS: After two years, the mean (+/- SE) percentage of patients who had had no upper gastrointestinal bleeding was 78 +/- 3 percent in the beta-adrenergic-antagonist treatment group and 65 +/- 3 percent in the control group (P = 0.002). The percentage of patients without fatal bleeding was 90 +/- 2 percent in the treatment group and 82 +/- 3 percent in the control group (P = 0.01). The percentage of patients surviving after two years was 71 +/- 3 percent in the treatment group and 68 +/- 3 percent in the control group (P = 0.34). After age and severity of cirrhosis were taken into account, the survival rate was better in the treatment group (P = 0.09). The percentage of surviving patients who had had no bleeding after two years was 62 +/- 3 percent in the treatment group and 53 +/- 3 percent in the control group (P = 0.04). Both propranolol and nadolol prevented a first episode of bleeding. Severe cirrhosis and especially the presence of ascites were associated with bleeding (P less than 0.001) and death (P less than 0.001) in both groups. The efficacy of beta-adrenergic-antagonist therapy in the prevention of bleeding (P less than 0.001) and of fatal bleeding (P = 0.004) and in the prevention of bleeding or death (P = 0.005) was the same after adjustment for cause and severity of cirrhosis, ascites, and size of varices. CONCLUSIONS: Propranolol and nadolol are effective in preventing first bleeding and reducing the mortality rate associated with gastrointestinal bleeding in patients with cirrhosis, regardless of severity.

Adrenergic beta-Antagonists↗
PubMed1991

[Medical treatment of portal hypertension].

Several agents can reduce portal pressure in patients with portal hypertension. These drugs act in different ways and have different actions. Several hemodynamic investigations have elucidated the effects of beta-blockade on the splanchnic circulation. Propranolol and other non-selective beta-blockers significantly decreased portal pressure in patients with cirrhosis. In some patients, beta-blockers did not decrease portal pressure while cardiac output and azygos blood flow significantly decreased. The cause and severity of cirrhosis do not influence the effects of beta-blockers. The efficacy of beta-blockers in the prevention of the first gastrointestinal bleeding is well established. Meta-analysis showed that among patients receiving beta-blockers, 10 per cent bled 1 year after inclusion as against 30 per cent in the placebo group. A significant difference in survival rate was also observed between the two groups. The efficacy of beta-blockers in the prevention of recurrent gastrointestinal bleeding is variable; 5 trials showed a significant difference while 3 did not show any significant difference between patients receiving beta-blockers and those receiving a placebo. Meta analysis showed a significant difference in the risk of rebleeding but did not show any difference in survival rate. Thus, beta-blockers reduce the degree of portal hypertension in patients with cirrhosis and decrease the risk of gastrointestinal bleeding in compliant patients.

Adrenergic beta-Antagonists↗
PubMed1991

Pulmonary hypertension complicating portal hypertension: prevalence and relation to splanchnic hemodynamics.

The prevalence of pulmonary hypertension in 507 patients hospitalized with portal hypertension but without known pulmonary hypertension who underwent cardiac catheterization was prospectively studied. Ten (2%) of these patients, 6 of whom were clinically asymptomatic, had primary pulmonary hypertension. Second, 26 patients with symptomatic pulmonary hypertension complicating portal hypertension were reviewed. Pulmonary hypertension occurred later after diagnosis of portal hypertension in patients with a surgical shunt (10 patients) than in those without a shunt (147 +/- 49 vs. 44 +/- 27 months; P less than 0.0001). Cardiac index correlated inversely with pulmonary arterial pressure (r = -0.45; P less than 0.01) and was lower in the 5 patients who died of pulmonary hypertension than in the 5 who died of liver failure (1.52 +/- 0.14 vs. 3.69 +/- 1.88 L/min.m2; P less than 0.05). Third, systemic and splanchnic hemodynamics were compared in 285 patients with alcoholic cirrhosis and 29 controls. No significant relation was found between elevated pulmonary vascular resistance and increased portal pressure, zzygos blood flow, or cardiac index. Pulmonary hypertension is considerably more frequent than was previously estimated in patients with portal hypertension. The risk of developing pulmonary hypertension could increase with the duration of portal hypertension without any clear relation to the degree of portal hypertension, hepatic failure, or amount of blood shunted.

Cardiac Catheterization↗
PubMed1991

Variability of hemodynamic values and plasma catecholamine concentrations over a one-hour period in conscious, restrained rats.

Restrained conscious rats have been widely used for physiological and pharmacological hemodynamic studies. In this condition, the variability of the circulation is unclear. Repeated measurements in restrained normal rats showed stable systemic hemodynamics (cardiac output ranging from 130 +/- 14 to 174 +/- 10 mL/min, mean arterial pressure ranging from 109 +/- 9 to 117 +/- 5 mmHg) and splanchnic hemodynamics (splanchnic blood flow ranging from 8.51 +/- 1.89 to 13.01 +/- 1.45 mL min-1 100 g-1 body wt) over a period of 1 hr. Slight but not significant hemodynamic variations, however, occurred in pulmonary blood flow. Similarly, plasma noradrenaline concentrations did not vary over this period (plasma noradrenaline level ranging from 186 +/- 36 to 358 +/- 64 pg/mL). These plasma noradrenaline concentrations were similar to those measured in a group of conscious unrestrained rats 3 hr after recovery from surgery (292 +/- 60 pg/mL). A significant correlation was observed between plasma noradrenaline concentration and heart rate.

Animals↗
PubMed1991

Clearance of atrial natriuretic peptide in patients with cirrhosis. Role of liver failure.

In non-cirrhotic patients, splanchnic, renal and pulmonary vascular beds are involved in the plasma clearance for atrial natriuretic peptide (ANP). In patients with cirrhosis, endogenous plasma ANP clearance by these vascular beds has not been systematically studied. In addition, the influence of the severity of liver failure on plasma ANP clearance is not known. Thus, in this study we determined plasma ANP clearance by splanchnic, renal and pulmonary circulations using both arteriovenous differences in plasma ANP concentrations and organ plasma flow in 11 patients with cirrhosis. The role of forearm circulation in plasma ANP extraction was also studied. Splanchnic plasma ANP extraction was 29 +/- 7% (mean +/- S.E.) and splanchnic plasma ANP clearance was 404 +/- 130 ml/min (n = 7). Renal plasma ANP extraction and clearance were 32 +/- 8% and 191 +/- 57 ml/min, respectively. Forearm plasma ANP extraction was 11 +/- 4%. Pulmonary plasma ANP extraction and clearance were 8 +/- 5% and 312 +/- 272 ml/min, respectively. A significant negative correlation was found between logarithm of serum bilirubin concentration, on one hand, and splanchnic and forearm plasma ANP extraction, on the other. A significant negative correlation was found between Pugh's score, on one hand, and renal plasma ANP extraction and clearance, on the other. No significant correlation was found between the severity of liver failure and pulmonary plasma ANP extraction and clearance. As a result, we conclude that in cirrhotic patients splanchnic, renal, forearm and pulmonary vascular beds are involved in plasma ANP extraction and clearance. Plasma ANP extraction and/or clearance may be attenuated in the splanchnic, renal and forearm circulations due to liver failure.

Atrial Natriuretic Factor↗
PubMed1991

Regional sympathetic activity, severity of liver disease and hemodynamics in patients with cirrhosis.

One hundred and eight patients with cirrhosis (23 grade A, 46 grade B and 39 grade C, according to Pugh's classification) underwent hemodynamic studies and plasma catecholamine concentration measurements. Blood samples were withdrawn from the pulmonary artery (n = 108), the hepatic vein (n = 108), the azygos vein (n = 59), the right renal vein (n = 66), the right jugular vein (n = 34) and the femoral vein (n = 33). Plasma noradrenaline concentrations in the pulmonary artery and the hepatic vein were more elevated in grade B (607 +/- 52 and 402 +/- 42 pg/ml, respectively) and C patients (630 +/- 59 and 475 +/- 53 pg/ml, respectively) than in grade A patients (411 +/- 51 and 243 +/- 40 pg/ml, respectively). Plasma noradrenaline concentrations from these two vessels were negatively correlated with indocyanine green clearance. These results indicate that both overall and splanchnic sympathetic activities are dependent on altered hepatic function. Significant correlations were found between the wedged hepatic venous pressure and plasma noradrenaline concentrations from either the pulmonary artery, the hepatic vein or the azygos vein. These correlations indicate that both overall and splanchnic sympathetic activities are dependent on the degree of portal hypertension. Moreover, significant correlations were found between hepatic venous plasma noradrenaline concentrations and systemic hemodynamic values, suggesting that splanchnic sympathetic nervous activity could either play a role in the systemic hyperkinetic syndrome or be a consequence of this hyperkinetic syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Early chronic administration of propranolol reduces the severity of portal hypertension and portal-systemic shunts in conscious portal vein stenosed rats.

We investigated the effects of early chronic administration of propranolol on systemic and splanchnic hemodynamic changes, and the development of portal-systemic shunts in conscious, unrestrained, portal vein stenosed rats. Compared to rats receiving placebo, early chronic propranolol (75 mg kg-1 day-1) administration to rats begun 3 days before portal vein stenosis and then continued for 10 consecutive days, resulted in a significant decrease in both portal pressure (11.8 +/- 1.5 mmHg) and portal-systemic shunts (48 +/- 18%) which were measured 2 to 3 h after the final dose of propranolol (15.2 +/- 1.5 mmHg and 84 +/- 5%, respectively). These beneficial effects were also observed 18 to 24 h after the final dose of chronic propranolol. In rats given propranolol continuously for 5 days starting 5 days after portal vein stenosis, portal pressure (11.8 +/- 1.2 mmHg) was significantly lower than in the placebo group but portal-systemic shunts (76 +/- 14%) were not significantly different. In rats receiving a single dose of propranolol (75 mg/kg) 10 days after portal vein stenosis and measured 2 to 3 h after propranolol administration, portal pressure (12.8 +/- 1.0 mmHg) was significantly lower than in the placebo group. Portal-systemic shunts (72 +/- 17%), however, showed no significant difference from the placebo group. Similar values in portal pressure (13.3 +/- 1.2 mmHg) and portal-systemic shunts (83 +/- 21%) were also observed in rats 18 to 24 h after a single dose of propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Divergent circulatory effects of betaxolol in conscious and anesthetized normal and portal hypertensive rats.

We aimed to define the circulatory effects of beta 1-blockade in conscious normal and portal hypertensive rats and determine if pentobarbital anesthesia affected these responses. A selective beta 1-antagonist, betaxolol, was given to four groups: conscious and anesthetized sham-operated and portal hypertensive rats. Cardiac output and splanchnic organ blood flows were measured by radioactive microspheres twice in each rat, before and 15 min after betaxolol. Both groups of conscious rats maintained mean arterial pressure despite significant decreases in cardiac output and heart rate, by increasing total peripheral resistance. Anesthetized rats were unable to do this and thus also diminished arterial pressure significantly, with portal hypertensive rats showing greater decreases than sham-operated rats. Portal tributary flow and portal pressure decreased only in the anesthetized rats. Autoregulation of splanchnic blood flow was not uniform between groups or organs: although splenic flow decreased in all four groups, intestinal blood flow decreased only in anesthetized portal hypertensive rats. The greatest decreases in several splanchnic organ blood flows were seen in this latter group. These results indicate that: (i) pentobarbital markedly changes systemic and splanchnic responses to beta 1-blockade; (ii) splanchnic autoregulation is not uniform--the intestinal circulation enjoys more protection than the splenic; and (iii) portal hypertensive rats seem to be more vulnerable to the circulatory effects of beta 1-blockade.

Animals↗
PubMed1991

Sinusoidal portal hypertension in hepatic amyloidosis.

Hepatic venous catheterisation and transvenous liver biopsy were performed in five patients with hepatic amyloidosis. In three patients, hepatic venous pressures were normal and histological examination of the liver biopsy specimen showed discrete and sparse perisinusoidal amyloid deposits. In the other two, however, the gradient between wedged and free hepatic venous pressures was increased (12 and 16 mmHg; normal 1-4 mmHg) and amyloid deposits were abundant and diffuse in the Disse's space. This study shows that portal hypertension in patients with hepatic amyloidosis is of the sinusoidal type and is related to the reduction of vascular space of hepatic sinusoids by massive perisinusoidal amyloid deposits. Furthermore, portal hypertension is associated with a poor prognosis in patients with hepatic amyloidosis.

Aged↗
PubMed1991

Adenosine and hemodynamic alterations in cirrhotic rats.

This study evaluated the hypothesis that adenosine may participate in the hemodynamic alterations observed in conscious unrestrained cirrhotic rats. In sham-operated rats, adenosine (20 micrograms.100 g body wt-1.min-1 iv) induced hyperdynamic circulation and significantly increased portal pressure, mimicking the hemodynamic changes observed in cirrhosis. Although adenosine significantly increased hyperdynamic circulation and portal pressure in cirrhotic rats, these changes were significantly less marked than in sham-operated rats. 8-Phenyltheophylline (20 micrograms.100 g body wt-1.min-1 iv), a specific and potent adenosine antagonist, significantly decreased portal tributary blood flow in sham-operated rats (-18.0 +/- 5.6%) but did not have a significant effect in cirrhotic rats. The limited effect of 8-phenyltheophylline was not due to an insufficient dose, since the dose administered antagonized the hemodynamic effect of exogenous adenosine up to 40 micrograms.100 g body wt-1.min-1. We conclude that in certain circumstances, although adenosine may aggravate the hyperdynamic circulation, in normal conditions, the hemodynamic alterations observed in cirrhotic rats are not mediated by adenosine.

Adenosine↗
PubMed1991

Splanchnic and systemic hemodynamics in cirrhotic patients with refractory ascites. Effect of peritoneovenous shunting.

The splanchnic and systemic hemodynamics of 14 patients with refractory ascites were studied and were compared to those of 15 patients with ascites responding to medical treatment. Among the 14 patients, 10 were grade B and 4 C, according to the Pugh classification. Of the 15 patients, 5 were Pugh B and 10 C. In patients with refractory ascites, free hepatic venous pressure was significantly higher and hepatic venous pressure gradient was significantly lower than in patients with responsive ascites. Hepatic and azygos blood flows were not significantly different between the two groups. Cardiac output was lower in patients with refractory ascites (p less than 0.05) than in those with responsive ascites. In patients with refractory ascites, six months after peritoneovenous shunting, there was a significant reduction of wedged and free hepatic venous pressures and azygos blood flow. Cardiac output increased by 20 % (p less than 0.02). This study shows that hemodynamic alterations in patients with refractory ascites is the consequence of increased intraabdominal pressure due to chronic ascites. Six months after peritoneovenous shunting splanchnic and systemic hemodynamics became similar to those observed in patients without ascites.

Adult↗
PubMed1991

Selective dopamine DA1 stimulation with fenoldopam in cirrhotic patients with ascites: a systemic, splanchnic and renal hemodynamic study.

We studied the effects of fenoldopam, a selective dopamine DA1 agonist on systemic and splanchnic hemodynamics, renal blood flow and sodium excretion in 12 patients with alcoholic cirrhosis and ascites. Hepatic, azygos and renal veins were catheterized before and after intravenous administration of fenoldopam, 0.05 micrograms/kg/min for 1 hr and increased to 0.1 micrograms/kg/min for another hour. Mean arterial pressure progressively decreased (from 83 +/- 7 to a minimum of 77 +/- 8 mm Hg 100 min after starting the infusion) but returned to baseline level at 120 min. Plasma norepinephrine and renin activity increased (respectively from 567 +/- 297 to 919 +/- 375 pg/ml, p less than 0.05, and from 17 +/- 14 to 23 +/- 15 ng/ml/hr, p less than 0.05). Renal blood flow, urine output or sodium excretion did not change. Sodium output decreased at 1 hr from 6.9 mumol/min to 4.0 mumol/min, p less than 0.05. Both hepatic venous pressure gradient and azygos blood flow significantly increased by 21%. We conclude that the acute administration of fenoldopam did not improve renal hemodynamics or function in patients with cirrhosis and ascites. In addition, dopamine DA1 agonism caused further increases in norepinephrine concentration and plasma renin activity. Portal pressure also increased, probably because of an increase in mesenteric blood flow. These results question the renal benefit and raise concern about the use of dopamine agonists in patients with cirrhosis and ascites.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗