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Biomedical subjects

A Hadengue

Publications and source records attributed to A Hadengue.

At least 145 records · Page 8Linked to original sources
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↗
PubMed1991

[Familial hepatocellular carcinoma in B or non-A non-B cirrhosis. Report of 4 families].

We report the cases of four families in whom 2 or 3 cases of hepatocellular carcinoma were observed. In the first family, the mother and 2 daughters had hepatocellular carcinoma. In 2 other families, 2 brothers had hepatocellular carcinoma. In the first three families, all patients with hepatocellular carcinoma, as well as other members of these three families, were chronic HBsAg carriers. In the fourth family, hepatocellular carcinoma developed in 2 brothers with HBsAg negative Mediterranean cirrhosis. Because of the high risk of hepatocellular carcinoma in chronic HBsAg carriers, it is conceivable that the occurrence of familial cases of hepatocellular carcinoma could be fortuitous. However, we cannot exclude the possibility of the familial predisposition to hepatocellular carcinoma. Therefore, it seems wise, when hepatocellular carcinoma develops in one patient in a family, to carefully monitor other members of this family, whether HBsAg positive or with non A non B chronic hepatitis, for the development of hepatocellular carcinoma.

Adult↗
PubMed1991

Giant hemangioma of the liver with pain, fever, and abnormal liver tests. Report of two cases.

In conclusion, we report the cases of two patients with large hemangiomas of the liver, abdominal pain, increased ESR and fibrinogen, increased serum alkaline phosphatase and gamma-glutamyltransferase activity, and normal white blood cell counts. Clinical and biochemical abnormalities disappeared after surgical resection. Increased ESR and fibrinogen are probably related to thrombosis within the tumor. This mode of presentation may suggest a diagnosis of hepatocellular carcinoma.

Adult↗
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

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

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

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↗
PubMed1991

Relationships between plasma atrial natriuretic peptide concentrations and hemodynamics and hematocrit in patients with cirrhosis.

We studied the relationships in 29 patients with cirrhosis between pulmonary arterial atrial natriuretic peptide concentrations and the following: systemic and splanchnic hemodynamics, the hematocrit, arterial oxyhemoglobin saturation, oxygen tension and the severity of cirrhosis. Plasma atrial natriuretic peptide concentrations ranged from 21 to 208 pg/ml and averaged 78 +/- 8 pg/ml (mean +/- S.E.M.). Simple regression analysis showed significant correlations between plasma atrial natriuretic peptide concentration and the following: hematocrit, mean pulmonary arterial pressure, wedged hepatic venous pressure, free hepatic venous pressure, pulmonary wedged pressure and serum bilirubin concentrations. No significant correlations were found between plasma atrial natriuretic peptide concentrations and all other hemodynamic values, arterial oxyhemoglobin saturation and oxygen tension. Multiple stepwise regression analysis showed that the hematocrit, mean pulmonary arterial pressure and wedged hepatic venous pressure were significant and independent predictors of pulmonary artery plasma atrial natriuretic peptide concentrations (R2 = 0.69). Partial regression coefficients were -0.74 (p less than 0.001), 0.61 (p less than 0.001) and 0.44 (p less than 0.05) for the hematocrit, the mean pulmonary arterial pressure and the wedged hepatic venous pressure, respectively. In conclusion, in patients with cirrhosis, increased plasma atrial natriuretic peptide concentrations were related to the degree of hemodilution, increased pulmonary arterial pressure and the degree of portal hypertension. Plasma atrial natriuretic peptide concentrations were not influenced by the arterial oxygenation levels.

Arteries↗
PubMed1991

Systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine in patients with cirrhosis.

The effects of dopamine on kidney function have not been elucidated in patients with cirrhosis. Moreover, although increased portal pressure has been observed with supradopaminergic doses of dopamine in these patients, the splanchnic hemodynamic effects of low doses of dopamine have not been previously studied. Thus we studied the acute systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine (1.5 micrograms/kg body wt min) in nine cirrhotic patients. Plasma dopamine levels increased markedly from 35 +/- 20 pg/ml to 31,400 +/- 4,900 pg/ml during dopamine administration. A significant diastolic pressure decrease of 10% was associated with a 15% increase in heart rate. Cardiac output was not altered. Although dopamine significantly increased azygos blood flow by 16%, wedged and free hepatic venous pressures were not altered. Dopamine significantly increased renal blood flow by 31%, but did not change the glomerular filtration rate. We conclude that a dopaminergic dose of dopamine increases azygos blood flow but not the hepatic venous pressure gradient. Finally, although it increases renal blood flow, dopamine does not seem to have any beneficial effects on glomerular filtration rate in cirrhotic patients.

Dopamine↗
PubMed1990

Hepatic vein thrombosis in Behçet's disease.

We describe four patients with hepatic vein thrombosis caused by Behçet's disease and review the 17 previously published cases. In addition, we compared these 21 cases of hepatic vein thrombosis to our 24 cases of hepatic vein thrombosis caused by primary myeloproliferative disorders. In patients with Behçet's disease, a male predominance (male/female ratio, 19:1) contrasted with the female predominance found in patients with hepatic vein thrombosis complicating primary myeloproliferative disorders (sex ratio = 1:3). The mean age at clinical onset was younger in patients with Behçet's disease than in those with primary myeloproliferative disorders (29 vs. 35 yr). Obstruction of the inferior vena cava was found in 90% of patients with hepatic vein thrombosis caused by Behçet's disease. Inferior vena caval thrombosis appears to be the main pathophysiological mechanism of hepatic vein thrombosis in patients with Behçet's disease. Unlike patients with primary myeloproliferative disorders who often had a progressive course, one third of patients with Behçet's disease had acute liver failure and died within 2 wk of clinical onset. These findings suggest that, in patients with Behçet's disease, hepatic vein thrombosis is a sudden event usually related to the extension of a caval thrombus to the ostium of the hepatic veins.

Adolescent↗
PubMed1990

Abnormal pressor response to vasopressin in patients with cirrhosis: evidence for impaired buffering mechanisms.

In patients with cirrhosis, vasopressin infusion induces sustained vasoconstriction and elevation of arterial pressure. The vasopressor effect could be caused by impairment of mechanisms normally aimed at buffering increases in arterial pressure (reflex bradycardia and decreases in arteriolar resistance). We studied the acute effects of continuous vasopressin infusion (0.4 IU/min) on systemic hemodynamics in seven patients with cirrhosis and in six patients without cirrhosis (controls). Vasopressin effects on systemic O2 consumption were also studied. In both groups, vasopressin infusion induced similar peak increases in arterial pressure, followed by similar decreases in heart rate and cardiac output. However, cirrhotic patients and controls differed 30 min after the start of vasopressin infusion. At 30 min, mean arterial pressure, diastolic arterial pressure and systemic vascular resistance remained significantly higher than preinfusion values in patients with cirrhosis. No decrease in systemic O2 consumption occurred in cirrhotic patients. In controls, at 30 min, mean arterial pressure and diastolic arterial pressure had returned to baseline. Systemic vascular resistance was not significantly higher than the preinfusion value and systemic O2 consumption had significantly decreased to below preinfusion values. We conclude that the vasopressor effect of vasopressin is abnormally sustained in patients with cirrhosis. This might be caused by insufficient buffering of vasopressin-induced arteriolar constriction rather than by abnormal vagal control of heart rate. In turn, as suggested by the lack of a decrease in systemic O2 consumption, persistent arteriolar constriction might be related to abnormally sustained sympathetic vascular tone in patients with cirrhosis.

Adult↗
PubMed1990

Calcified hepatic and renal cysts in adult dominant polycystic kidney disease.

We report the case of a 56-year-old woman suffering from adult dominant polycystic kidney disease, treated by hemodialysis, in whom calcifications of the wall of hepatic and renal cysts developed. The possibility that cystic calcifications might be the consequence of secondary hyperparathyroidism is discussed.

Calcinosis↗