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Biomedical subjects

D Lebrec

Publications and source records attributed to D Lebrec.

At least 253 records · Page 14Linked to original sources
PubMed1986

[Prevention of recurrent hemorrhage due to portal hypertension].

Gastrointestinal bleeding due to portal hypertension is a severe complication in patients with cirrhosis. Recurrent hemorrhage occurs in 75% of patients at 2 years, and medical treatment aims to induce a permanent decrease in portal pressure. A controlled study demonstrated that continuous administration of propranolol significantly decreased the risk of recurrent gastrointestinal bleeding in selected cirrhotic patients in good health. This efficacy was not found in unselected patients. The risk of recurrent gastrointestinal bleeding correlates with the development of hepatocellular carcinoma and poor compliance. Sclerotherapy of esophageal varices consists in obstruction of the varicosities. It has been demonstrated that esophageal sclerotherapy significantly reduces recurrent gastrointestinal bleeding, although a number of complications may occur.

Double-Blind Method↗
PubMed1986

Comparison of the circulation between fed and fasted normal and portal hypertensive rats.

The radioactive microsphere technique with the reference sample method was used for simultaneous determinations of splanchnic organ blood flow and cardiac output in fed and fasted anesthetized control rats and in rats with portal hypertension due to portal vein stenosis. Portal tributary blood flow was significantly higher in control (27.35 +/- 1.82 versus 14.60 +/- 0.96 ml/min) and in portal hypertensive (25.45 +/- 0.71 versus 20.09 +/- 1.27 ml/min) fed animals than in fasted rats, respectively. This difference was due to an increase in most of the splanchnic organ blood flows expressed in terms of either milliliter per minute or milliliter per minute per gram of tissue. The distribution of the cardiac output to the portal venous territory was also increased in fed animals as compared to fasted rats. In contrast, hepatic arterial blood flow was lower in fed animals than in fasted rats in both groups. Cardiac output was also significantly elevated in fed animals. This study demonstrates that the baseline circulatory state that depends on the digestive condition of these rats must be considered for splanchnic hemodynamic studies.

Animals↗
PubMed1986

Circulatory actions of vasopressin in anaesthetized rats with portal hypertension subjected to haemorrhage.

To assess the influence of vasopressin on splanchnic and renal circulatory changes induced by haemorrhage in portal hypertension, we studied 4 groups of 7 rats with chronic portal vein stenosis. Two groups received saline (C and H) and two groups vasopressin, 0.01 IU/kg/min (VP and VP-H). Ten minutes after starting drug infusion, group H and VP-H animals were allowed to bleed from the superior mesenteric vein. Both haemorrhage and vasopressin alone, decreased portal venous tributary blood flow and pressure but their association was not additive (as reflected by comparable bleeding rate in groups H and VP-H). By contrast, vasopressin increased renal perfusion in bleeding and non-bleeding animals whereas haemorrhage alone decreased renal perfusion. These results indicate that the effects of vasopressin on the splanchnic circulation in bleeding anaesthetized animals differ from the effects observed when blood volume is normal. Therefore, in patients with cirrhosis the effects of vasopressin during bleeding might also differ from those observed in patients in stable condition.

Anesthesia↗
PubMed1986

Alteration in response of the portal tributary vascular bed to the beta-agonist dobutamine in rats with extrahepatic portal hypertension.

The acute effects of 2 doses of the beta-agonist dobutamine on systemic and splanchnic haemodynamics were studied in normal rats and in rats with portal hypertension due to portal vein stenosis. Cardiac output and splanchnic organ blood flow were estimated with the radioactive microsphere method and portal pressure was measured. Low dose (5 micrograms/kg) of dobutamine did not change significantly arterial pressure and portal pressure but, cardiac output was significantly higher after dobutamine than after placebo in both groups of rats. Similar results were observed with 15 micrograms/kg of dobutamine except for a significant decrease in arterial pressure in portal-hypertensive rats. In sham-operated rats, dobutamine significantly increased portal tributary blood flow; this rise was parallel to cardiac output. In contrast, in portal-hypertensive rats, portal tributary blood flow did not change significantly after dobutamine. Accordingly in the former group, portal tributary vascular resistance significantly decreased, whereas in the latter group, no change in this resistance was observed with a low dose and a significant decrease was noted with a high dose. In both groups of rats, hepatic arterial blood flow was not significantly different after dobutamine than after placebo. This study demonstrates that the vasodilatory response of the portal tributary vascular bed to an increase in cardiac output is altered in anaesthetized rats with portal hypertension due to portal vein stenosis.

Animals↗
PubMed1986

Haemodynamic rebound phenomena after abrupt cessation of propranolol therapy in portal hypertensive rats.

The haemodynamic effect of sudden termination of propranolol therapy was studied in sham-operated and portal hypertensive rats. All animals were injected with propranolol (20 mg/kg/day) or saline i.p. for 10 days, then had an isoproterenol infusion test performed 48 h or 72 h after cessation of injections. The dose of isoproterenol required to increase the heart rate by 50 beats/min (CD50), was significantly lower in both sham-operated and portal hypertensive rats at 48 h after propranolol withdrawal. Maximum chronotropic response (Rmax), was significantly higher only in portal hypertensive rats at 48 h after propranolol withdrawal. These results show the existence of a transient beta-adrenergic hypersensitivity state following propranolol withdrawal in normal and portal hypertensive rats.

Animals↗
PubMed1986

Noncirrhotic intrahepatic portal hypertension.

Portal hypertension, widely recognized as a complication of cirrhosis, may also develop as an intrahepatic consequence of numerous hepatic disorders in the absence of cirrhosis. When gastrointestinal bleeding occurs in such cases, ruptured esophageal varices must be considered. Among chronic liver diseases, some, such as schistosomiasis, are commonly associated with portal hypertension and its complications. In others, including tuberculosis, amyloidosis, and polycystic disease, well-documented portal hypertension has been reported in only a small minority of cases. Nevertheless, because of the ever-present possibility of variceal hemorrhage whenever portal hypertension occurs, clinicians should be aware of these disorders. Acute conditions associated with noncirrhotic intrahepatic portal hypertension include acute (and particularly fulminant) viral or drug-induced hepatitis, acute alcoholic hepatitis, acute veno-occlusive disease, and acute fatty liver of pregnancy. Portal hypertension may be reversible following recovery in these settings. Particular attention is called to the increasing frequency of acute veno-occlusive disease on bone marrow transplant units, presumably as a complication of high-dose chemo- and radiotherapy.

Adolescent↗
PubMed1986

Alterations in isoprenaline sensitivity in patients with cirrhosis: evidence of abnormality of the sympathetic nervous activity.

Isoprenaline sensitivity and plasma catecholamine concentrations were studied to assess the sympathetic nervous activity in 13 patients with alcoholic cirrhosis and were compared with five controls. In patients with cirrhosis, the dose of isoprenaline required to increase the resting heart rate by 25 beats min-1 (chronotropic dose 25 or CD25) ranged from 2.50 to 34.73 micrograms (median: 4.47 micrograms) and was significantly higher than in controls (range: 0.66 to 2.76 micrograms, median: 1.34 micrograms). In cirrhotic patients, CD25 values were significantly correlated with plasma albumin concentration, resting heart rate and wedged hepatic venous pressure. In patients with cirrhosis, plasma noradrenaline concentrations ranged from 192 to 978 pg ml-1 (median: 444 pg ml-1) and adrenaline concentrations ranged from 5 to 183 pg ml-1 (median: 47 pg ml-1). No correlation was found between noradrenaline or adrenaline concentrations and CD25 values in cirrhotic patients. In conclusion, in patients with cirrhosis, beta-adrenoceptor responsiveness assessed by isoprenaline sensitivity is altered.

Adult↗
PubMed1986

Influence of the degree of liver failure on systemic and splanchnic haemodynamics and on response to propranolol in patients with cirrhosis.

Systemic and splanchnic haemodynamics were studied in patients with cirrhosis who had been classified in three groups (A, B, and C) according to the degree of liver failure (modified Pugh's classification). In patients of group A, cardiac index was significantly lower than that of group C and systemic vascular resistance was higher, but not significantly so, than that of patients with liver failure. Wedged hepatic venous pressure was significantly lower in the former group than in the latter. In patients in group B, corresponding values fell between those of groups A and C. Azygos blood flow averaged 0.477 +/- 0.242 l/min (mean +/- SD) in group A and it was significantly lower than in groups B and C (0.642 +/- 0.224 and 1.061 +/- 0.476 l/min, respectively). In the three groups, acute administration of propranolol induced statistically significant changes in systemic and splanchnic haemodynamics. In patients of group C but not of group B, the mean value of azygos blood flow after propranolol remained significantly higher than in group A. Moreover, the fraction of azygos blood flow to cardiac output decreased in groups A and B while slightly increased in group C. This study shows that in patients with cirrhosis, the degree of liver failure may be a determinant for the haemodynamic responses to drugs acting on portal hypertension.

Female↗
PubMed1986

Hemodynamic characterization of chronic bile duct-ligated rats: effect of pentobarbital sodium.

Systemic and splanchnic hemodynamics of the chronic bile duct-ligated rat were characterized by radioactive microspheres. Conscious and pentobarbital sodium-anesthetized, bile duct-ligated and sham-operated rats had cardiac output and regional organ blood flows determined. The conscious bile duct-ligated rat compared with the sham-operated showed a hyperdynamic circulation with an increased cardiac output (153.3 +/- 9.8 vs. 112.6 +/- 6.0 ml/min, P less than 0.005) and portal tributary blood flow (21.32 +/- 1.43 vs. 12.79 +/- 1.47 ml/min, P less than 0.005). Pentobarbital sodium anesthesia induced marked hemodynamic changes in both sham-operated and bile duct-ligated rats. The latter group was especially sensitive to its effects; thus, comparison of cardiac output and portal tributary blood flow between anesthetized bile duct-ligated and sham-operated rats showed no significant differences. We conclude that the rat with cirrhosis due to chronic bile duct ligation is an excellent model for hemodynamic investigations but should be studied in the conscious state, since pentobarbital sodium anesthesia eliminates the hyperdynamic circulation.

Anesthesia, General↗
PubMed1986

Domperidone-induced increase in lower oesophageal sphincter pressure does not affect azygos blood flow in patients with cirrhosis.

An increase in lower oesophageal sphincter pressure induced by domperidone has previously been reported to decrease superior portosystemic collateral flow in patients with portal hypertension owing to cirrhosis. Although a 10-mg intravenous dose of domperidone was effective in increasing lower oesophageal sphincter tone in a group of six patients with cirrhosis, the same dose failed to affect azygos blood flow in a matched group of six patients. The results do not support the hypothesis that an increase in lower oesophageal sphincter tone can decrease flow through oesophageal varices in patients with cirrhosis.

Domperidone↗
PubMed1986

Role of portasystemic shunts in the hyperkinetic circulation of the portal hypertensive rat.

We evaluated the role of portasystemic shunts in the hyperkinetic circulatory state in rats with portal hypertension. Cardiac output and regional blood flow were measured by the radioactive microsphere technique in rats with portal hypertension caused by portal vein stenosis, in rats with end-to-side portacaval shunts, and in sham-operated rats. Cardiac output was significantly higher in rats with surgical shunts than in those of the two other groups and was significantly lower in sham-operated rats compared with portal hypertensive rats. Portal tributary blood flow and hepatic arterial blood flow expressed in absolute flow as well as in percentage of cardiac output were significantly increased in rats with surgical shunts compared with other groups. These blood flows were also significantly higher in portal hypertensive rats than in sham-operated animals. A significant correlation was found between cardiac output and portal tributary blood flow in rats with portal vein stenosis and in rats with surgical shunts; this correlation was absent in sham-operated rats. This study shows that the hyperkinetic circulatory state in rats with portal hypertension and a normal liver is related to the presence of portasystemic shunts but not to portal hypertension per se.

Animals↗
PubMed1985

Relationship between dose, blood level and haemodynamic response in patients with cirrhosis receiving propranolol.

Fifty-two patients with cirrhosis receiving continuous administration of propranolol in doses reducing the heart rate by 25% were studied. The doses and plasma levels varied widely - 185 +/- 98 mg/day (mean +/- SD) and 208 +/- 153 ng/ml, respectively. These values were significantly correlated. No significant correlation was found between the dose of the drug or plasma level and the liver function tests. Although propranolol significantly decreased cardiac output and the hepatic venous pressure gradient, no correlation was found between drug dose or plasma level and these haemodynamic effects.

Adult↗
PubMed1985

Granulomonocytic colony forming cells in myelofibrosis: concentrations within hepatic blood and peripheral blood.

Hepatic and peripheral blood GM-CFC concentrations were compared in 8 cases of myelofibrosis. Hepatic blood concentrations were significantly higher (p less than 0.05). The density-distribution profile for hepatic blood GM-CFCs shifted to the left as compared to peripheral blood in 4 cases out of 5. The maximal blood transit time for circulating GM-CFCs was about 1 min. These results suggest that spleen and liver are a production site of blood GM-CFCs in myelofibrosis. In particular, they would be responsible for the presence in blood of the lightest GM-CFCs (less than 1.060 g cm-3). Increased GM-CFC inflow from bone marrow and/or liver and spleen to blood is the single explanation for the increased value of the circulating GM-CFCs.

Blood Circulation↗
PubMed1985

Acute effects of captopril on systemic and renal hemodynamics and on renal function in cirrhotic patients with ascites.

The reduction of angiotensin II production by captopril--an angiotensin-converting enzyme inhibitor--could suppress hyperaldosteronism without impairment of renal function and could thereby be useful in the treatment of ascites in patients with cirrhosis. Systemic and renal hemodynamics and renal function were studied in 6 nonazotemic patients with cirrhosis and ascites with a low-sodium diet before and after oral administration of 25 mg of captopril. Cardiac output and renal blood flow did not change significantly after administration of captopril, whereas mean arterial pressure significantly decreased. Systemic and renal vascular resistances were significantly reduced. There was a statistically significant reduction of glomerular filtration rate, filtration fraction, and urinary output. Plasma renin activity significantly increased in all patients after administration of captopril. A statistically significant correlation was found between the decrease in mean arterial pressure and the reduction of glomerular filtration, but no relationship was found between basal values of plasma renin activity and the other observed variations. We concluded that captopril mainly induces hypotension due to an increase in renal vasodilatation in ascitic patients with cirrhosis.

Ascites↗
PubMed1985

Superior portosystemic collateral circulation estimated by azygos blood flow in patients with cirrhosis. Lack of correlation with oesophageal varices and gastrointestinal bleeding. Effect of propranolol.

In patients with cirrhosis, superior portosystemic collateral circulation was evaluated by the continuous thermodilution method in the azygos vein. Azygos blood flow was 5 times higher in a group of patients with cirrhosis (alcoholic in 27, cryptogenic in 8, post-hepatitic in 2 and primary biliary cirrhosis in 1), than in a group of patients without portal hypertension (steatosis in 2, granulomatous hepatitis in 2, persistent chronic hepatitis in 2 and Hodgkin's disease in 1). Azygos blood flow was not different in cirrhotic patients with no visible, in those with small-sized, and in those with large sized oesophageal varices. Azygos blood flow was not different in cirrhotic patients with and without a previous episode of gastrointestinal bleeding. Fifteen min after intravenous administration of 15 mg of propranolol, azygos blood flow significantly decreased whereas azygos blood flow did not change after placebo. The decrease in azygos blood flow was significantly more marked than the reduction in cardiac output. It is concluded that superior portosystemic collateral blood flow is elevated in patients with cirrhosis and that the reduction in this collateral circulation might explain the efficiency of propranolol in the prevention of recurrent gastrointestinal bleeding.

Azygos Vein↗
PubMed1985

Acute effect of propranolol on splanchnic circulation in normal and portal hypertensive rats.

Propranolol decreases portal venous pressure in patients with cirrhosis but no method is available in man to study the effect of this beta-blocker on splanchnic organ blood flow. Because in rats, the microsphere method allows evaluation of regional blood flow, the acute effect of propranolol on both splanchnic and systemic circulations was studied in normal rats and in rats with portal hypertension due to portal vein stenosis. Portal venous pressure significantly decreased during propranolol administration in normal (5.6 +/- 1.0-4.7 +/- 1.1 mm Hg; mean +/- SD) as well as in portal hypertensive rats (11.7 +/- 2.3-10.3 +/- 1.8 mm Hg). Propranolol slightly decreased cardiac output and arterial pressure in all rats. Portal tributary blood flow was significantly reduced by propranolol in normal rats (17.4 +/- 3.0-11.3 +/- 2.2 ml/min) and in portal hypertensive rats (23.7 +/- 5.0-16.6 +/- 3.3 ml/min). Accordingly vascular resistance of the different organs in the portal venous territory increased in these rats receiving propranolol. The percentage of the decrease in portal tributary blood flow was significantly more marked than the percentage of reduction in cardiac output in portal hypertensive rats but, in normal rats, these percentages were parallel. Hepatic arterial blood flow did not change or slightly increased and, consequently, hepatic arterial vascular resistance decreased. These findings further clarify the marked effects of propranolol on splanchnic circulation.

Animals↗