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Biomedical subjects

A Braillon

Publications and source records attributed to A Braillon.

At least 55 records · Page 3Linked to original sources
PubMed1989

Somatostatin analogue improves survival in conscious cirrhotic rats subjected to gastrointestinal bleeding.

1. The continuing doubt concerning the value of vasoconstrictive therapy for gastrointestinal bleeding may be related to the complexity of clinical trials in such a situation. 2. The effect of SM 201-995, a somatostatin analogue, was investigated in conscious cirrhotic rats before, during and after experimental bleeding from the portal territory. 3. Before haemorrhage, somatostatin analogue (8 micrograms h-1 kg-1 body weight, intravenously) produced a significant decrease in portal pressure (17%), whereas a placebo (saline) lacked significant effect. 4. The rats were then subjected to spontaneous bleeding, by disconnection of the portal catheter from the pressure gauge, for a 5 min period. At the end of the haemorrhage, haemodynamic parameters did not significantly differ between the group receiving somatostatin analogue and that receiving placebo. 5. Fifteen minutes after the end of the bleeding period, portal pressure was significantly lower in rats receiving somatostatin analogue [8.5 +/- 0.5 mmHg (1.13 +/- 0.07 kPa), mean +/- SEM] than in rats receiving placebo [11.0 +/- 1.1 mmHg (1.50 +/- 0.15 kPa)]. 6. The volume of blood lost and mortality were significantly lower in the group treated with somatostatin analogue (2.3 +/- 0.1 ml/100 g body weight and 8%, respectively) than in the group receiving placebo (3.0 +/- 0.1 ml/100 g body weight and 50%, respectively). 7. These results demonstrate, in an experimental model, the beneficial effect of somatostatin analogue for the treatment of gastrointestinal bleeding due to portal hypertension. They suggest that administration of this substance should be started as soon as possible after the beginning of haemorrhage and continued after the cessation of bleeding.

Animals↗
PubMed1989

Hemodynamic effects of a combination of clonidine and propranolol in conscious cirrhotic rats.

The hemodynamic effects of the combination of clonidine and propranolol were studied in conscious rats with portal hypertension owing to secondary biliary cirrhosis. Pressure and blood flow measurements (radioactive microsphere method) were performed in three groups of eight rats before and after drug administration. The combined effects of clonidine (2 micrograms/100 g body wt., i.v.) and propranolol (0.2 mg/min for 10 min) were compared with those observed after administration of either clonidine alone or propranolol alone. The association of clonidine and propranolol induced significant decreases in portal pressure (30%) and portal tributary blood flow (43%), the magnitude of these changes being significantly more marked than that after administration of either clonidine alone (12 and 20%, respectively) or propranolol alone (16 and 17%, respectively). After the combination, no significant change in arterial pressure was observed, but cardiac output significantly decreased and systemic vascular resistance significantly increased. Renal blood flow decreased to a similar extent (40%) in the three groups. These findings indicate that the combination of clonidine and propranolol is more effective for reversing splanchnic hemodynamic changes than clonidine alone or propranolol alone. The additive effects of this association are in agreement with the action of clonidine and propranolol at different levels (central and peripheral) and on different receptors (alpha and beta). It suggests that an increase in sympathetic activity may play a major role in hemodynamic changes observed in experimental cirrhosis.

Animals↗
PubMed1989

[Tissue hypoxia and hepatocellular insufficiency in patients with cirrhosis].

To determine whether tissue hypoxia occurred in cirrhosis, oxygen contents, mixed venous and hepatic venous lactate concentrations as well as systemic hemodynamics were studied in 53 patients with cirrhosis. The influence of liver failure on tissue oxygenation was also studied. Cardiac index and mixed venous and hepatic venous lactate concentrations were significantly higher in patients with cirrhosis than in 20 control subjects. Oxygen consumption, oxygen extraction ratio and mixed venous and hepatic venous carbon dioxide tensions were significantly lower in the former than in the latter. Oxygen transport was not significantly different between the two groups. Cardiac index and oxygen transport were not significantly different between grade A (Pugh's classification) and grade C patients. Mixed venous as well as hepatic venous lactate concentrations were significantly higher while oxygen consumption, oxygen extraction ratio and carbon dioxide tensions were significantly lower in grade C than in grade A patients. We conclude that tissue hypoxia occurs in patients with cirrhosis and hepatic insufficiency. This tissue hypoxia might be due to arteriovenous shunting-related limitation of tissue oxygen extraction.

Adult↗
PubMed1989

[Influence of ascites on splanchnic and systemic hemodynamics in patients with alcoholic cirrhosis].

The effect of ascites on splanchnic and systemic hemodynamics was retrospectively studied in 256 patients with alcoholic cirrhosis. The patients were divided into 3 classes: no ascites, moderate ascites, and large ascites. They were also classed into 3 groups according to a modified Pugh classification (ascites was not taken into account). In patients without ascites, cardiac output was positively related to the severity of liver disease. This result was not found in patients with large ascites. Similarly, in patients with no or moderate ascites, the degree of portal hypertension estimated by the hepatic venous pressure gradient was associated with liver failure. In patients with large ascites, hepatic venous pressure gradient was higher than in patients without ascites but this relation was observed only in patients without liver failure. These results show that ascites reduces the relation between cardiac output and liver failure and increases the degree of portal hypertension but not cardiac output.

Ascites↗
PubMed1988

A simple method for chronic cannulation of the portal vein in intact unrestrained rats.

A simple new method is described for chronic cannulation of the portal vein in rats. A Silastic catheter (0.64 mm OD) with an internal metallic leader is directly inserted in the junction of the two small ileal veins. The catheter is advanced into the mesenteric vein to the portal vein. Then the leader is removed and the catheter tunneled out the back of the neck. This method allows for the measurement of portal vein pressure, direct injection of substances in the portal vein, or blood samples for at least 1 wk in intact unrestrained rats. Validation included the presence of elevated portal vein pressure in portal hypertensive rats compared with normal rats and the absence of clot development in the portal vein. This method should help provide a better understanding of hepatic physiology and pharmacology in normal and disease states.

Animals↗
PubMed1988

Continuous monitoring of portal vein and hepatic artery hemodynamics in unrestrained rats.

Continuous measurement of portal vein and hepatic artery blood flows during physiological experimental conditions, even in large animals, poses difficult problems. We report the successful use of miniaturized flow probes and pulsed Doppler flowmetry for chronic monitoring of hepatic artery and portal vein flows in intact unrestrained rats and describe the probe construction and implantation. Proportionality between portal vein velocity and portal flow was made possible by a technique for stabilizing the diameter of the venous segment from which velocity is recorded. The accuracy of the method in detecting changes in portal vein flow was established by the high statistically significant correlation between changes in velocity recorded simultaneously from portal vein and superior mesenteric artery in a series of rats with ligated celiac and inferior mesenteric arteries. In these preparations all portal vein flow is derived from the superior mesenteric artery. Complex dynamic changes in the hepatic circulation of conscious unrestrained rats were recorded in response to systemic injections of glucagon and angiotensin II. In the resting state several characteristic velocity patterns were recorded from the portal vein. Oscillations linked to respiration were not observed while the animals rested quietly but were noted during sleep and anesthesia. Two hitherto unrecognized patterns produced respectively by the pulsations of the superior mesenteric artery and by spontaneous contractions of the portal vein were also observed. The method described here provides the first opportunity to study hepatic circulation in chronically instrumented rats during physiological experimental conditions.

Animals↗
PubMed1988

Comparative haemodynamic effects of betaxolol and propranolol in patients with cirrhosis.

The acute effects of betaxolol (10 mg, intravenously), a new cardioselective beta-blocker, and propranolol (15 mg, intravenously) on splanchnic and systemic circulations were studied in two matched groups of six patients with portal hypertension due to cirrhosis. Similar decreases in hepatic venous pressure gradient and azygous blood flow--an estimation of superior portosystemic shunts--were observed after both drugs, whereas hepatic blood flow was not modified. The decreases in heart rate and cardiac index were also similar after betaxolol and propranolol. Both drugs induced a significant decrease in the fraction of cardiac output flowing through superior portosystemic shunts. These findings confirm that the marked effect of beta-adrenoceptor blocking agents on splanchnic circulation results both from the reduction in cardiac output and from a vasoconstriction of the portal vein territory, and demonstrate that this vasoconstriction of the portal vein area does not necessitate a beta 2-blocking activity of the drug. The similar efficiency of the two agents in decreasing the hyperkinetic circulation suggests that betaxolol merits further long-term study in the pharmacologic treatment of portal hypertension.

Adrenergic beta-Antagonists↗
PubMed1987

Pseudomonas aeruginosa liver abscesses following endoscopic retrograde cholangiography. Report of a case without biliary tract disease.

We report a case of Pseudomonas aeruginosa liver abscesses following endoscopic retrograde cholangiopancreatography (ERCP) in a patient without evidence of biliary tract disease and of any known cause of hepatic infection. Computer tomography (CT) scan was the best method of diagnosis, allowing, through guided percutaneous puncture of the abscesses, isolation of the organism, which was sensitive to carbenicillin. One month of antibiotherapy with repeated aspirations of the largest abscesses was successful. This report suggests that ERCP may induce cholangitic sepsis by inoculating pathogens in the biliary tree even in the absence of extrahepatic obstruction.

Adult↗
PubMed1987

Reduction of intrahepatic vascular space in the pathogenesis of portal hypertension. In vitro and in vivo studies in the rat.

To elucidate a possible role for reduction of intrahepatic vascular space in the pathogenesis of portal hypertension, we studied a partially hepatectomized rat model in vitro and in vivo. The in vitro study used livers from normal, 1/3-hepatectomized, and 2/3-hepatectomized rats, and rats with cirrhosis caused by chronic bile duct ligation, for isolated, perfused flow-pressure plotting. Resistance to perfusion increased such that significant differences were found between all groups except the last two, which showed similar resistances. The in vivo study measured splanchnic blood flow by radioactive microspheres and portal pressure in anesthetized sham-operated and 1/3- and 2/3-hepatectomized rats. Although absolute portal tributary blood flows did not change, portal flow per gram of remnant liver showed significant increases: 1.57 +/- 0.32 ml/min X g liver, 2.52 +/- 0.60 ml/min X g liver, p less than 0.01; 3.48 +/- 1.04 ml/min X g liver, p less than 0.01, respectively. Although intrahepatic resistance increased significantly only in the 2/3-hepatectomized group, portal pressures increased significantly in both groups of hepatectomized rats: normal, 7.5 +/- 1.1 mmHg; 1/3-hepatectomized, 9.4 +/- 1.1 mmHg; and 2/3-hepatectomized, 11.1 +/- 1.2 mmHg. Thus, decreased intrahepatic vascular space caused by resection and hepatocellular hypertrophy leads to portal hypertension, thereby suggesting that this reduction in space may be the pathogenic factor common to a number of different theories of portal hypertension.

Animals↗
PubMed1987

Reversal of adrenaline-induced increase in azygos blood flow in patients with cirrhosis receiving propranolol.

In patients with cirrhosis, endogenous catecholamines may influence the circulatory effects of propranolol. We intended to evaluate the interaction of adrenaline and propranolol on azygos blood flow, an estimate of blood flow in the superior portosystemic collateral circulation. We investigated 6 patients with cirrhosis, 5 with good liver function, receiving an intravenous infusion of adrenaline (50 ng/kg/min) before and after administration of propranolol. The median value for baseline azygos blood flow was increased from 700 ml/min (range 340-1 470 ml/min) to 1 050 (range 570-1 840 ml/min) with adrenaline alone (P less than 0.05), and decreased to 610 ml/min (range 260-1 190 ml/min) with propranolol alone (P less than 0.05). The infusion of adrenaline given after propranolol further reduced azygos blood flow to a median value of 530 ml/min (range 200-730 ml/min) (P less than 0.05). Thus, following beta-adrenergic blockade, there is a reversal of the effects of adrenaline on azygos blood flow, which corresponds to a potentiation of the effects of propranolol. Similar endogenous adrenaline-propranolol interactions may play a role in preventing recurrent variceal bleeding in cirrhotic patients.

Adult↗
PubMed1987

Failure of haemodynamic measurements to predict recurrent gastrointestinal bleeding in cirrhotic patients receiving propranolol.

In an attempt to identify the haemodynamic factors predicting the recurrence of gastrointestinal bleeding in cirrhotic patients receiving propranolol, haemodynamic measurements were prospectively collected. Systemic and splanchnic haemodynamics were assessed before propranolol administration. Among 77 patients receiving propranolol, 24 re-bled and 53 did not re-bleed in a follow-up period of 30-730 days (median 540). There was no difference between patients with and without recurrent bleeding with regard to the initial value of heart rate, mean arterial pressure, cardiac index, and hepatic venous pressure gradient. A subgroup of 43 patients was further investigated for the haemodynamic response to one single dose of 40 mg of propranolol. No difference was observed in the propranolol-induced changes of heart rate, mean arterial pressure, cardiac index or hepatic venous pressure gradient, between patients with (n = 14) and those without (n = 29) recurrent bleeding while taking propranolol. In conclusion, systemic haemodynamics and hepatic venous pressure gradient have no predictive value in evaluating the risk of recurrent bleeding in cirrhotic patients receiving propranolol. Furthermore, therapeutic efficacy of propranolol cannot be predicted from the haemodynamic response to a single first dose of this substance.

Adult↗
PubMed1987

[Hepatocellular carcinoma invading the right atrium: clinical, echographic and angiographic study].

The authors report the case of a 54 year old woman suffering from hepatocellular carcinoma with tumor growth into right hepatic vein, inferior vena cava and right atrium. On cardiac examination, a pansystolic bruit and a diastolic rumble were audible at the tricuspid focus. Diagnosis was confirmed by inferior vena cavography and two-dimensional echocardiography, which demonstrated a large mobile mass in the right atrium moving to and fro through the tricuspid valve. This case report emphasizes the value of routine cardiac examination during the course of hepatocellular carcinoma.

Carcinoma, Hepatocellular↗