PubMed Health⌕ Search

Biomedical subjects

D Valla

Publications and source records attributed to D Valla.

At least 163 records · Page 9Linked to original sources
PubMed1985

Budd-Chiari syndrome: US evaluation.

Twelve patients with proved Budd-Chiari syndrome (eight acute and four chronic cases) were examined, using real-time ultrasonography (US). In all acute cases, US study showed at least one hepatic vein with findings suggestive of the syndrome, such as stenosis, dilatation, thick wall echoes, thrombosis, abnormal course, or extrahepatic anastomosis. In chronic cases, hepatic veins were usually not visible. Modifications of liver morphology were present in all patients except those with recent onset of the disease. Caudate lobe hypertrophy was present in only six cases. US study is therefore the procedure of choice for initial diagnosis of acute Budd-Chiari syndrome. Pitfalls were the failure to detect two caval thromboses and one hepatic vein web. Cavography should still be performed systematically, but hepatic phlebography is useful in selected cases only.

Adult↗
PubMed1985

Effects of pentobarbital sodium anesthesia on splanchnic hemodynamics of normal and portal-hypertensive rats.

To determine the effect of pentobarbital sodium anesthesia on the rat with portal hypertension due to portal vein stenosis, four groups of rats were studied. Cardiac output and regional blood flow were measured by radioactive microspheres in anesthetized and conscious sham-operated and portal-hypertensive rats. Anesthesia markedly decreased cardiac output in both sham-operated (109.7 +/- 4.6 vs. 77.8 +/- 1.4 ml/min, P less than 0.001) and portal-hypertensive rats (130.1 +/- 7.6 vs. 93.8 +/- 5.3 ml/min, P less than 0.01). In spite of this diminution in cardiac output, pentobarbital did not significantly change absolute blood flow values of splanchnic organs in either group. However, the fractions of cardiac output perfusing the splanchnic organs were significantly increased by pentobarbital in both groups because of the decrease in cardiac output: sham operated, anesthetized, 22.86 +/- 1.19% vs. conscious, 14.83 +/- 1.02%, P less than 0.001; and portal hypertensive, anesthetized, 26.67 +/- 0.71% vs. conscious, 19.07 +/- 1.44%, P less than 0.001. The hyperdynamic circulation of the portal vein-stenosed rat compared with the sham-operated rat continued to manifest itself with significantly increased portal pressure, cardiac output, and splanchnic blood flow, whether the animal was anesthetized or awake. We conclude that, despite marked hemodynamic changes induced by pentobarbital, the rat with portal vein stenosis remains a useful experimental model of portal hypertension.

Anesthesia, General↗
PubMed1985

Primary myeloproliferative disorder and hepatic vein thrombosis. A prospective study of erythroid colony formation in vitro in 20 patients with Budd-Chiari syndrome.

We assessed the prevalence of overt and latent primary myeloproliferative disorders in hepatic vein thrombosis. Cultures of bone marrow or peripheral blood mononuclear cells were done in 20 patients with Budd-Chiari syndrome. Erythroid colony formation in the absence of erythropoietin, which is a reliable indicator for a primary myeloproliferative disorder, was seen in 16 patients in whom Budd-Chiari syndrome was due to hepatic vein thrombosis, including 13 women aged 18 to 45 years. Among these 16 patients, the conventional criteria for the diagnosis of a primary myeloproliferative disorder were met in only 2. Primary myeloproliferative disorder, often without peripheral blood changes, is a major cause of hepatic vein thrombosis in young women.

Adolescent↗
PubMed1985

[Effects of glypressin on the splanchnic and systemic circulation in patients with cirrhosis].

Although not demonstrated in patients with cirrhosis, it is generally claimed that administration of vasopressin in the form of triglycyl-lysine-vasopressin (glypressin) may prevent untoward systemic effects of this former hormone. The aim of this study was to assess the effects of intravenous administration of 2 mg of glypressin on splanchnic and systemic hemodynamics in 9 patients with cirrhosis under stable circulatory conditions. One hour after the injection, the following statistically significant changes were observed as compared to the baseline values (m +/- SEM): wedged hepatic venous pressure, -9 +/- 2 p. 100; hepatic venous pressure gradient, -16 +/- 3 p. 100; azygos blood flow, -24 +/- 6 p. 100; heart rate, -16 +/- 3 p. 100; cardiac index, -23 +/- 2 p. 100; systemic vascular resistances, +47 +/- 11 p. 100; wedged pulmonary arterial pressure, +44 +/- 15 p. 100. In conclusion, in patients with cirrhosis in a stable hemodynamic condition, intravenous administration of glypressin decreased portal venous pressure and blood flow into the superior portal systemic collateral circulation but did not prevent the untoward systemic hemodynamic effects of vasopressin.

Adult↗
PubMed1984

Vasopressin perfusion of esophageal varices in cirrhotic patients: cineangiographic study.

Portal cineangiography after umbilicoportal cannulation was used to evaluate esophageal vein perfusion and diameter in 13 cirrhotic patients with severe portal hypertension, prior to and during intravenous vasopressin infusion (0.35 IU per min). Between the 15th and the 20th minute of infusion no change had occurred in the diameters of left gastric veins, esophageal varices, portal veins, or splenic veins. Considerable reduction in the left gastric vein perfusion was indirectly documented by prolongation of washout time (greater than + 145%) and increase in vascular density. These modifications were disproportionate in relation to the simultaneous changes in portal pressure (-16%). These results demonstrate that during vasopressin infusion: (a) there is no constriction of the varices at the level of the lower esophageal sphincter; (b) there is a marked decrease in the perfusion of left gastric vein and esophageal varices; and (c) there is a moderate portal pressure decrease which, by itself, may not be a reliable index of the splanchnic hemodynamic response to vasopressin in cirrhotic patients.

Adult↗
PubMed1984

Effects of propranolol on renal blood flow and renal function in patients with cirrhosis.

Systemic and splanchnic hemodynamics, renal blood flow, and renal function were studied in 13 patients with cirrhosis both before and 1 h after oral administration of 40 mg of propranolol (acute administration) and 1 mo after continuous administration of this substance at doses reducing the heart rate by 25% (chronic administration). Cardiac output and the gradient between wedged and free hepatic venous pressures significantly decreased after acute and chronic administration of propranolol; mean arterial pressure did not change significantly and systemic vascular resistance significantly increased. Renal blood flow and renal vascular resistance did not change significantly after acute administration of propranolol and renal function did not change significantly after acute or chronic administration of propranolol. We conclude that propranolol does not alter renal function in patients with cirrhosis who are in good physical condition.

Aldosterone↗
PubMed1984

Discrepancy between wedged hepatic venous pressure and portal venous pressure after acute propranolol administration in patients with alcoholic cirrhosis.

In patients with alcoholic cirrhosis, wedged hepatic venous pressure closely reflects portal venous pressure. This study was carried out to determine if propranolol-induced reductions in portal venous pressure are accurately evaluated by the measurement of wedged hepatic venous pressure. Hepatic venous cannulation and percutaneous transhepatic catheterization of the portal vein were simultaneously performed in 7 patients with alcoholic cirrhosis. One hour after oral administration of 40 mg of propranolol, wedged hepatic and portal venous pressures significantly decreased from 24.3 +/- 3.5 (mean +/- SD) to 19.0 +/- 3.0 mmHg, and from 24.7 +/- 3.9 to 22.4 +/- 3.6 mmHg, respectively. Although no significant difference was found between baseline wedged hepatic and portal venous pressures, a significant difference was found between these pressures after propranolol administration. We concluded that during acute administration of a drug acting on the splanchnic circulation, the measurement of wedged hepatic venous pressure may not provide a reliable estimation of the magnitude of the changes in portal venous pressure. There is, however, no evidence that the direction of the changes might not be adequately assessed by wedged hepatic venous pressure measurement.

Aged↗
PubMed1984

[Systemic circulatory hyperkinetic syndrome in patients with cirrhosis. Relation with hepatocellular failure and portal hypertension].

Hyperkinetic circulatory state is common in patients with cirrhosis but the cause of this syndrome has not been clearly elucidated. Systemic hemodynamic changes and their relationship to liver failure and splanchnic hemodynamics were studied in 100 patients with cirrhosis and were compared to a group of 15 patients without portal hypertension. Cardiac output was significantly higher and systemic vascular resistance was significantly lower in cirrhotic patients than in control patients. Multivariate analysis revealed that among different clinical, biochemical and splanchnic hemodynamic data, serum albumin, serum bilirubin, plasma prothrombin, and gastrointestinal bleeding significantly and independently explained the variation of cardiac output and systemic vascular resistance. No relationship was found between hepatic venous pressures or the presence of ascites and the hyperkinetic syndrome. From these results, it is concluded that in patients with cirrhosis liver failure is partly responsible for the hyperkinetic state.

Adult↗
PubMed1983

Right-sided endocarditis complicating peritoneovenous shunting for ascites.

We describe two patients with alcoholic cirrhosis in whom staphylococcal right-sided endocarditis developed after insertion of a peritoneovenous shunt (PVS). Massive pulmonary embolism caused early death in one patient. In the other patient, staphylococcal septicemia was cured after shunt removal and antibiotic treatment; recurrent endocarditis due to Corynebacterium xerosis ultimately caused the patient's death. No clinical manifestation of tricuspid valve dysfunction was noted in either patient, and right-sided endocarditis was recognized only at autopsy. The protracted contact of the tip of the venous line of PVS with the atrial wall is likely to be a major factor in the development of right-sided endocarditis in these patients.

Adult↗
PubMedDate not supplied

Hemodynamic changes in patients with portal venous obstruction.

Splanchnic and systemic hemodynamics were evaluated in five adult patients with portal hypertension due to portal venous obstruction and were compared with those of patients with cirrhosis and those of a control group. In patients with portal venous obstruction, the gradient between wedged and free hepatic venous pressures ranged from 2 to 3 mm Hg, as in the control group, and was significantly lower than in patients with cirrhosis. Hepatic blood flow averaged 0.521 +/- 0.127 liter per min per m2 (mean +/- S.D.) and was significantly lower than that measured in cirrhotic and normal patients. Cardiac index averaged 3.788 +/- 0.629 liters per min per m2; this high value for cardiac index was not significantly different from that measured in cirrhotic patients, but was significantly higher than in patients of the control group. It is suggested that a hyperkinetic circulatory state may result from the development of portal-systemic venous collateral circulation in patients with portal venous obstruction having normal liver and hepatic venous pressures.

Adult↗
PubMedDate not supplied

Assessment of beta-adrenergic blockade with propranolol in patients with cirrhosis.

Fourteen patients with cirrhosis and bleeding esophageal varices were treated with propranolol. The dose of propranolol was determined by decreasing the resting heart rate by 25% 12 hr after an oral dose of propranolol which was given twice a day. Significant decreases in the hepatic venous pressure gradient and cardiac output after 1 month of propranolol administration was observed. To assess beta-adrenergic blockade, the isoproterenol test and plasma propranolol levels were evaluated. Increasing doses of isoproterenol were injected to increase the resting heart rate 25 beats per minute (chronotropic dose 25 or CD25 ). Plasma propranolol concentrations were measured in blood samples drawn 4 hr after the last oral dose. The mean CD25 was 5 +/- 2 micrograms before and 146 +/- 84 micrograms after 1 month of propranolol administration. The plasma propranolol level after 1 month of drug administration was 0.69 +/- 0.47 microM per liter i.e. 2.33 +/- 1.59 micrograms per ml. A significant correlation was found between the CD25 measured after continuous propranolol administration and plasma propranolol level. In conclusion, the efficacy of beta-adrenergic blockade was estimated by the isoproterenol test which correlates with the plasma propranolol level in patients with cirrhosis. This study suggests that the isoproterenol test is useful in assessing beta-adrenergic blockade with propranolol in patients with cirrhosis.

Cardiac Output↗
PubMedDate not supplied

Lack of vasopressin action on splanchnic hemodynamics during bleeding: a study in conscious, portal hypertensive rats.

Due to the marked effects of hemorrhage on cardiac output and splanchnic hemodynamics, the circulatory actions of vasopressin may differ during bleeding as opposed to stable conditions. We evaluated this hypothesis in conscious rats with portal hypertension due to chronic portal vein stenosis, by comparing the effects of a vasopressin infusion (0.02 IU per kg per min) to those of a control saline infusion, during and after a hypotensive hemorrhage (25 ml per kg). We also studied unbled portal hypertensive rats receiving an identical infusion of vasopressin or saline. During and after hemorrhage, vasopressin induced significant changes in systemic hemodynamics but had no effect on portal pressure, portal tributary blood flow and nonhepatic splanchnic arteriolar resistance. In unbled animals, by contrast, vasopressin decreased portal pressure and portal tributary blood flow and increased nonhepatic splanchnic arteriolar resistance. Our data further indicate that hemorrhage alone caused an early vasoconstriction in the portal tributaries and a delayed vasoconstriction in the nonsplanchnic vascular bed while vasopressin during hemorrhage induced an early and sustained vasoconstriction in the nonsplanchnic vascular bed as well as in the portal tributaries. The results show that, during and after severe bleeding, vasopressin exerts little influence on portal hemodynamics. Although these data do not allow firm conclusions concerning the therapeutic efficacy of vasopressin in bleeding esophageal varices, they demonstrate that the splanchnic actions of vasoactive substances cannot be readily extrapolated from stable conditions to hemorrhage.

Animals↗
PubMedDate not supplied

Transfusion-associated or nosocomial hepatitis G virus infection in patients undergoing surgery.

BACKGROUND: Despite blood donor screening, there are still cases of transfusion-associated hepatitis. From 1988 to 1992, a prospective study was conducted on the incidence of non-A, non-B posttransfusion hepatitis (PTH). STUDY DESIGN: The present investigation was designed to determine if transfusion recipients with PTH who are negative for hepatitis C virus (HCV) were positive for hepatitis G virus (HGV). Patients admitted for surgery who had normal liver tests and no transfusions during the previous 6 months were enrolled. Alanine amino transferase levels were determined monthly for 6 months after surgery and for 1 year in the case of PTH (defined as alanine aminotranferase twice the upper limit of normal in two consecutive assays). HGV RNA and E2 antibodies were tested for in samples from transfusion recipients with or without PTH and from nontransfused patients. RESULTS: Of the 308 blood recipients who were enrolled in the study, 21 (6.8%) had PTH. HGV RNA was detected at the onset of hepatitis in 3 patients with PTH (14%), 2 of whom were also anti-HCV and HCV RNA positive. One patient developed E2 antibodies without detectable HGV RNA. Three (10.7%) of 28 recipients of an allogeneic transfusion without PTH developed HGV infection. HGV RNA was also found in two nontransfused patients, which suggests nosocomial transmission of HGV. CONCLUSION: Some cases of PTH are associated with HGV; most cases of postoperative HGV infection are not associated with liver abnormalities; and most PTH cases are not associated with known hepatotropic viruses.

Adult↗