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Biomedical subjects

A Braillon

Publications and source records attributed to A Braillon.

88 records · Page 5Linked to original sources
PubMed1983

Metronidazole in prevention of cholestasis associated with total parenteral nutrition.

The effect of metronidazole on liver function tests was studied in patients given total parenteral nutrition (TPN) for an acute attack of Crohn's disease. In those receiving TPN and metronidazole, serum activities of alkaline phosphatase and gamma-glutamyl-transferase decreased or remained normal after 30 days of TPN. In contrast, serum activities of these enzymes increased significantly after 30 days of TPN alone. These results suggest that intrahepatic cholestasis associated with TPN may be related to intestinal overgrowth of anaerobic bacteria.

Acute Disease↗
PubMed1983

Bleeding cecal typhoid ulcer. Value of emergency angiography for selective surgical hemostasis.

A case of bleeding cecal typhoid ulcer in a 22-year-old patient demonstrated by superior mesenteric arteriography is described. An attempt to stop hemorrhage using intraarterial vasopressin infusion, failed. However, arteriography proved helpful in locating the bleeding site, and in permitting conservative surgery, namely cecal ulcer suture to achieve hemostasis. On the basis of this case and a review of the literature, management of complicating hemorrhage resulting from typhoid fever is discussed, with particular reference to radiological procedures.

Adult↗
PubMed1983

[Nodular regenerative hyperplasia of the liver. Study of 15 cases and review of the literature].

The authors report 15 cases of nodular regenerative hyperplasia (NRH) of the liver observed in 10 women and 5 men during a 9 year period. Gastrointestinal bleeding due to ruptured esophageal varices revealed the liver disease in 11 cases. Hepatomegaly and splenomegaly were noted in 9 cases and ascites in 7. Anicteric cholestasis was demonstrated in 10 cases. Another disease, e. g. myelofibrosis and monoclonal gammapathy, was present in 11 patients. In 10 patients, portal diversion was performed; outcome being favorable with a follow-up of one to six years. The analysis of these cases and of the 113 previously published reports calls for the following comments: 1) In most cases, NRH is characterized by small-sized hepatocytic nodules scattered throughout the entire liver with no surrounding fibrosis; however this histological pattern may vary somewhat, with adjacent normal zones being found adjacent to typical cirrhotic fibrosis; although a precise morphometric study was not performed in our patients, obstruction of the tiny branches of intrahepatic portal veins was not observed. 2) Histological diagnosis of NRH is difficult and in most cases requires surgical biopsy specimens and specific coloration of the reticulin network. 3) NRH must be considered as a new cause of intrahepatic (sinusoidal or presinusoidal) portal hypertension and/or of chronic anicteric cholestasis. 4) A number of various conditions may be associated with NRH, the most frequent being Felty's syndrome and myeloproliferative disorders. 5) The pathogenesis of NRH remains unknown. 6) Portal diversion generally has a favorable outcome in this disease.

Adult↗
PubMedDate not supplied

Hemodynamic effects of a clonidine-induced decrease in sympathetic tone in patients with cirrhosis.

A decrease in plasma noradrenaline--a reflection of sympathetic nervous system activity--by clonidine, a centrally acting alpha 2-agonist, could reduce the hyperdynamic circulation observed in cirrhosis and may thereby decrease portal hypertension. Plasma noradrenaline concentration and plasma renin activity as well as systemic and splanchnic hemodynamics were measured in 12 patients with cirrhosis and ascites before and after administration of either 150 micrograms of clonidine or placebo. Plasma noradrenaline concentration significantly decreased in all patients after clonidine administration, whereas plasma renin activity did not change significantly. There were statistically significant reductions of cardiac output (-17.4%), mean arterial pressure (-12.2%), hepatic venous pressure gradient (-19.7%) and azygos blood flow (-26.6%) after administration of clonidine. No significant correlation was found between the reduction of plasma noradrenaline concentration and changes in systemic or splanchnic hemodynamics. Hepatic blood flow was not changed by clonidine. Placebo administration had no effect on any laboratory or hemodynamic measurement. We conclude that the reduction in sympathetic nervous system activity by clonidine and the subsequent decrease in the hyperdynamic circulation suggests that sympathetic overactivity contributes to the circulatory derangements in patients with cirrhosis.

Aged↗
PubMedDate not supplied

Beneficial hemodynamic effects of ketanserin in patients with cirrhosis: possible role of serotonergic mechanisms in portal hypertension.

We studied the acute effects of ketanserin, a serotonin S2 antagonist, on systemic and splanchnic hemodynamics in 11 patients with cirrhosis. Mean arterial pressure decreased moderately but significantly after ketanserin. This effect was maximal at 5 min and correlated to the severity of cirrhosis. Cardiac index and systemic vascular resistance were not significantly changed. The hepatic venous pressure gradient, used as an index of portal pressure, significantly decreased after ketanserin (-23%). Azygos blood flow, a reflection of superior portosystemic collateral blood flow, also significantly decreased (-26%), but this effect was delayed, progressive and not correlated to the arterial pressure decrease. Hepatic blood flow was unchanged. These findings suggest that the systemic and splanchnic circulations may be hypersensitive to ketanserin in cirrhotic patients, and that serotonergic mechanisms may contribute to maintain portal hypertension. New specific antiserotonergic drugs deserve further evaluation for potential therapeutic implications in portal hypertension.

Azygos Vein↗
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

Effects of alpha 1 and beta-adrenergic antagonists and 5-hydroxytryptamine receptor antagonist on portal-systemic collateral vascular resistance in conscious rats with portal hypertension.

In order to study the acute effects of pharmacological agents on the vascular resistance of portal-systemic collaterals, a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the conscious rat. The haemodynamic effects of several vaso-active substances were evaluated in this model and compared with those obtained after saline administration. Prazosin (0.5 mg), an alpha 1-adrenergic antagonist, significantly reduced mean arterial pressure by 29%, portal pressure from 13.8 +/- 1.0(mean +/- s.e.m.) to 10.1 +/- 0.4 mmHg and portal tributary blood flow (radioactive microspheres) from 13.6 +/- 2.1 to 11.7 +/- 1.2 mL/min. It also decreased portal-systemic vascular resistance from 95 +/- 16 to 73 +/- 9 dyn s/cm5 x 10(3). Propranolol (4 mg), a beta-adrenergic antagonist, significantly reduced mean arterial pressure by 12% and portal pressure from 15.5 +/- 1.2 to 13.3 +/- 0.9 mmHg while reducing portal tributary blood flow from 14.6 +/- 1.5 to 11.0 +/- 1.7 mL/min and increasing portal systemic collateral vascular resistance from 88 +/- 7 to 103 +/- 8 dyn s/cm5 x 10(3). Ketanserin (0.25 mg/kg), a 5-hydroxytryptamine receptor antagonist, reduced portal pressure from 15.8 +/- 1.0 to 13.3 +/- 0.7 mmHg at a dose that did not alter mean arterial pressure or portal tributary blood flow. It achieved this by reducing portal-systemic collateral vascular resistance from 90 +/- 14 to 74 +/- 13 dyn s/cm5 x 10(3). Saline had no significant effect on systemic and splanchnic haemodynamics. This study shows that ketanserin decreases vascular resistance of portal-systemic collaterals while propranolol increases it. Thus, it is suggested that collateral vascular resistance is accessible to pharmacological manipulation.

Animals↗
PubMedDate not supplied

[Relation between plasma catecholamines, the severity of the liver disease and hemodynamics in patients with cirrhosis].

Plasma noradrenaline and adrenaline concentrations were measured in 75 patients with cirrhosis in order to attempt to correlate these concentrations and liver failure and hemodynamic changes. The increased noradrenaline concentration was not correlated with the degree of liver failure estimated by Pugh's classification, with the cause of cirrhosis, with the presence of acute alcoholic hepatitis or with the presence of ascites. Adrenaline concentration was higher in cirrhotic patients with acute alcoholic hepatitis than in those without these lesions. Noradrenaline concentration was significantly correlated with heart rate, wedged hepatic venous pressure and renal blood flow. Noradrenaline concentration was also negatively correlated with stroke volume and adrenaline concentration was negatively correlated with cardiac output and stroke volume. These findings confirm the relationships between portal hypertension, sympathetic hyperactivity and renal function in patients with cirrhosis.

Adult↗
PubMedDate not supplied

[Effect of the development of portosystemic shunts in the maintenance of portal hypertension in rats].

We studied the role of portosystemic shunt development in the maintenance of portal hypertension in a prehepatic portal hypertension rat model. A first group was studied two days after partial portal vein ligation. When portosystemic shunts were negligible; the second group was studied 3 weeks after the partial portal vein ligation, when large portosystemic shunts were present. Portal pressure was significantly higher in the first group than in the second group (19.9 +/- 0.8 mmHg (mean +/- 1 SD) and 12.8 +/- 2.3 mmHg, respectively; p less than 0.001). When compared with sham operated rats: a) portal tributary blood flow (measured with the radioactive microspheres method) was decreased in the first group (- 34 p. 100; p less than 0.01) and increased in the second group (+ 32 p. 100; p less than 0.02); b) portal system vascular resistance was markedly increased in the first group (+ 269 p. 100; p less than 0.001) and did not significantly change in the second group (+ 30 p. 100). These results suggest that portosystemic shunt development decreases portal pressure but not to normal value because portal tributary blood flow is increased. Moreover the increase in portal system vascular resistance and in portal tributary blood flow play different roles in the maintenance of portal hypertension depending on the stage of evolution of portal hypertension.

Acute Disease↗