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PubMed1988

Propranolol reduces the response of serum bile acids to oral chenodeoxycholic acid, possibly as a reflex reaction to reduced portal blood flow in healthy and cirrhotic subjects.

To evaluate if a drug that affects splanchnic and portal flow reduces intestinal bile acid absorption, we studied the effect of propranolol (40 mg oral dose) both on the response of total bile acids (SBA) to oral chenodeoxycholic acid (CDCA 250 mg) and on the estimated hepatic flow by indocyanine green kinetics in 10 healthy and 14 cirrhotic subjects. In 18 subjects who showed a reduction in resting heart rate of almost -5%, propranolol significantly reduced the SBA area under the curve after CDCA in both healthy (mumol/l/h m +/- SD from 181.7 x 144.9 to 56.5 +/- 36.4 p less than 0.02) and cirrhotic (from 1412.1 +/- 1044.8 to 1129.2 +/- 978.8 p less than 0.01) subjects. Variable but not significant modifications were observed in estimated hepatic flow. These results suggest that the propranolol-induced changes in SBA response to CDCA could be a reflex reaction to changes in splanchnic/portal flow.

Bile Acids and Salts↗
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↗
PubMed1985

Comparison of the short-term effects of mepindolol and propranolol on splanchnic and systemic haemodynamics in patients with cirrhosis.

The splanchnic and systemic haemodynamic effects of mepindolol (0.6 mg, IV), a beta-blocker with a marked beta 2-blockade activity and propranolol (15 mg, IV) were studied in two groups of eight patients with portal hypertension due to cirrhosis. Similar decreases in the hepatic venous pressure gradient were observed after mepindolol and propranolol, whereas hepatic blood flow significantly decreased after mepindolol but did not significantly do so after propranolol. The decreases in cardiac output and heart rate were statistically significant and similar after mepindolol and propranolol. Mepindolol slightly decreased mean arterial pressure and propranolol slightly increased this pressure. Both beta-blockers significantly increased systemic vascular resistance. From these observations, it was not possible to demonstrate that mepindolol offered a beneficial effect on splanchnic haemodynamics in patients with portal hypertension due to cirrhosis.

Adult↗
PubMed2000

Reversal of the vasoconstrictor step of hyperacute xenogeneic rejection of the liver by endothelin antagonists.

The role of endothelin in the initial vasoconstrictor step of hyperacute xenogeneic rejection was investigated. Isolated rat livers were perfused in recirculation. Perfusion with human sera provided an ex vivo model of hyperacute rejection in a discordant combination. Perfusion of 10% xenogeneic serum induced a marked (70%) and sustained reduction of the liver flow and induced the release of endothelin into the perfusion medium. In contrast, perfusion of 10% allogeneic serum or of 10% decomplemented human serum induced a weak (25%) and transient reduction of the liver flow and induced the release of minimal amounts of endothelin. The simultaneous administration of BQ 123 and BQ 788, the respective antagonists of ET(A) and ET(B) endothelin receptors, or that of bosentan, a mixed ET(A)/ET(B) antagonist, antagonized the vasoconstrictor effect of 10% xenogeneic human serum, as well as that of 10(-9) M endothelin-1. The vasoconstrictor effects of xenogeneic serum on liver circulation are, at least partly, mediated through the release of endothelin by the graft.

Animals↗
PubMed1999

Regulation of endothelin-1 synthesis by endothelin-converting enzyme-1 during wound healing.

Endothelin-1 (ET-1) is involved in the pathogenesis of a number of diseases, including wound healing. In cirrhosis, the wounding response of the liver, circulating ET-1 levels are elevated; moreover, ET-1 has potent effects on hepatic stellate cells, the key effectors of cirrhosis. In this study, we have examined the regulatory role of ECE-1, a critical enzyme involved in ET-1 synthesis, in the two major cellular sources of hepatic ET-1. ET-1 release from normal hepatic endothelial cells was 25-fold higher than that from normal stellate cells. However, after liver injury, ET-1 release was increased in stellate cells but markedly decreased in endothelial cells. The two major isoforms of ECE-1, ECE-1alpha/1beta, made up 80% and 20%, respectively, of total ECE-1 in both stellate and endothelial cells. Following liver injury, ECE-1alpha mRNA was decreased by 44.2% in stellate cells, and by 16.1% in endothelial cells. ECE-1beta mRNA expression remained unchanged after injury. In contrast to ECE-1 mRNA, ECE-1 protein expression was increased by 43.9% in stellate cells but decreased in endothelial cells, while relative ECE-1 enzymatic activity was unchanged. In mRNA stability experiments, the half-life of ECE-1alpha mRNA in normal stellate cells was 13 h compared with 38 h in cells from injured livers. Thus, during hepatic wound healing, differential regulation of ECE-1 mRNA and protein appears to be critical in controlling ET-1 production.

Animals↗
PubMed1987

Tissue glycogen and lactate levels in starved and in protein-fed domestic fowl chicks (Gallus domesticus).

The levels of glycogen, protein and lactate in the tissues of 3- and 5-day-old domestic fowl chicks either starved or fed a protein diet (hard-boiled egg white) have been studied. The patterns of change in the parameters studied were much similar in both experimental groups compared to fed controls. Tissue and circulating levels of lactate were very low in protein-fed chicks, they are lowest in the starved ones. Plasma glucose levels were diminished in starved and protein-fed groups vs. controls, as were their tissue glycogen levels, the latter being lowest in starved chicks. The availability of dietary amino acids could not prevent the effects of the lack of dietary carbohydrate observed in starved chicks, as the weight of liver, circulating glucose and lactate levels were significantly lowered in these animals compared with controls.

Animals↗
PubMed1988

Intraarterial digital subtraction angiography with carbon dioxide: superior detectability of arteriovenous shunting.

Intraarterial digital subtraction angiography (IADSA) with carbon dioxide (CO2) was performed on 41 patients with liver or renal diseases. CO2 produced no hypersensitivity reactions, and the pain or feeling of warmth was relatively mild compared with iodinated contrast media. Although the image quality of the arterial or capillary phase was inferior to that with iodinated contrast media, the detectability of arteriovenous shunting was excellent. IADSA with CO2 may become an effective method for detecting arteriovenous shunting which cannot be demonstrated with conventional angiography or DSA with iodinated contrast medium.

Adult↗
PubMed1981

Measurement of portal-systemic shunting in the rat by using gamma-labeled microspheres.

A method for determining the extent of portal-systemic shunting (PSS) is described and evaluated in lightly anesthetized (ketamine) rats. This method relies on the intrasplenic injection of 15-micrometers gamma-labeled spheres and the subsequent measurement of liver and lung radioactivities. After the splenic injection of the microspheres, a fraction of microspheres shunting the hepatic sinusoidal bed will be entrapped in the lungs. Thus, the ratio, lung/(lung + liver) radioactivities, will indicate the degree of PSS. The percent of PSS was determined in normal (n = 13; 1.2 +/- 0.3%), in cirrhotic (n = 9; 15.0 +/- 4.5%; P less than 0.01), and in portal vein-ligated animals (n = 14; 95.0 +/- 0.9%; P less than 0.001 for normal and cirrhotic). In addition, PSS was sequentially quantitated (n = 3) before (3.0%) and after (89%) partial portal vein ligation. The variability of PSS found in cirrhotic rats (0.7-41.0%) is in agreement with the reported data for PSS in patients. This technique, which is simple, rapid, and reproducible, allows the quantitation of PSS in small laboratory animals.

Animals↗
PubMed2002

Acute effects of nitric oxide synthase inhibition on systemic, hepatic, and renal hemodynamics in patients with cirrhosis and ascites.

BACKGROUND: Nitric oxide synthase (NOS) inhibition has been demonstrated to correct systemic vasodilation and renal hypoperfusion in studies of patients with cirrhosis. In patients with decompensated cirrhosis, NOS blockade increases arterial pressure, but the acute effects on hepatic and renal hemodynamics are not known. METHODS: We examined the acute systemic, hepatic, and renal hemodynamic effects of N(G)-monomethyl-L-arginine (L-NMMA) in 10 patients with decompensated cirrhosis. After baseline measurements, 3 mg/kg L-NMMA was administered as an IV bolus. At 20 minutes, if mean arterial pressure did not increase by at least 10 mm Hg above the baseline value, a second injection of 6 mg/kg was administered. RESULTS: In 5 of 10 patients, the second injection of L-NMMA 6mg/kg was necessary to achieve at least a 10 mm Hg increase in mean arterial pressure. Acute NOS inhibition increased systemic vascular resistance and decreased cardiac output, without causing changes in the hepatic venous pressure gradient. Hepatic blood flow decreased, but the indocyanine green intrinsic clearance and extraction remained unchanged. Plasma renin activity (from 9.5 +/- 2.9 to 6.7 +/- 1.6 ng/ml/h) and urinary prostaglandin E2 (from 299 +/- 40 to 112 +/- 36 pg/ml) significantly decreased. No significant changes in glomerular filtration rate, renal plasma flow, and natriuresis occurred, however. CONCLUSIONS: Acute L-NMMA infusion in patients with decompensated cirrhosis reduced hepatic blood flow and decreased plasma renin activity and urinary prostaglandin E2, without causing significant changes in renal hemodynamics.

Adult↗
PubMed1981

Effect of somatostatin on splanchnic hemodynamics in patients with cirrhosis of the liver and in normal subjects.

The effect of somatostatin on splanchnic hemodynamics was determined in 8 patients with cirrhosis of the liver and in 18 normal subjects using arterial-hepatic-venous catheterization. Estimated hepatic blood flow determined by indocyanine green infusion was 1.36 +/- 0.23 L/min (+/- SEM) in patients with cirrhosis and remained unaffected during 30 min of somatostatin (250 microgram/h) administration. Wedged hepatic venous pressure which was elevated to 23 +/- 1.8 mmHg was also uninfluenced. In contrast to somatostatin, an infusion of vasopressin (12 U/h for 30 min) given to the same patients, lowered estimated blood flow by 28% (p < 0.05) and wedged hepatic venous pressure by 18% (p < 0.02). Arterial gastrin and insulin levels were lowered during somatostatin infusion by 33% (p < 0.02) and by 75% (p < 0.005), respectively. In contrast to the cirrhosis, infusion of 250 microgram/h somatostatin into normal subjects was associated with a decrease of estimated hepatic blood flow from 1.20 +/- 0.16 to 0.88 +/- 0.12 L/min (p < 0.01) representing a 27% decline. Arterial gastrin and insulin concentrations were lower (p < 0.01) than in cirrhosis, but the basal levels were lowered by somatostatin to a similar degree in both groups of patients. A higher dose of somatostatin (500 microgram/h) administered to normal subjects resulted in a similar decrease of gastrin and of estimated hepatic blood flow as that seen with 250 microgram/h, whereas a lower dose (125 microgram/h) decreased gastrin but failed to influence estimated hepatic blood flow. Thus, somatostatin at a dose which has been used in the treatment of acute peptic ulcer hemorrhage (250 microgram/h) failed to influence estimated hepatic blood flow and wegded hepatic venous pressure in patients with cirrhosis but lowered splanchnic blood flow in normal subjects. Assuming that this effect contributes to somatostatin's therapeutic efficacy, these results cast doubt on its potential value in the treatment of upper gastrointestinal bleeding of cirrhotics with portal hypertension.

Dose-Response Relationship, Drug↗
PubMed1993

Studies on the relationship between hepatic and splenic density change in dynamic CT in the presence of a large splenorenal shunt in patients with liver cirrhosis.

Using dynamic computerized tomography (CT), we studied liver and spleen hemodynamics in one group of patients with a large splenorenal shunt and another group without a large shunt. Specifically, we measured the time-to-peak hepatic and splenic enhancement and the loss of enhancement, i.e., decay time. The time-to-peak liver enhancement (61 +/- 21 s vs. 81 +/- 14 s, p < 0.05) and the splenic decay time (24 +/- 16 s vs. 48 +/- 28 s, p < 0.05) were significantly shorter in patients with a large splenorenal shunt compared to those without. The groups had similar hepatic decay times and times to peak splenic enhancement. We found dynamic CT useful in assessing the effect of a large splenorenal shunt on portal and splenic hemodynamics.

Adult↗
PubMed2004

Changes in extrathymic T cells in the liver and intestinal intraepithelium in mice with obstructive jaundice.

Recently, T cells were classified into two categories: intrathymic T cells (ITCs; thymus-derived T cells) and extrathymic T cells (ETCs). ETC, localized in the liver and intestinal intraepithelium (IE), play an important immunologic role in the suppressed condition of T-cell development in the thymus. Given the fact that complications of surgery in patients with obstructive jaundice are often related to immunosuppression in the gut-liver circulation, we attempted to investigate the changes in the proportion of ETCs in mice with obstructive jaundice. Three mice models were prepared ( n = 10 per group): sham group with simple laparotomy; ligation group with common bile duct ligation; deoxycholic acid (DCA) group with an oral intake of DCA as a model of the presence of bile salts in the gut lumen. In each model, total mononuclear cells (MNCs), ITCs in the thymus, and ETCs in the liver and IE were counted using monoclonal antibodies in conjunction with a two-color immunofluorescence test by flow cytometry. In the ligation group the number of MNCs was reduced in the thymus and IE, and only those in the IE recovered after oral intake of DCA. A decrease of ITCs in the thymus and the increase in ETCs in the liver and IE occurred simultaneously during the early phase of biliary obstruction. At day 7 after biliary obstruction, ETCs in the livers of the DCA and ligation groups decreased to nearly the level in the sham group. However, on day 7 the ETCs in the IE remained significantly higher in the DCA group than in the ligation group. These results suggested that ETCs can act in place of ITCs at an early phase of obstructive jaundice, and the presence of bile in the gut lumen may be associated with the consumption of ETCs in the IE, a reaction that may bring about improved immunoreactivity.

Animals↗