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The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.

ABSTRACT: BACKGROUND: Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting. AIMS: To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver. METHODS: Different sized microspheres were sequentially injected into the portal vein of male Wistar rats. RESULTS: Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 microns diameter microspheres, respectively. Sequential injection of 15, 40, and 80 microns diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 x 10(5) 80 microns microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p > 0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 microns microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 microns microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow. CONCLUSION: It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.

SUBMITTER: Li X

PROVIDER: S-EPMC1726987 | biostudies-other | 1998 Feb

REPOSITORIES: biostudies-other

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Project description:Background and aimsTransjugular intrahepatic portosystemic shunt (TIPS) is used for decompressing clinically significant portal hypertension. The aims of this study were to evaluate clinical outcomes and adverse events associated with this procedure.MethodsRetrospective single-center study including 78 patients submitted to TIPS placement between January 2015 and November 2018. Follow-up data were missing in 27 patients, and finally 51 patients were included in the study sample. Data collected from individual registries included demographics, comorbidities, laboratory results, complications, and clinical results according to the indication.ResultsAverage pre-TIPS portosystemic pressure gradient decreased from 18.1 ± 5 to 6 ± 3 mm Hg after TIPS placement. Indications for TIPS were refractory ascites (63%, n = 49), recurrent or uncontrolled variceal bleeding (36%, n = 28), and Budd-Chiari syndrome (1.3%, n = 1). TIPS-related adverse events occurred in 29/51 (56.8%) patients, with hepatic encephalopathy (HE) in 21 (41%) patients, sepsis in 3, liver failure in 2, hemolytic anemia in 1, acute pulmonary edema in 1, and capsular perforation in 1 patient. Mean follow-up was 15.7 ± 15 months. First-month mortality was 11.7% (n = 6) (sepsis, n = 3; acute liver failure, n = 2; and recurrence of variceal bleeding, n = 1) and was significantly higher for patients with Child-Pugh >9 points (p = 0.01), model of end-stage liver disease (MELD) scores >19 (p = 0.02), and for patients with a history of HE before the procedure (p = 0.001). Older age (p = 0.006) and higher levels of creatinine (p = 0.008) were significantly higher in patients developing HE after TIPS. Ascites persisted in 21.2% (7/33 patients) and was more frequent in patients with lower baseline albumin levels (p = 0.003). Recurrent variceal bleeding occurred in 22% (n = 4/18 patients) and was more frequent in patients with lower baseline hemoglobin levels (p = 0.03).ConclusionTIPS is effective in up to 80% of patients presenting with variceal bleeding or refractory ascites. Careful patient selection based on age and HE history may reduce adverse events after TIPS.

Project description:BackgroundHydrogen sulfide (H(2)S) displays vasodilative, anti-oxidative, anti-inflammatory and cytoprotective activities. Impaired production of H(2)S contributes to the increased intrahepatic resistance in cirrhotic livers. The study aimed to investigate the roles of H(2)S in carbon tetrachloride (CCl(4))-induced hepatotoxicity, cirrhosis and portal hypertension.Methods and findingsSodium hydrosulfide (NaHS), a donor of H(2)S, and DL-propargylglycine (PAG), an irreversible inhibitor of cystathionine ?-lyase (CSE), were applied to the rats to investigate the effects of H(2)S on CCl(4)-induced acute hepatotoxicity, cirrhosis and portal hypertension by measuring serum levels of H(2)S, hepatic H(2)S producing activity and CSE expression, liver function, activity of cytochrome P450 (CYP) 2E1, oxidative and inflammatory parameters, liver fibrosis and portal pressure. CCl(4) significantly reduced serum levels of H(2)S, hepatic H(2)S production and CSE expression. NaHS attenuated CCl(4)-induced acute hepatotoxicity by supplementing exogenous H(2)S, which displayed anti-oxidative activities and inhibited the CYP2E1 activity. NaHS protected liver function, attenuated liver fibrosis, inhibited inflammation, and reduced the portal pressure, evidenced by the alterations of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), albumin, tumor necrosis factor (TNF)-?, interleukin (IL)-1?, IL-6 and soluble intercellular adhesion molecule (ICAM)-1, liver histology, hepatic hydroxyproline content and ?-smooth muscle actin (SMA) expression. PAG showed opposing effects to NaHS on most of the above parameters.ConclusionsExogenous H(2)S attenuates CCl(4)-induced hepatotoxicity, liver cirrhosis and portal hypertension by its multiple functions including anti-oxidation, anti-inflammation, cytoprotection and anti-fibrosis, indicating that targeting H(2)S may present a promising approach, particularly for its prophylactic effects, against liver cirrhosis and portal hypertension.

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The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.

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