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Splenectomy ameliorates portal pressure and anemia in animal models of cirrhotic and non-cirrhotic portal hypertension

Portal hypertension (PH)-associated splenomegaly is caused by portal venous congestion and splanchnic hyperemia. This can trigger hypersplenism, which favors the development of cytopenia. We investigated the time-dependent impact of splenectomy on portal pressure and blood cell counts in animal mode...

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Published in:Advances in medical sciences 2022-03, Vol.67 (1), p.154-162
Main Authors: Schwabl, Philipp, Seeland, Berit Anna, Riedl, Florian, Schubert, Tim Lukas, Königshofer, Philipp, Brusilovskaya, Ksenia, Petrenko, Oleksandr, Hofer, Benedikt, Schiefer, Ana-Iris, Trauner, Michael, Peck-Radosavljevic, Markus, Reiberger, Thomas
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Language:English
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Summary:Portal hypertension (PH)-associated splenomegaly is caused by portal venous congestion and splanchnic hyperemia. This can trigger hypersplenism, which favors the development of cytopenia. We investigated the time-dependent impact of splenectomy on portal pressure and blood cell counts in animal models of non-cirrhotic and cirrhotic PH. Ninety-six rats underwent either partial portal vein ligation (PPVL), bile duct ligation (BDL), or sham operation (SO), with subgroups undergoing additional splenectomy. Portal pressure, mean arterial pressure, heart rate, blood cell counts and hemoglobin concentrations were evaluated throughout 5 weeks following surgery. Following PPVL or BDL surgery, the animals presented a progressive rise in portal pressure, paralleled by decreased mean arterial pressure and accelerated heart rate. Splenectomy curbed the development of PH in both models (PPVL: 16.25 vs. 17.93 ​mmHg, p ​= ​0.083; BDL: 13.55 vs. 15.23 ​mmHg, p ​= ​0.028), increased mean arterial pressure (PPVL: +7%; BDL: +9%), and reduced heart rate (PPVL: −10%; BDL: −13%). Accordingly, splenectomized rats had lower von Willebrand factor plasma levels (PPVL: −22%; BDL: −25%). Splenectomy resulted in higher hemoglobin levels in PPVL (14.15 vs. 13.08 ​g/dL, p ​
ISSN:1896-1126
1898-4002
DOI:10.1016/j.advms.2022.02.005