{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T15:48:52Z","timestamp":1758815332523,"version":"3.27.0"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":6421,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,2]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>The influence of hepatocyte enlargement on intrahepatic hemodynamics was assessed in the isolated perfused rat liver preparation (IPRL) using two experimental models: hypotonic liver cell swelling and phenobarbitone-induced hepatocyte hypertrophy. The analysis of pressure-flow data obtained from the portal vascular bed over a flow range of 0 to 70 mL\/min in the presence of a maximally-effective concentration of the vasodilator agent papaverine hydrochloride (6 \u00d7 10<jats:sup>\u22124<\/jats:sup> mol\/L) enabled the calculation of P<jats:sub>0<\/jats:sub>, an estimate of the pressure required to passively distend the intrahepatic vasculature, and G<jats:sub>max<\/jats:sub>, the maximal portal vascular conductance. By comparison with an isotonic perfusion medium (Krebs-Henseleit buffer [KH] containing 2.5% bovine serum albumin [BSA]), perfusion with a hypotonic medium induced a significant increase in mean hepatocyte cross-sectional area (H<jats:sub>A<\/jats:sub>) (590 \u00b1 21 vs. 324 \u00b1 23 \u03bcm <jats:sup>2<\/jats:sup>, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .05), a fall in G<jats:sub>max<\/jats:sub> (0.39 \u00b1 0.08 vs. 2.02 \u00b1 0.18 mL\/min\/g\/mm hg, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .001), and an increase in P<jats:sub>0<\/jats:sub> (2.96 \u00b1 0.38 vs. 1.58 \u00b1 0.07 mm hg, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .001). Phenobarbitone administered in drinking water (0.5 g\/L) over a period of 60 days also induced a significant degree of hepatocyte enlargement (H<jats:sub>A<\/jats:sub>, 510 \u00b1 29 \u03bcm<jats:sup>2<\/jats:sup>, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .05). On day 7, portal pressure measured <jats:italic toggle=\"yes\">in vivo<\/jats:italic> in this group was significantly elevated compared with untreated controls (10.5 \u00b1 0.3 vs. 8.4 \u00b1 0.2 mm hg, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .001), while in the IPRL G<jats:sub>max<\/jats:sub> was reduced (0.48 \u00b1 0.01 mL\/min\/g\/mm hg, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .001), and P<jats:sub>0<\/jats:sub> was increased (2.23 \u00b1 0.17 mm hg, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .05). However, with continued phenobarbitone treatment portal pressure, G<jats:sub>max<\/jats:sub> and P<jats:sub>0<\/jats:sub> returned toward control values. The results confirm that hepatocyte enlargement is associated with a significant disturbance of intrahepatic hemodynamics but also that some adaptation occurs if hepatocyte enlargement is sustained over a prolonged period of time.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.510270219","type":"journal-article","created":{"date-parts":[[2004,7,27]],"date-time":"2004-07-27T23:44:13Z","timestamp":1090971853000},"page":"446-451","update-policy":"http:\/\/dx.doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":11,"title":["The effect of hepatocyte enlargement on the hemodynamic characteristics of the isolated perfused rat liver preparation"],"prefix":"10.1097","volume":"27","author":[{"given":"Howard J.","family":"Grossman","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Virginia 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