{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T05:25:25Z","timestamp":1777699525150,"version":"3.51.4"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":4383,"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":[[2003,9]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague\u2013Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin\u2013II and endothelin\u20131 (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01), 87% increase in cardiac index and 30% increase in heart weight (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01) increase in cross\u2013sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK\u2013B genes (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01). Isolated perfused CBDL hearts showed pressure\/end\u2013diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with <jats:italic toggle=\"yes\">N<\/jats:italic>\u2013nitro\u2013L\u2013arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1053\/jhep.2003.50369","type":"journal-article","created":{"date-parts":[[2003,9,23]],"date-time":"2003-09-23T22:01:25Z","timestamp":1064354485000},"page":"589-598","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":48,"title":["Left Ventricular Hypertrophy in Rats With Biliary 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