Effectofadriamycinonmyocardialfibrosisandpossiblemechanismsinrats

doi:10.3969/j.issn.10073205.2016.03.002

Abstract

Abstract: [
Abstract ] Objective Todeterminetheeffectofadriamycinon myocardialfibrosisand
possible mechanismsin rats.Methods A rat myocardialfibrotic model wasinduced by
intravenousinjectionofadriamycin ( 3 mg /
kg
, onceaweek ) forsix weeks.Duringthetest ,
generalconditionandbodyweightwereobserved.Attheseventhweek , hemodynamicparameters
andhydroxyprolineconcentrationaswellasmorphologicaltransformationofhearttissueswere
detected.Results Comparedtothoseincontrolgroup , hydroxyprolinecontentwasmarkedly
increasedinadriamycininducedrats.Histopathologicalexaminationfurtherconfirmedthesame
alteration.Moreover , hemodynamicsshowedasignificantdeclineinleft-ventricularsystolic
pressure , maximumandminimumrateofdevelopedleftventricularpressure ,
accompaniedbyan
incrementofleftventricularend-diastolicpressure ( P <0.05 ) .Conclusion Thesefindings
suggestedthatadriamycincouldinducemyocardialfibrosisandinhibitcardiacfunction.

Key words: [ Keywords ] endomyocardialfibrosis , adriamycin , rats

BAOYun-feng1, WANGJing-jing 2,ZHUGE Ming-ning3,ZHANG Hong-zhen2*. Effectofadriamycinonmyocardialfibrosisandpossiblemechanismsinrats[J]. Journal of Hebei Medical University, doi: 10.3969/j.issn.10073205.2016.03.002.

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Effectofadriamycinonmyocardialfibrosisandpossiblemechanismsinrats

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