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Objective:To studytheaorticremodelingproducedby chronicsinoaorticdenervation(SAD)anditstime course,andto studytheroleof humoralfactorintheSAD-inducedaorticremodeling.Methods:In ratswithchronicSAD or shamoperation,theaorticstructurewasmeasuredby computer-assistedimageanalysis,theaorticfunctionby isolated arterypreparation,andangiotensinⅡconcentrationby radioimmunoassay.Results and Conclusion:Theaorticstructural remodelingdevelopedprogressivelyat4,8,16and32weeksafterSAD.AorticstructuralremodelingafterSADexpressed mainlyas aortichypertrophydue to SMC growthand collagenaccumulation.The aorticcontractionelicitedby nore-pinephrine(NE)wasprogressivelyincreased8,16and32weeksafterSAD.Theaorticrelaxationelicitedby acetylcholine(ACh)wasdepressed8,16and32weeksafterSAD.Inaddition,in32-weekSADratstheNE-inducedcontractionwasnot increasedby endothelialdenudation.TheseindicatedthattheincreasedcontractionanddepressedrelaxationafterSAD wererelatedto thechangeof endotheliumand/orthechangeof interactionbetweenendotheliumandSMC.In10-week SADrats,plasmaangiotensinⅡconcentrationremainedunchanged,whereasaorticangiotensinⅡconcentrationwas sig-nificantlyincreased,suggestingthatactivationof tissuerenin-angiotensinsystemmaybe involvedin SAD-inducedaortic remodeling.
Objective: To studytheaorticremodelingproducedby chronicsinoaorticdenervation (SAD) anditstime course, andto studytheroleof humoralfactorintheSAD-inducedaorticremodeling.Methods: In ratswithchronicSAD or shamoperation, theaorticstructurewasmeasuredby computer-assistedimageanalysis, theaorticfunctionby isolated arterypreparation, andangiotensinⅡconcentrationby radioimmunoassay.Results and Conclusion: Theaorticstructural remodelingdevelopedprogressivelyat4,8,16and32weeksafterSAD.AorticstructuralremodelingafterSADexpressed mainlyas aortichypertrophydue to SMC growthand collagenaccumulation.The aorticcontractionelicitedby nore-pinephrine (NE) wasprogressivelyincreased8,16and32weeksafterSAD.Theaorticrelaxationelicitedby acetylcholine (ACh) wasdepressed8,16and32weeksafterSAD.Inaddition, in32-weekSADratstheNE-inducedcontractionwasnot increasedby endothelialdenudation.TheseindicatedthattheincreasedcontractionanddepressedrelaxationafterSAD wererelatedto thechangeof endotheliumand / orthechangeof interactionb etweenendotheliumandSMC.In10-week SADrats, plasmaangiotensinⅡconcentrationremainedunchanged, andaorticangiotensinⅡconcentrationwas sig-nificantly established, suggestingthatactivationof tissuerenin-angiotensin systemmaybe involvedin SAD-inducedaortic remodeling.