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Electrophysiological, structural and molecular remodeling of chronically infarcted rabbit heart

Li, Li
http://rave.ohiolink.edu/etdc/view?acc_num=case1130882699

Abstract Details

2006, Doctor of Philosophy, Case Western Reserve University, Biomedical Engineering.
Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. In the US, approximately 1.5 million cases of MI occur each year. The infarcted canine model has been investigated for a long time, which is characterized by structural and molecular remodeling in the infarcted area and epicardial border zone (BZ). However, clinical findings suggest primarily endocardial BZ. In our recent studies, we found that the infarcted rabbit heart developed endocardial BZ, providing a more appropriate model for MI studies. The goal of this study was to explore the electrophysiological, structural and molecular remodeling of chronic infarcted rabbit heart, especially in the BZ area. Whole heart electrophysiology during shock application and sustained arrhythmia were optically recorded and analyzed for both normal and chronically MI rabbit hearts. The gap junction remodeling, fibroblast and cell morphology were accessed by histology and immunohistochemistry studies. The major findings of this study are: 1) the rabbit model of healed MI consistently reproduces the endocardial BZ. 2) A significant increase of shock-induced vulnerability is observed in infarcted versus control hearts. This is reflected in increased incidences of shock-induced arrhythmias and increased severity and duration of arrhythmias. 3) The infarction BZ is responsible for both the initiation and maintenance of shock-induced arrhythmias, which results in increased upper limit of vulnerability. 4) In the BZ area of the chronically infarcted rabbit hearts, Cx43 distribution was heavily disturbed. The amount of Cx43 proteins decreased significantly in the BZ area versus control hearts and the non-infarcted area in the infarcted hearts. 5) Cx45 distribution was observed in the intercalated disk area of both the control and infarcted rabbit ventricles. The amount of Cx45 proteins decreased significantly in the BZ area versus control hearts and the non-infarcted area in the infarcted hearts. 6) There is no Cx45/Cx40 gap junction formation between myocyte and fibroblast or between fibroblasts. We didn’t find determinant evidence of Cx43 gap junction formation between myocyte and fibroblast or between fibroblasts. The results of the study provide knowledge of basic mechanisms of MI and facilitate future improvement of clinical pharmacological and device therapies.
Igor Efimov (Advisor)
arrhythmias; BZ; INFARCTED; Cx43; infarction; infarcted hearts; endocardial

Recommended Citations

Citations

  • Li, L. (2006). Electrophysiological, structural and molecular remodeling of chronically infarcted rabbit heart [Doctoral dissertation, Case Western Reserve University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=case1130882699

    APA Style (7th edition)

  • Li, Li. Electrophysiological, structural and molecular remodeling of chronically infarcted rabbit heart. 2006. Case Western Reserve University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=case1130882699.

    MLA Style (8th edition)

  • Li, Li. "Electrophysiological, structural and molecular remodeling of chronically infarcted rabbit heart." Doctoral dissertation, Case Western Reserve University, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1130882699

    Chicago Manual of Style (17th edition)

case1130882699
1,169
© 2005, all rights reserved.
This open access ETD is published by Case Western Reserve University School of Graduate Studies and OhioLINK.