Background. Congestive Heart Failure (CHF) causes arrhythmogenic remodeling in both atria and ventricles, but potential differences between atrial and ventricular remodeling in CHF have not been studied. / Methods and results. We examined atrial and ventricular tissues from dogs with CHF induced by ventricular tachypacing (VTP, 240/min) for 0 (control) or 24 hrs, 1, 2, or 5 wks. Tissue angiotensin-II concentration (ELISA) increased to steady state at 24 hrs, and was significantly higher in LA than LV. VTP caused tissue apoptosis, inflammatory-cell infiltration and cell-death, with maximum changes in LA being transient and larger than in LV. MAP kinase activation (Western blot) was rapid (within 24 hrs) in LA, but smaller and slower (p38, JNK) or non-significant (ERK) in LV. The 25-kDa activated form of TGFbeta1, a particularly important profibrotic mediator in atria, increased significantly (Western blot) in LA at 24 hrs and 1 wk, but was not changed in LV. Substantial fibrosis developed in LA, but was much less important in LV. / Conclusions. There are qualitative and quantitative differences in LA and LV remodeling in experimental CHF, with important potential consequences for underlying mechanisms and therapeutic approaches.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.80286 |
| Date | January 2003 |
| Creators | Hanna, Nessrine |
| Contributors | Nattel, Stanley (advisor) |
| Publisher | McGill University |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Format | application/pdf |
| Coverage | Master of Science (Department of Pharmacology & Therapeutics.) |
| Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
| Relation | alephsysno: 002032433, proquestno: AAIMQ98655, Theses scanned by UMI/ProQuest. |
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