Isoproterenol induces primary loss of dystrophin in rat hearts: correlation with myocardial injury
| Autor: | Cibele M. Prado, Minna Moreira Dias Romano, Erica C. Campos, Marcos A. Rossi |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Chronotropic
medicine.medical_specialty Sarcolemma Membrane permeability Cardiac muscle Cell Biology Biology medicine.disease Pathology and Forensic Medicine medicine.anatomical_structure Endocrinology Ventricle Internal medicine cardiovascular system medicine biology.protein Myofibril Dystrophin Molecular Biology Myocytolysis |
| Zdroj: | International Journal of Experimental Pathology. 89:367-381 |
| ISSN: | 0959-9673 |
| DOI: | 10.1111/j.1365-2613.2008.00604.x |
| Popis: | Isoproterenol has been used as an infarct-like myocardial necrosis-inducing drug in experimental animals since 1959 (Rona et al. 1959). The morphological changes have been claimed as comparable to those taking place in human myocardial infarction (Ferrans et al. 1964). The cardiac lesions are generally localized in the apex, lower aspect of the left ventricle, interventricular septum, and, occasionally, in the right ventricle. These lesions are focal, many coalescent, and characterized by capillary dilatation, interstitial and intracellular oedema, lysis of myofibrils and granular disintegration or hyaline necrosis of myofibres (Chappel et al. 1959). The lysis of myofibrils is known as myocytolysis (Schlesinger & Reiner 1955) or myofibrilar degeneration (Reichenbach & Benditt 1970). Isoproterenol stimulates cardiac muscle cells due to its positive inotropic and chronotropic effect (Csapoet al. 1972) and causes complex changes leading to alterations in membrane permeability (Handforth 1962; Rona 1985). The exact mechanism of isoproterenol-induced myocardial damage is still unknown, but a mismatch of oxygen supply vs. demand following coronary hypotension and myocardial hyperactivity is the best explanation for the complex morphological alterations observed in the presence of a patent vasculature (Grimm et al. 1998). Severe alterations in the structural integrity of the sarcolemma of cardiomyocytes have been demonstrated to be caused by isoproterenol (Yunge et al. 1989). Taking into account that the sarcolemmal integrity is stabilized by the dystrophin-glycoprotein complex (DGC) that connects actin and laminin in contractile machinery and extracellular matrix (McNally et al. 2003) and by integrins that also are essential to define cellular–extracellular interaction, this study was undertaken to test the hypothesis that isoproterenol affects sarcolemmal stability through changes in the DGC and integrins. |
| Databáze: | OpenAIRE |
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