Sinoaortic denervation induces cardiac damage in rats, which is associated with increased cardiomyocyte apoptosis and altered expression of apoptosis-regulating proteins.
Sinoaortic denervation may promote cardiomyocyte apoptosis in rats; hypothesis-generating for autonomic contributions to human cardiac injury.
The arterial baroreflex plays an important role in the maintenance of the stability of blood pressure. Sinoaortic denervation (SAD) produces severe organ damage in rats. The present study was designed to investigate whether apoptosis, which is a ubiquitous physiological mode of cell death distinct from cell mortality induced by injury and necrosis, is involved in SAD-induced cardiac damage. 2. Male Sprague-Dawley rats (10 weeks old) were used. Rats underwent SAD (n = 9) or sham operation (n = 10). Sixteen weeks after operation, the heart tissues were taken for investigations including electron microscopy, immunohistochemistry, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL) and reverse transcription-polymerase chain reaction (RT-PCR). 3. Cardiac hypertrophy and fibrosis was found in SAD rats. The number apoptotic cardiomyocytes was increased in SAD rats compared with sham-operated rats. 4. The expression of Bcl-2mRNA and protein (an inhibitory factor of apoptosis) in cardiomyocytes was decreased in SAD rats. In contrast, the expression of Bax, Fas and Fas ligand mRNA and proteins (promoters of apoptosis) in cardiomyocytes was significantly increased in SAD rats. 5. In conclusion, the present study reveals a high level of apoptosis in cardiomyocytes in SAD rats. It is proposed that apoptosis is involved in SAD-induced cardiac damage.
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Zhang et al. (2003) studied this question.
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