Calpain I inhibition prevents pacing-induced structural remodeling for atrial fibrillation in canine / 中华心血管病杂志
Chinese Journal of Cardiology
;
(12): 132-136, 2007.
Artigo
em Chinês
| WPRIM
| ID: wpr-304954
ABSTRACT
<p><b>OBJECTIVE</b>To study the relation of the structural remodeling processes and activation of calpain I.</p><p><b>METHODS</b>Fifteen dogs were randomly divided into three groups. The dogs in pacing group (n=5) and inhibitor group (n=5) were subjected to 3 weeks of rapid atrial pacing at 600 beats/min, control dogs (n=5) were in sham-operated group. The dogs in inhibitor group were administered intravenous N-Acetyl-Leu-Leu-Met (ALLM), a calpain inhibitor, and in pacing group and sham-operated group were administered intravenous DMSO. The activity of calpain I was measured by hydrolyzing Suc-Leu-Leu-Val-Tyr-7-amino-4-methyl-coumarin. The ultrastructure of atrium was examined by light and electron microscopy. TnT expression was assessed by Western blot. Echocardiography examination was performed in all the three groups.</p><p><b>RESULTS</b>Calpain I activity was significantly increased in pacing group (2.3-fold, P<0.01), and decreased in inhibitor group (1.1-fold, P>0.05), compared to sham-operated group respectively. The percentages of myolysis were (76.7 +/- 5.9)% and (20.8 +/- 8.1)% in pacing group and inhibitor group respectively (P<0.01). TnT expression decreased in the rapid pacing-induced persistent atrial fibrillation, and these effects were inhibited by calpain I inhibitor ALLM. The area and volume of left atrium tended to increase after 3 weeks ALLM treatment in inhibitor group, but the change was not as prominent as in pacing group (P<0.05).</p><p><b>CONCLUSIONS</b>ALLM can decrease calpain I activity, and prevent canine atrial cardiomyocyte structural remodeling during atrial fibrillation. This study provided a capacity of atrial cardiomyocyte protection.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fibrilação Atrial
/
Calpaína
/
Estimulação Cardíaca Artificial
/
Função do Átrio Esquerdo
/
Troponina T
/
Modelos Animais de Doenças
/
Átrios do Coração
/
Metabolismo
/
Miocárdio
Limite:
Animais
Idioma:
Chinês
Revista:
Chinese Journal of Cardiology
Ano de publicação:
2007
Tipo de documento:
Artigo
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