International journal of cardiology · 2006
Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.
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Bregagnollo Edson A, Zornoff Leonardo A M, Okoshi Katashi, Sugizaki Mario, Mestrinel Marco A, Padovani Carlos R, Cicogna Antonio C
Аннотация
OBJECTIVES: To analyze the potential contribution of contractility state and ventricular geometry to the development of heart failure in rats with aortic stenosis.
METHODS: Rats were divided into three groups: compensated aortic stenosis (AS, n=11), heart failure AS (n=12) and control rats (C, n=13).
RESULTS: After 21 weeks, failing AS rats presented higher systolic (C=36.6+/-3.1, AS=78.6+/-4.8*, failing AS=104.6+/-7.8*(dagger)) and diastolic meridian stress (C=6.9+/-0.4, AS=20.1+/-1.1*, failing AS=43.2+/-3.2*(dagger)), hydroxyproline (C=3.6+/-0.7 mg/g, AS=6.6+/-0.6* mg/g, failing AS=9.2+/-1.4*(dagger) mg/g) and cross-sectional area (C=338+/-25 microm2, AS=451+/-32* microm2, failing AS=508+/-36*(dagger) microm2), in comparison with control and compensated AS animals (*p<0.05 vs. control, (dagger)p<0.05 vs. AS). In the isometric contraction study, considering the time from peak tension to 50% relaxation (RT50), the relative variation responses, following post-rest contraction and increase in Ca2+ concentration, were higher in failing AS than compensated AS animals. In contrast, following post-rest contraction, compensated AS group presented higher values of the peak developed tension (DT) than failing AS group. Following beta-adrenergic stimulation, control animals presented higher values of +dT/dt and -dT/dt than AS animals. In addition, failing AS animals presented higher TPT values than compensated AS animals.
CONCLUSION: Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.
METHODS: Rats were divided into three groups: compensated aortic stenosis (AS, n=11), heart failure AS (n=12) and control rats (C, n=13).
RESULTS: After 21 weeks, failing AS rats presented higher systolic (C=36.6+/-3.1, AS=78.6+/-4.8*, failing AS=104.6+/-7.8*(dagger)) and diastolic meridian stress (C=6.9+/-0.4, AS=20.1+/-1.1*, failing AS=43.2+/-3.2*(dagger)), hydroxyproline (C=3.6+/-0.7 mg/g, AS=6.6+/-0.6* mg/g, failing AS=9.2+/-1.4*(dagger) mg/g) and cross-sectional area (C=338+/-25 microm2, AS=451+/-32* microm2, failing AS=508+/-36*(dagger) microm2), in comparison with control and compensated AS animals (*p<0.05 vs. control, (dagger)p<0.05 vs. AS). In the isometric contraction study, considering the time from peak tension to 50% relaxation (RT50), the relative variation responses, following post-rest contraction and increase in Ca2+ concentration, were higher in failing AS than compensated AS animals. In contrast, following post-rest contraction, compensated AS group presented higher values of the peak developed tension (DT) than failing AS group. Following beta-adrenergic stimulation, control animals presented higher values of +dT/dt and -dT/dt than AS animals. In addition, failing AS animals presented higher TPT values than compensated AS animals.
CONCLUSION: Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis.