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Mechanisms of Beneficial Effects of β-adrenoceptor Blockers in Heart Failure Due to Myocardial Infarction

机译:β-肾上腺素受体阻滞剂因心肌梗塞引起的β-肾上腺素受体阻滞剂的有益效果

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Although several β-adrenoceptor (β-AR) blockers are widely used for the treatment of heart failure due to myocardial infarction (MI), mechanisms of their action are not fully understood. By employing a rat model of heart failure due to MI, we have observed that cardiac dysfunction in the failing heart was associated with depressed myofibrillar Ca2+-stimulated ATPase, sarcoplasmic reticular Ca2+-transport and sarcolemmal Na+-K+ ATPase activities. Such abnormalities were attenuated by treatments of infarcted animals with different β-AR blocking agents such as propranolol and atenolol. The beneficial effects of these agents on cardiac and subcellular remodeling may not only be elicited due to the blockade of β-AR mediated signal transduction but may also be a consequence of reductions in the level of plasma catecholamines, development of oxidative stress and occurrence of intracellular Ca2+-overload.
机译:虽然几种β-肾上腺素依有剂(β-AR)阻滞剂由于心肌梗塞(MI)而被广泛用于治疗心力衰竭(MI),但其作用的机制尚不完全理解。通过采用由于MI而导致的心力衰竭大鼠模型,我们观察到失败心脏中的心脏功能障碍与抑制的myofibrillAca2 +刺激的ATP酶,Sarcoplasmic网状Ca2 + -Transport和Sarcolemal Na + -k + ATP酶活性有关。这些异常通过用不同β-Ar阻断剂如普萘洛尔和阿替洛尔的治疗梗死的动物进行衰减。由于β-AR介导的信号转导的阻断,这些药物对心脏和亚细胞重塑的有益效果可能也可能是降低血浆儿茶酚胺水平,氧化应激和细胞内发生的结果的后果。 ca2 + -overload。

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