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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Influence of long-term treatment of imidapril on mortality, cardiac function, and gene expression in congestive heart failure due to myocardial infarction.
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Influence of long-term treatment of imidapril on mortality, cardiac function, and gene expression in congestive heart failure due to myocardial infarction.

机译：咪咪普利的长期治疗对心肌梗塞引起的充血性心力衰竭的死亡率，心脏功能和基因表达的影响。

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Although it is generally accepted that the efficacy of imidapril, an angiotensin-converting enzyme inhibitor, in congestive heart failure (CHF) is due to improvement of hemodynamic parameters, the significance of its effect on gene expression for sarcolemma (SL) and sarcoplasmic reticulum (SR) proteins has not been fully understood. In this study, we examined the effects of long-term treatment of imidapril on mortality, cardiac function, and gene expression for SL Na+/K+ ATPase and Na+–Ca2+ exchanger as well as SR Ca2+ pump ATPase, Ca2+ release channel (ryanodine receptor), phospholamban, and calsequestrin in CHF due to myocardial infarction. Heart failure subsequent to myocardial infarction was induced by occluding the left coronary artery in rats, and treatment with imidapril (1 mg.kg–1.day–1) was started orally at the end of 3 weeks after surgery and continued for 37 weeks. The animals were assessed hemody nam ically and the heart and lung were examined morphologically. Some heartswere immediately frozen at –70 degrees C for the isolation of RNA as well as SL and SR membranes. The mortality of imidapril-treated animals due to heart failure was 31% whereas that of the untreated heart failure group was 64%. Imidapril treatment improved cardiac performance, attenuated cardiac remodeling, and reduced morphological changes in the heart and lung. The depressed SL Na+/K+ ATPase and increased SL Na+–Ca2+ exchange activities as well as reduced SR Ca2+ pump and SR Ca2+ release activities in the failing hearts were partially prevented by imidapril. Although changes in gene expression for SL Na+/K+ ATPase isoforms as well as Na+–Ca2+ exchanger and SR phospholamban were attenuated by treatments with imidapril, no alterations in mRNA levels for SR Ca2+ pump proteins and Ca2+ release channels were seen in the untreated or treated rats with heart failure. These results suggest that the beneficial effects of imidapril in CHF may be due to improvements in cardiac performance and changes in SL gene expression.
机译：尽管普遍认为血管紧张素转化酶抑制剂咪达普利在充血性心力衰竭（CHF）中的功效是由于血液动力学参数的改善，其对肌膜（SL）和肌浆网基因表达的影响的重要性（尚未完全了解SR）蛋白。在这项研究中，我们研究了长期服用咪达普利对SL Na + / K + ATPase和Na + –Ca2 +交换子以及SR Ca2 +泵ATPase，Ca2 +释放通道（ryanodine受体）的死亡率，心脏功能和基因表达的影响。 ，心肌梗死导致CHF中的磷酸化，磷lamban和Calsequestrin升高。通过闭塞大鼠左冠状动脉诱发心肌梗死后的心力衰竭，并在手术后3周结束时开始口服咪达普利（1 mg.kg–1.day-1）治疗，并持续37周。对动物进行了血液动力学评估，并对心脏和肺进行了形态学检查。立即将一些心脏冷冻在–70摄氏度，以分离RNA以及SL和SR膜。因心力衰竭而用吡虫啉治疗的动物死亡率为31％，而未经治疗的心力衰竭组为64％。咪达普利治疗可改善心脏性能，减弱心脏重塑并减少心脏和肺部的形态变化。咪达普利可部分预防心衰时SL Na + / K + ATPase的降低和SL Na + –Ca2 +交换活性的增加以及SR Ca2 +泵和SR Ca2 +释放活性的降低。尽管通过咪达普利处理可减轻SL Na + / K + ATPase亚型以及Na + -Ca2 +交换子和SR磷酸lamban的基因表达变化，但未处理或未处理的SR Ca2 +泵蛋白和Ca2 +释放通道的mRNA水平均未改变。心力衰竭的大鼠。这些结果表明，咪达普利对CHF的有益作用可能是由于心脏功能的改善和SL基因表达的改变。

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