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Effects of omacor? on left ventricular remodelling consecutive to post myocardial infarction special issue-myocardial infarction

机译:omacor的影响?心肌梗死后连续发生左心室重构的特殊问题-心肌梗塞

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Ventricular remodelling is the main trigger of the development of heart failure. Therefore, the reduction of structural remodelling is known to prevent the development of heart failure. The aim of the present study was to investigate the effects of OMACOR?, a well known mixture of EPA and DHA in an experimental model of heart failure induced by occlusion of left descending coronary artery and the reperfusion within 2 months. After a long term treatment of 2 months; OMACOR? (100 mg/kg) statistically significantly reduced the expansion of infarcted zone (35% ± 4%, P ± 3% in the vehicle group). The phosphorylation of Cx43 as biomarker of the cardiac remodelling was visualised by immunofluorescence in rat’s heart at the end of the study. In the vehicle-infarcted group, a significant de-phosphorylation of Cx43 was observed (8.2 ± 1.0 u.a, n = 8 compared to 11.8 ± 1.3 u.a in the sham group, n = 9) confirming a remodelling process in the infarcted group. In the group treated with OMACOR?,the de-phosphorylation of Cx43 was no longer observed compared to the sham group (16.4 ± 2.9 u.a, n = 9, NS). The present results demonstrate that a long term treatment with OMA-COR? reduced the infarcted size in experimental models of heart failure and that these anti-remodelling effects are due at least in part by resynchronizing the gap junction activity.
机译:心室重构是心力衰竭发展的主要触发因素。因此,已知减少结构重塑可防止心力衰竭的发展。本研究的目的是研究OMACORα(一种著名的EPA和DHA混合物)在2个月内由左冠状动脉下降闭塞和再灌注引起的心力衰竭实验模型中的作用。经过2个月的长期治疗; OMACOR? (100 mg / kg)在统计学上显着减少了梗塞区的扩张(媒介物组为35%±4%,P±3%)。研究结束时,通过免疫荧光在大鼠心脏中观察到了Cx43磷酸化作为心脏重构的生物标志物。在媒介物梗死组中,观察到Cx43的显着去磷酸化(8.2±1.0 u.a,n = 8,而假手术组为11.8±1.3 u.a,n = 9),证实了梗死组的重塑过程。与假手术组(16.4±2.9u.a,n = 9,NS)相比,在用OMACORα治疗的组中,不再观察到Cx43的去磷酸化。目前的结果表明,OMA-COR®可以长期治疗。减少了心力衰竭实验模型中的梗塞面积,并且这些抗重塑作用至少部分归因于使间隙连接活动重新同步。

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