首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart
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Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart

机译:Lasalocid立即完全防止冠状动脉缺血再灌注造成的心肌损伤

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摘要

Lasalocid, a specific mobile membrane ionophore for calcium, dopamine and norepinephrine was assayed in its capacity to reduce or maintain unaltered the cardiovascular function in conditions of imminent myocardial injury. In experiments of coronary blockade and reperfusion carried out in rat heart, it was found that when administered from 5 to 30 minutes prior to the induction of coronary blockade, at a concentration of 2 mg/kg of body weight, the ionophore immediately, simultaneously, and completely interrupts the blood pressure decay, cardiac frequency increase, electrical ventricular tachycardia and fibrillation, as well as the fall of mitochondrial oxidative phosphorylation and decay of mitochondrial oxygen uptake provoked by the induced myocardial injury. It appears that the molecular mode of action of the lasalocid is associated with its unique ability to transport both calcium and the catecholamines, dopamine and norepinephrine, across mitochondrial and bimolecular lipid membranes, as well as through synaptic cell membrane terminals from rat heart, myocardial fibers of the heart and heart chromaffin membrane vesicles. It is suggested that for the potential medical use of lasalocid to detain incoming ischemic myocardial damage, there exists a need to develop a personal electronic device able to simultaneously monitor, detect, and inform on the very early and simultaneous signs of cardiac alterations of electrical, mechano-chemical, metabolic and hydraulic nature, all which precede heart failure and to administer the lasalocid.
机译:Lasalocid,用于钙,多巴胺和去甲肾上腺素的特定移动膜离子素,其能力减少或维持在迫在眉睫的心肌损伤条件下的心血管功能。在大鼠心脏中进行的冠状动脉膜障碍和再灌注的实验中,发现当在冠状动脉α诱导前5至30分钟施用时,以2mg / kg体重,离子载体同时,并完全中断血压衰减,心脏频率增加,电动心室心动过速和颤动,以及线粒体氧化磷酸化的下降和由诱导的心肌损伤引发的线粒体氧气吸收的衰减。似乎朗洛考的分子作用模式与其在线粒体和双分子脂膜上运输钙和儿茶酚胺,多巴胺和去甲肾上腺素的独特能力,以及通过大鼠心脏,心肌纤维的突触细胞膜末端心脏和心脏染色体膜囊泡。有人建议,对于延长延髓癌的潜在医学用来扣留入境缺血性心肌损伤,需要开发一种能够同时监测,检测和通知电气的早期和同步迹象的个人电子设备,机械化学,代谢和液压性质,所有这些都在心脏衰竭之前并施用Lasalocid。

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