Centro de Invención e Innovación Tecnológica de México, S.C., Dakota 14-8, Col. Nápoles, C. P. 03810, Ciudad de México, Deleg. Benito Juárez, México.
, Retorno de Los Leones 58, C. P. 01710, Ciudad de México, Mexico.
Mol Cell Biochem. 2019 Mar;453(1-2):121-130. doi: 10.1007/s11010-018-3437-2. Epub 2018 Sep 6.
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.
拉沙里菌素是一种专门的可移动膜钙离子载体、多巴胺和去甲肾上腺素载体,用于评估其在即将发生心肌损伤的情况下减少或维持心血管功能不变的能力。在大鼠心脏进行的冠状动脉阻断和再灌注实验中发现,当在诱导冠状动脉阻断前 5 至 30 分钟内以 2 毫克/千克体重的浓度给药时,该载体立即、同时且完全中断血压下降、心率增加、电室性心动过速和纤维性颤动,以及诱导性心肌损伤引起的线粒体氧化磷酸化下降和线粒体耗氧量下降。拉沙里菌素的分子作用模式似乎与其独特的能力有关,即能够跨线粒体和双分子脂膜以及通过突触细胞膜末端从大鼠心脏、心肌纤维和心脏嗜铬细胞膜小泡转运钙和儿茶酚胺,多巴胺和去甲肾上腺素。因此,为了将拉沙里菌素潜在地用于阻止传入性缺血性心肌损伤,需要开发一种能够同时监测、检测和报告早期和同时发生的电、机械化学、代谢和液压性质的心脏改变的个人电子设备,所有这些都发生在心力衰竭之前,并给予拉沙里菌素。