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Poor glycemic control impairs the cardioprotective effects of red blood cells on myocardial ischemia/reperfusion injury.
Nitric Oxide ( IF 3.2 ) Pub Date : 2020-01-22 , DOI: 10.1016/j.niox.2020.01.008
Johanna M Muessig 1 , Luise Moellhoff 1 , Johanna Noelle 1 , Sema Kaya 1 , Leonie Hidalgo Pareja 1 , Maryna Masyuk 1 , Michael Roden 2 , Malte Kelm 3 , Christian Jung 1
Affiliation  

Red blood cells (RBCs) play an important role in the cardiac ischemia/reperfusion (I/R) injury. Cardiovascular risk factors impair the RBC function in an endothelial nitric oxide synthase (eNOS) dependent manner. However, it is unclear whether the protective role of RBCs can be rescued by modifying cardiovascular risk factors or by pharmacologic intervention. RBCs obtained from elderly patients with or without diabetes as well as from young volunteers were treated with vehicle, eNOS inhibitor l-NAME and/or arginase inhibitor nor-NOHA before loading to the coronary system of isolated murine hearts in a Langendorff system before 40 min of global ischemia. RBCs from young and healthy volunteers as well as from aged persons and elderly diabetes patients with satisfying blood glucose control improved left ventricular function upon 60 min of reperfusion with Krebs-Henseleit buffer and reduced the infarct size compared to buffer treated controls. This cardioprotective effect was abolished in RBCs from aged diabetes patients with poor blood glucose control. Treatment of RBCs from elderly diabetes patients with nor-NOHA partly rescued the cardioprotective function. Thus, effective glucose control in aged diabetes patients rescues RBC-dependent cardioprotection in an ex-vivo model of myocardial I/R injury.

中文翻译:

血糖控制不良会损害红细胞对心肌缺血/再灌注损伤的心脏保护作用。

红细胞(RBC)在心脏缺血/再灌注(I / R)损伤中起重要作用。心血管危险因素以内皮一氧化氮合酶(eNOS)依赖性方式损害RBC功能。但是,尚不清楚是否可以通过改变心血管危险因素或通过药物干预来挽救红细胞的保护作用。在40分钟之前,将载有单独的鼠心的冠状动脉系统加载到Langendorff系统中,然后用赋形剂,eNOS抑制剂l-NAME和/或精氨酸酶抑制剂nor-NOHA处理从患有或不患有糖尿病的老年患者以及年轻志愿者中获得的RBC。全球缺血。与缓冲液治疗的对照组相比,Krebs-Henseleit缓冲液再灌注60分钟后,年轻,健康志愿者以及血糖水平令人满意的老年人和老年糖尿病患者的RBC改善了左心室功能,并减少了梗塞面积。在血糖控制不佳的老年糖尿病患者的红细胞中,这种心脏保护作用被取消。nor-NOHA治疗老年糖尿病患者的红细胞部分恢复了心脏保护功能。因此,在老年糖尿病患者中,有效的葡萄糖控制可以在心肌I / R损伤的体内模型中恢复RBC依赖性的心脏保护作用。在血糖控制不佳的老年糖尿病患者的红细胞中,这种心脏保护作用被取消。nor-NOHA治疗老年糖尿病患者的红细胞部分恢复了心脏保护功能。因此,在老年糖尿病患者的体内模型中,有效的葡萄糖控制可以恢复RBC依赖性的心脏保护作用。在血糖控制不佳的老年糖尿病患者的红细胞中,这种心脏保护作用被取消。nor-NOHA治疗老年糖尿病患者的红细胞部分恢复了心脏保护功能。因此,在老年糖尿病患者的体内模型中,有效的葡萄糖控制可以恢复RBC依赖性的心脏保护作用。
更新日期:2020-01-22
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