Uysal Erdal, Dokur Mehmet, Altınay Serdar, Saygılı Eyup İlker, Batcıoglu Kadir, Ceylan Mehmet S, Kazımoglu Hatem, Uyumlu Burcin A, Karadag Mehmet
a Department of General Surgery , Sanko University School of Medicine , Gaziantep , Turkey.
b Emergency, Dr. Necip Fazil City Hospital , Kahramanmaras , Turkey.
J Invest Surg. 2018 Oct;31(5):402-411. doi: 10.1080/08941939.2017.1343880. Epub 2017 Jul 14.
In our study, it was aimed to investigate the preventive effect of milrinone on renal damage in experimental controlled non-heart-beating donors (NHBDs) model.
Sixteen rats randomly divided into 2 groups, 8 rats in each were used. Group 1 was control, group 2 was milrinone group. Group 1 rats received 1.25 ml 0.09% NaCl intraperitoneally equivalent to the milrinone diluted volume. Group 2 rats were administered intraperitoneally with 0.5 mg/kg of milrinone 2 hours before cardiac arrest. After the cardiac arrest, left nephrectomy was applied to the rats. Malondialdehyde, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) activities, Caspase-3 (apoptotic index) and histopathological evaluation were performed in the tissues.
In the milrinone group, the total injury score was significantly lower relative to the control group (p = 0.001). Caspase-3 staining was moderately strong in the control group but weaker in the milrinone group. Apoptotic index was significantly lower in the milrinone group compared to the control group (p = 0.001). In comparison between groups, SOD and GPx in the milrinone group was significantly higher than the control group (p = 0.008, p = 0.006).
Milrinone has been shown to be effective in the prevention of tissue damage due to oxidative stress and inflammatory process in the renal of warm ischemia in the experimental NHBDs model and in protecting the renal. Milrinone increases antioxidant activity while reducing apoptosis. Systemic administration of milrinone prior to cardiac arrest may be beneficial. Administration of milrinone to the recipient in the perioperative period may contribute to donor function.
在我们的研究中，旨在探讨米力农对实验性控制性非心脏跳动供体（NHBDs）模型中肾脏损伤的预防作用。
将16只大鼠随机分为2组，每组8只。第1组为对照组，第2组为米力农组。第1组大鼠腹腔注射1.25 ml 0.09%氯化钠，其体积等同于米力农稀释后的体积。第2组大鼠在心脏骤停前2小时腹腔注射0.5 mg/kg米力农。心脏骤停后，对大鼠实施左肾切除术。对组织进行丙二醛、超氧化物歧化酶（SOD）、过氧化氢酶、谷胱甘肽过氧化物酶（GPx）活性、半胱天冬酶-3（凋亡指数）检测及组织病理学评估。
米力农组的总损伤评分相对于对照组显著降低（p = 0.001）。半胱天冬酶-3染色在对照组中中等强度，但在米力农组中较弱。米力农组的凋亡指数与对照组相比显著降低（p = 0.001）。组间比较，米力农组的SOD和GPx显著高于对照组（p = 0.008，p = 0.006）。
在实验性NHBDs模型中，米力农已被证明在预防热缺血肾脏中氧化应激和炎症过程导致的组织损伤以及保护肾脏方面是有效的。米力农增加抗氧化活性同时减少细胞凋亡。心脏骤停前全身给予米力农可能有益。围手术期向受体给予米力农可能有助于供体功能。
