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体外冲击波治疗减轻了心肾综合征小型猪的左心室功能障碍和重塑。

Extracorporeal shock wave treatment attenuated left ventricular dysfunction and remodeling in mini-pig with cardiorenal syndrome.

作者信息

Sheu Jiunn-Jye, Ali Hani E E, Cheng Ben-Chung, Chiang Hsin-Ju, Sung Pei-Hsun, Chen Kuan-Hung, Yang Chih-Chao, Chen Yen-Ta, Chiang John Y, Lin Pao-Yuan, Chua Sarah, Chai Han-Tan, Chung Sheng-Ying, Sun Cheuk-Kwan, Yip Hon-Kan

机构信息

Division of Thoracic and Cardiovascular Surgery, Department of Surgery, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

出版信息

Oncotarget. 2017 May 30;8(33):54747-54763. doi: 10.18632/oncotarget.18287. eCollection 2017 Aug 15.

DOI:10.18632/oncotarget.18287
PMID:
28903379
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5589618/
Abstract

This study tested the hypothesis that extracorporeal shock wave (ECSW) treatment can improve ischemia-induced left ventricular (LV) dysfunction in mini-pig with co-existing chronic kidney disease (CKD). LV ischemia in mini-pigs was induced by applying an ameroid constrictor over mid-left anterior descending artery (LAD), while model of CKD was established by right nephrectomy with partial ligation of left renal arterioles 2 weeks before LAD constriction. Thirty mini-pigs were randomly divided into group 1 (sham-control), group 2 (LV-ischemia), group 3 (LV-ischemia + CKD), Group 4 [LV-ischemia + ECSW (applied 1200 shots at 0.1 mJ/m/equally to 4-ischemic regions by day-90 after LAD constriction], and group 5 (LV-ischemia-CKD + ECSW). By day-180 after CKD induction, echocardiography showed that LV ejection fraction (LVEF) was highest in group 1, lowest in group 3, significantly lower in group 2 than that in groups 4 and 5, and significantly lower in group 5 than that in group 4, whereas LV-end systolic and diastolic dimensions displayed an opposite pattern (all p<0.001). Protein expressions of oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptotic (cleaved-caspase-3/cleaved-PARP/mitochondrial-Bax), fibrotic (TGF-β/Smad3), pressure/volume-overload (BNP/β-MHC), endothelial (CD31/vWF) and mitochondrial-integrity (PGC-1/mitochondrial-cytochrome-C) biomarkers exhibited a pattern identical to that of LVEF, whereas angiogenesis factors (VEGF/CXCR4/SDF-1α) showed significant progressive increase among all groups (all p<0.0001). Microscopic findings of CD31+cells/vWF+cells/small-vessel density/sarcomere-length showed an identical pattern, whereas collagen-deposition area/fibrotic area/apoptotic nuclei expressed an opposite pattern compared to that of LVEF among all groups (all p<0.0001). In conclusion, CKD aggravated ischemia-induced LV dysfunction and remodeling and molecular-cellular perturbations that were reversed by ECSW treatment.

摘要

本研究检验了以下假设

体外冲击波（ECSW）治疗可改善合并慢性肾脏病（CKD）的小型猪缺血诱导的左心室（LV）功能障碍。通过在左前降支（LAD）中段上方应用阿梅氏缩窄环诱导小型猪LV缺血，而在LAD缩窄前2周通过右肾切除并部分结扎左肾小动脉建立CKD模型。30只小型猪随机分为1组（假手术对照组）、2组（LV缺血组）、3组（LV缺血+CKD组）、4组[LV缺血+ECSW组（在LAD缩窄后90天对4个缺血区域等能量施加1200次，能量为0.1 mJ/m）]和5组（LV缺血-CKD+ECSW组）。在诱导CKD后180天，超声心动图显示，1组的LV射血分数（LVEF）最高，3组最低，2组显著低于4组和5组，5组显著低于4组，而LV收缩末期和舒张末期内径呈现相反模式（均p<0.001）。氧化应激（NOX-1/NOX-2/氧化蛋白）、凋亡（裂解的半胱天冬酶-3/裂解的聚ADP核糖聚合酶/线粒体Bax）、纤维化（转化生长因子-β/Smad3）、压力/容量超负荷（脑钠肽/β-肌球蛋白重链）、内皮（CD31/vWF）和线粒体完整性（PGC-1/线粒体细胞色素C）生物标志物的蛋白表达呈现与LVEF相同的模式，而血管生成因子（血管内皮生长因子/CXCR4/基质细胞衍生因子-1α）在所有组中均呈现显著的逐渐增加（均p<0.0001）。CD31+细胞/vWF+细胞/小血管密度/肌节长度的微观观察结果呈现相同模式，而胶原沉积面积/纤维化面积/凋亡细胞核在所有组中与LVEF相比呈现相反模式（均p<0.0001）。总之，CKD加重了缺血诱导的LV功能障碍、重塑以及分子细胞紊乱，而ECSW治疗可使其逆转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/97175504be7a/oncotarget-08-54747-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/f7b12fe3fff5/oncotarget-08-54747-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/97175504be7a/oncotarget-08-54747-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/d2b692ef23d6/oncotarget-08-54747-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/f449f1e00fc3/oncotarget-08-54747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/703ccc0157e1/oncotarget-08-54747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d723/5589618/9bff7c1b8400/oncotarget-08-54747-g006.jpg
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