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High-NaCl Diet Aggravates Cardiac Injury in Rats with Adenine-Induced Chronic Renal Failure and Increases Serum Troponin T Levels

机译:高NaCl饮食加重腺嘌呤诱发的慢性肾功能衰竭大鼠的心脏损伤,并增加血清肌钙蛋白T水平

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Aims: To examine the effects of 2 weeks of high-NaCl diet on left ventricular (LV) morphology and serum levels of cardiac troponin T (cTnT) in rats with adenine-induced chronic renal failure (ACRF). Methods: Male Sprague-Dawley rats either received chow containing adenine or were pair-fed an identical diet without adenine [controls (C)]. Approximately 10 weeks after the beginning of the study, the rats were randomized to either remain on a normal NaCl diet (NNa; 0.6%) or to be switched to high-NaCl chow (HNa; 4%) for 2 weeks, after which acute experiments were performed. Results: Rats with ACRF showed statistically significant increases (p < 0.001) in arterial pressure (AP), LV weight and fibrosis, and serum cTnT levels compared to controls. Two weeks of high-NaCl intake augmented the increases in AP, LV weight and fibrosis, and serum cTnT concentrations only in ACRF rats (p < 0.05 for group x NaCl intake interaction). Compared to group C-NNa, cTnT levels were elevated approximately 6-fold in group ACRF-NNa and 24-fold in group ACRF-HNa. Focal LV injury with cardiomyocyte necrosis, scarring, and fibrinoid necrosis of small arteries were only detected in group ACRF-HNa. There was a strong correlation between the degree of LV fibrosis and serum cTnT levels in ACRF rats (r = 0.81, p < 0.01). Conclusion: Two weeks of high-NaCl diet in rats with ACRF produces LV injury and aggravates increases in serum cTnT levels, presumably by causing hypertension-induced small artery lesions leading to myocardial ischemia. This model may be suitable for studying pathophysiological mechanisms in chronic renicardiac syndromes. (C) 2016 S. Karger AG, Basel
机译:目的:研究2周高NaCl饮食对腺嘌呤诱发的慢性肾衰竭(ACRF)大鼠左心室(LV)形态和心肌肌钙蛋白T(cTnT)血清水平的影响。方法:雄性Sprague-Dawley大鼠要么接受含腺嘌呤的食物,要么配对饲喂不含腺嘌呤的相同饮食[对照组(C)]。在研究开始约10周后,将大鼠随机分组,以正常的NaCl饮食(NNa; 0.6%)或改用高NaCl的食物(HNa; 4%)喂养2周,此后急性进行了实验。结果:与对照组相比,ACRF大鼠的动脉压(AP),LV重量和纤维化以及血清cTnT水平有统计学上的显着增加(p <0.001)。仅在ACRF大鼠中,高NaCl摄入量的两周增加了AP,LV重量和纤维化以及血清cTnT浓度的增加(对于组x NaCl摄入相互作用,p <0.05)。与C-NNa组相比,ACRF-NNa组的cTnT水平升高了约6倍,ACRF-HNa组的cTnT水平升高了24倍。仅在ACRF-HNa组中检测到局灶性LV损伤并伴有心肌细胞坏死,瘢痕形成和小纤维蛋白样坏死。 ACRF大鼠的左心室纤维化程度与血清cTnT水平密切相关(r = 0.81,p <0.01)。结论:ACRF大鼠高NaCl饮食两周会导致LV损伤,并加剧血清cTnT水平升高,可能是由于高血压引起的小动脉病变导致心肌缺血。该模型可能适合研究慢性肾综合征的病理生理机制。 (C)2016 S.Karger AG,巴塞尔

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