Kashioulis Pavlos, Hammarsten Ola, Marcussen Niels, Shubbar Emman, Saeed Aso, Guron Gregor
Department of Molecular and Clinical Medicine/Nephrology, University of Gothenburg, Gothenburg, Sweden.
Department of Clinical Chemistry and Transfusion Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Cardiorenal Med. 2016 Aug;6(4):317-27. doi: 10.1159/000446547. Epub 2016 Jun 22.
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).
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.
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 × 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).
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.
研究高盐饮食2周对腺嘌呤诱导的慢性肾衰竭（ACRF）大鼠左心室（LV）形态及血清心肌肌钙蛋白T（cTnT）水平的影响。
雄性Sprague-Dawley大鼠，一部分给予含腺嘌呤的饲料，另一部分给予不含腺嘌呤的相同饲料作为对照（C组）。研究开始约10周后，将大鼠随机分为两组，一组继续给予正常NaCl饮食（NNa组，0.6%），另一组改为高盐饲料（HNa组，4%），持续2周，之后进行急性实验。
与对照组相比，ACRF大鼠的动脉血压（AP）、左心室重量和纤维化程度以及血清cTnT水平均有统计学显著升高（p < 0.001）。高盐摄入2周仅使ACRF大鼠的AP、左心室重量和纤维化程度以及血清cTnT浓度进一步升高（组×NaCl摄入交互作用，p < 0.05）。与C-NNa组相比，ACRF-NNa组的cTnT水平升高约6倍，ACRF-HNa组升高约24倍。仅在ACRF-HNa组检测到左心室局灶性损伤，伴有心肌细胞坏死、瘢痕形成和小动脉纤维蛋白样坏死。ACRF大鼠左心室纤维化程度与血清cTnT水平之间存在强相关性（r = 0.81，p < 0.01）。
ACRF大鼠高盐饮食2周会导致左心室损伤并加重血清cTnT水平升高，可能是通过引起高血压诱导的小动脉病变导致心肌缺血。该模型可能适用于研究慢性肾心综合征的病理生理机制。
