Rossi G, Bond M, Fouad-Tarazi F M
Research Institute of the Cleveland Clinic Foundation, OH 44106.
Am J Med Sci. 1989 Mar;297(3):153-7. doi: 10.1097/00000441-198903000-00004.
Increased myocardial contractility was found in the perfused heart isolated from sodium depleted Sprague-Dawley rats. Previously, it was reported that in vitro exposure of different cardiac preparations to low Na+ buffers was associated with both an increased contractility and an increased Ca2+ content in the cells. Therefore, this study was designed to examine increases in ventricular Ca2+ content in the hearts of chronically sodium depleted rats. Two groups of 12-week-old Sprague-Dawley rats were studied. One group (n = 5) received furosemide (5 mg/kg/day IP for 4 days), a low Na+ diet and distilled drinking water for 6 weeks (low sodium plus diuretics group = LSD). The other group (n = 5) received the same low Na+ diet, but 0.5% NaCl was supplemented in drinking water (regular sodium group = RS). Body weight and blood pressure were measured weekly during the dietary period in all rats. At the end of the 6 weeks, heart weight as well as water and electrolyte contents of the heart were measured in all animals. Results showed that both body weight and heart weight were significantly lower in LSD than in RS. Moreover, ventricular Na+ content was reduced while ventricular Ca2+ content was doubled in LSD compared to RS (8.2 +/- 0.2 units vs. 9.2 +/- 0.3 units, p less than .05 and 0.45 +/- 0.13 units vs. 0.23 +/- 0.01 units, p less than .01, respectively). We conclude that in vivo sodium depletion induces an increase in ventricular calcium content; this increased myocardial calcium may be related to the increased in vitro cardiac contractility observed after chronic in vivo sodium depletion, but its distribution between intracellular and extracellular compartments needs to be determined.
在从缺钠的斯普拉格 - 道利大鼠分离出的灌注心脏中发现心肌收缩力增强。此前有报道称，不同心脏制剂在体外暴露于低钠缓冲液时，细胞内收缩力增强且钙含量增加。因此，本研究旨在检测长期缺钠大鼠心脏心室钙含量的增加情况。研究了两组12周龄的斯普拉格 - 道利大鼠。一组（n = 5）接受呋塞米（5毫克/千克/天，腹腔注射，共4天）、低钠饮食和蒸馏水饮用6周（低钠加利尿剂组 = LSD）。另一组（n = 5）接受相同的低钠饮食，但饮用水中补充0.5%氯化钠（正常钠组 = RS）。在饮食期间，每周测量所有大鼠的体重和血压。6周结束时，测量所有动物的心脏重量以及心脏的水和电解质含量。结果显示，LSD组的体重和心脏重量均显著低于RS组。此外，与RS组相比，LSD组心室钠含量降低，而心室钙含量增加了一倍（分别为8.2±0.2单位对9.2±0.3单位，p < 0.05；0.45±0.13单位对0.23±0.01单位，p < 0.01）。我们得出结论，体内缺钠会导致心室钙含量增加；这种心肌钙含量的增加可能与长期体内缺钠后体外观察到的心脏收缩力增强有关，但其在细胞内和细胞外区室之间的分布需要确定。
