Hori K, Mirsky I, Fouad-Tarazi F M
Department of Heart and Hypertension Research, Cleveland Clinic Foundation, Ohio 44195-5069.
Cardiovasc Res. 1989 May;23(5):432-42. doi: 10.1093/cvr/23.5.432.
Since in vivo ejection fraction is said to be reduced in chronically sodium depleted dogs, this study was conducted to investigate the direct effects of sodium deprivation on intrinsic ventricular contractility, independent of haemodynamic or adrenergic influences. Since low sodium diet and/or diuretics are commonly used in the treatment of hypertension, we included a hypertensive group in the study. Normotensive male Sprague-Dawley rats and age matched renovascular hypertensive rats were subdivided into three groups. The first group was fed regular sodium diet (RS) for 6 weeks. The second (LS) and third (LSD) groups received low sodium diet for 6 weeks, and the LSD group also received diuretic (frusemide) treatment to achieve marked sodium depletion (last dose given 2 weeks before the cardiac study). Left ventricular (LV) contractility was investigated in the isolated isovolumetric rat heart (Langendorff preparation) paced at 180 beats-min-1. Results showed that LV +dP/dt max at zero LV end diastolic pressure was higher (p less than 0.01) in the LSD group than in the other groups in normotensive rats [2672 (SEM127) mm Hg.s-1 in LSD, 2267(96) in LS, 2174(111) in RS] and higher in LSD (p less than 0.01) and LS (p less than 0.05) groups than in the RS group in hypertensive rats [2332(110) mm Hg.s-1, 2287(93), 1781(104), respectively]. Calculated LV balloon volume at zero LV end diastolic pressure was not significantly different in any dietary group. These results suggested that after 6 weeks of in vivo sodium depletion, in vitro LV contractility was enhanced rather than depressed under these experimental conditions. This enhancement is contrary to the in vivo findings in the dog model and could not be explained by differences in myocardial flow rate, LV chamber stiffness or myocardial stiffness constant. The mechanism of this accentuated ventricular contractility under these experimental conditions remains to be determined.
由于据说长期缺钠的犬体内射血分数会降低，因此进行本研究以探讨缺钠对心室固有收缩性的直接影响，而不受血流动力学或肾上腺素能的影响。由于低钠饮食和/或利尿剂常用于治疗高血压，我们在研究中纳入了一个高血压组。将正常血压的雄性Sprague-Dawley大鼠和年龄匹配的肾血管性高血压大鼠分为三组。第一组喂食常规钠饮食（RS）6周。第二组（LS）和第三组（LSD）接受低钠饮食6周，并且LSD组还接受利尿剂（速尿）治疗以实现明显的钠耗竭（在心脏研究前2周给予最后一剂）。在以180次/分钟起搏的离体等容大鼠心脏（Langendorff标本）中研究左心室（LV）收缩性。结果显示，在正常血压大鼠中，LSD组在零左心室舒张末期压力时的LV +dP/dt max高于其他组（p<0.01）[LSD组为2672（标准误127）mmHg·s-1，LS组为2267（96），RS组为2174（111）]，在高血压大鼠中，LSD组（p<0.01）和LS组（p<0.05）的LV +dP/dt max高于RS组[分别为2332（110）mmHg·s-1，2287（93），1781（104）]。在零左心室舒张末期压力时计算的左心室球囊容积在任何饮食组中均无显著差异。这些结果表明，在体内钠耗竭6周后，在这些实验条件下，体外左心室收缩性增强而非减弱。这种增强与犬模型中的体内研究结果相反，并且不能用心肌流速、左心室腔硬度或心肌硬度常数的差异来解释。在这些实验条件下这种增强的心室收缩性的机制仍有待确定。
