Ahn Jwari, Varagic Jasmina, Slama Michel, Susic Dinko, Frohlich Edward D
Ochsner Clinic Foundation, New Orleans, Louisiana 70121, USA.
Am J Physiol Heart Circ Physiol. 2004 Aug;287(2):H767-72. doi: 10.1152/ajpheart.00047.2004. Epub 2004 Apr 1.
Increased dietary salt intake induces cardiac fibrosis in the spontaneously hypertensive rat (SHR), yet little information details its effects on left ventricular (LV) function. Additionally, young normotensive rats are more sensitive to the trophic effect of dietary sodium than older rats. Thus cardiac responses to salt loading were evaluated at two ages in the SHR; LV collagen content was also examined. SHR (8 or 20 wk of age) were given an 8% salt diet; their age-matched controls received standard chow. Echocardiographic indexes, arterial pressure, and LV hydroxyproline concentration were measured at 16 and 52 wk in the younger and older SHR groups, respectively. In most SHR, salt excess increased arterial pressure, LV mass, and hydroxyproline concentration and impaired LV relaxation manifested by prolonged isovolumic relaxation time, decreased early and atrial filling velocity ratio (V(E)/V(A)), and slower propagation velocity of E wave (V(P)). LV systolic function remained normal. However, one-quarter of the young salt-loaded SHR developed cardiac failure with systolic and diastolic dysfunction associated with greater LV mass and ventricular fibrosis. They also had lower arterial pressure, decreased fractional shortening, and a restrictive pattern of mitral flow. Moreover, the shorter deceleration time of the E wave and increased V(E)/V(P), an index of LV filling pressure, indicated increased LV stiffness in these rats. These findings demonstrated that sodium sensitivity in SHR is manifested not only by further pressure elevation but also by significant LV functional impairment that most likely is related to enhanced ventricular fibrosis. Moreover, the SHR are more susceptible to cardiac damage when high dietary salt is introduced earlier in life.
饮食中盐摄入量增加会诱发自发性高血压大鼠（SHR）的心脏纤维化，但关于其对左心室（LV）功能影响的详细信息却很少。此外，年轻的正常血压大鼠比老年大鼠对饮食中钠的营养作用更敏感。因此，在两个年龄段评估了SHR对盐负荷的心脏反应；还检测了左心室胶原蛋白含量。给8周龄或20周龄的SHR喂食8%的高盐饮食；与之年龄匹配的对照组给予标准饲料。分别在16周和52周时测量年轻和老年SHR组的超声心动图指标、动脉血压和左心室羟脯氨酸浓度。在大多数SHR中，盐过量会导致动脉血压升高、左心室质量增加和羟脯氨酸浓度升高，并损害左心室舒张功能，表现为等容舒张时间延长、早期和心房充盈速度比（V(E)/V(A)）降低以及E波传播速度减慢（V(P)）。左心室收缩功能保持正常。然而，四分之一的年轻高盐负荷SHR出现了心力衰竭，伴有收缩和舒张功能障碍，且左心室质量和心室纤维化程度更高。它们的动脉血压也较低，缩短分数降低，二尖瓣血流呈限制性模式。此外，E波减速时间缩短和V(E)/V(P)增加（左心室充盈压指标）表明这些大鼠的左心室僵硬度增加。这些发现表明，SHR的钠敏感性不仅表现为血压进一步升高，还表现为明显的左心室功能损害，这很可能与心室纤维化增强有关。此外，当在生命早期引入高盐饮食时SHR更容易受到心脏损伤。
