血量扩张与高钠负荷对内源性洋地黄样因子释放的影响

Effect of Volume expansion and intracerebroventricular infusion of artificial sodium-rich cerebrospinal fluid on the release of endogenous digitalis-like factor

目的 探讨血量扩张 (volumeexpansion ,VE)与高钠负荷对内源性洋地黄样因子 (endogenousdigitalis likefactor ,EDLF)释放的调节作用。方法 在大鼠VE或双侧迷走神经切断术后VE以及在大鼠侧脑室注射高钠人工脑脊液或高渗蔗糖人工脑脊液处理后 ,放射免疫方法测定血清EDLF浓度的变化。结果 ①大鼠VE后 ,血清EDLF浓度明显下降。②大鼠双侧迷走神经切断术后再VE后 ,血清EDLF浓度与VE前相比无明显差异。③侧脑室注射高钠人工脑脊液后大鼠血清EDLF浓度显著升高 :而侧脑室注射高渗蔗糖人工脑脊液后大鼠血清EDLF浓度无明显变化。结论 VE可抑制EDLF的释放 ,而脑室内高钠可促进EDLF的释放。表明EDLF可能参与了容量感受性反射引起的心血管调节反应和体内钠平衡的调节。

Objective To assess the role of volume expansion(VE) and sodium-rich load in the release of endogenous digitalis-like factor(EDLF). Methods Tritact rats or rats with bilateral vagotomy were treated with VE and rats were treated with intracerebroventricular infusion of artifical sodium-rich cerebrospinal fluid or hypertonic sucrose cerebrospinal fluid.After treatments,EDLF concentration in serum was measured with radioimmunoassay. Results ①EDLF concentration in serum was decreased after treatments with VE in the intact rats.②Following treatment with VE in rats with bilateral vagotomy.EDLF concentration in serum did not change.③EDLF concentration in serum increased significantly in rats treated with intracerebroventricular infusion of artifical sodium-rich cerebrospinal fluid;but EDLF concentration in serum did not change in rats treated with intracerebroventricular infusion of hypertonic sucrose cerebrospinal fluid.Conlusions Thesc findings suggest that VE stimulation decreased the release of EDIF and intracerebroventricular sedtum-rich stimulation increased the release of EDLE, and EDLF may play an important role in the regulation of cardiovascular and sodium homeostasis. [