肾缺血增强大鼠延髓腹外侧头端区神经元电话动和Fos蛋白表达

在67只切断两侧缓冲神经的麻醉Sprague-Dawley大鼠,应用细胞外记录的电生理方法和免疫组织化学技术,分别观察肾缺血对延髓腹外侧头端区巨细胞旁外侧核神经元自发放电活动和Fos蛋白表达的影响.所得结果如下(1)左肾动脉阻断后,28个单位的放电频率由11.40±1.08增至21.1±1.74spikes/s(P<0.001),血压和心率无明显变化(P>0.05);(2)在17个放电单位中,应用腺苷受体拮抗剂8-苯茶碱(8-phenyltheophylline,10mg/kg)可明显抑制肾缺血的兴奋效应(P<0.05);(3)肾缺血后,延髓腹外侧头端区的Fos蛋白样免疫反应神经元显著增加(P<0.01);(4)预先应用8-苯茶碱可明显减弱肾缺血所激活的Fos蛋白表达反应(P<0.05).以上结果提示肾缺血增强延髓腹外侧头端区神经元的放电活动和Fos蛋白表达,而此作用可能与肾脏缺血所产生的腺苷激活肾内感受器有关.

Renal ischemia enhances electrical activity and Fos protein expression of the rostral ventrolateral medullary neurons in rats

The effects of renal ischemia on spontaneous electrical activity and Fos protein expression of nucleus paragigantocellularis lateralis (PGL) in rostral ventrolateral medulla (RVLM) were observed in 67 anesthetized Sprague-Dawley rats with sinoaortic denervation by using extracellular recording and immunohistochemical techniques. The results obtained are as follows. (1) Renal ischemia increased the discharge rate from 11.40 +/- 1.08 to 21.1 +/- 1.74 spikes/s (P < 0.001) in 28 out of 30 PGL neurons, while blood pressure and heart rate had no significant change (P > 0.05). (2) Administration of 8-phenyltheophylline (8-PT), an adenosine receptor antagonist, did not affect the discharge rate of PGL neurons, but could partially inhibit the effects of renal ischemia in 17 units (P < 0.05). (3) Renal ischemia resulted in a remarkable increase in the number of Fos-like protein immunoreactive PGL neurons in the RVLM (P < 0.01). (4) Fos protein expression induced by renal ischemia was significantly inhibited by pretreatment with 8-PT (P < 0.05). Taken together, it is concluded that renal ischemia induces an increase in spontaneous electrical activity and Fos protein expression in PGL neurons of RVLM, and that adenosine released within ischemic kidney may be involved in such effects.