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目的探索心力衰竭(HF)时下丘脑室旁核(PVN)氧化应激反应是否能够增强肾交感神经(RSNA)活动,进而促进HF的发生发展。方法取SD大鼠行冠脉结扎术制作心衰模型,对照组(SHAM)大鼠不结扎冠脉,两天后通过侧脑室插管给予tempol(氧自由基清除剂)或人工脑脊液(VEH)。正常饲养4周后,测量各组大鼠血流动力学、RSNA、PVN区域NADPH亚基gp91 phox的表达。结果HF组大鼠心功能明显低于SHAM组大鼠,RSNA增强、PVN区域NADPH亚基gp91 phox的表达增加。HF大鼠给予tempol治疗后心功能各项指标有所改善,RSNA减弱,PVN区域gp91 phox的表达降低,但达不到SHAM组水平。结论心衰时PVN区域氧化应激反应增强与RSNA增加有关,降低该区域氧自由基水平可能延缓HF的发生发展过程。
Objective To explore whether oxidative stress in the hypothalamic paraventricular nucleus (PVN) in heart failure (HF) can enhance the renal sympathetic nerve (RSNA) activity and then promote the development of HF. Methods A rat model of heart failure was established by coronary artery ligation in SD rats. The rats in the control group (SHAM) were not ligated with coronary artery. Two days later, tempol (oxygen free radical scavenger) or artificial cerebrospinal fluid (VEH) was administered through the lateral ventricle. After 4 weeks of normal feeding, hemodynamics, expression of gp91 phox of NADPH subunit in RSNA and PVN were measured. Results The cardiac function in HF group was significantly lower than that in SHAM group. RSNA increased and the expression of gp91 phox in NADPH subunit of PVN increased. The indexes of cardiac function in HF rats were improved after treatment with tempol, RSNA weakened, while the expression of gp91 phox in PVN decreased but not reached the level in SHAM group. Conclusions The increase of oxidative stress response in PVN is related to the increase of RSNA in heart failure. Decreasing the level of oxygen free radicals in this area may delay the occurrence and development of HF.