中文摘要：

目的交感神经活动亢进是慢性心力衰竭（CHF）的主要心血管改变特征之一，并与压力交感反射的功能低下密切相关。孤束核（NTS）是压力反射中枢传递的关键核团，本研究将明确心血管中枢NTS超氧阴离子在介导CHF压力交感反射低下中的作用。方法SD大鼠通过结扎冠状动脉左前降支后获得CHF模型，对照为假手术组（Sham），并通过NTS微量注射超氧化物歧化酶模拟剂Tempol比较观察两组动物肾交感神经活动和压力交感反射敏感性的影响。结果在麻醉动物模型上，CHF交感神经活动基础值高于Sham组（P〈0．05），而压力交感反射敏感性低于Sham组。Sham组NTS微量注射Tempol（10nmol／50nL）不影响基础肾交感神经活动和压力交感反射敏感性，而在CHF组，Tempol能降低肾交感神经活动（P〈0．05），并增加压力反射敏感性。结论NTS超氧阴离子不仅参与CHF交感兴奋性的增加，而且具有降低压力交感反射敏感性作用，提示NTS氧化应激是CHF心血管活动异常的重要机制。

英文摘要：

Objective To determine the role of the nucleus tractus solitarii （NTS） superoxide in mediating the chronic heart failure （CHF）-induced reduction in baroreflex control of sympathetic activity. Methods CHF model was produced by coronary ligation in SD rats, and rats receiving sham operation （Sham） served as controls. Changes in renal sympathetic nerve activity （RSNA） and baroreflex sensitivity control of sympathetic activity were observed after microinjections of SOD mimic Tempol into the NTS in Sham and CHF rats. Results In anesthetized rats, the baseline level of sympathetic nerve activity was significantly higher in CHF group than in Sham group （P~0.05）, whereas the baroreflex sensitivity control of sympathetic activity was lower in CHF group than in Sham group. Bilateral microinjection of Tempol （10 nmol in 50 nL） into the NTS had no effect on baseline RSNA and baroreflex sensitivity in the Sham group. In contrast, injection of Tempol notably reduced the baseline RSNA and increased baroreflex sensitivity in CHF group. Conclusion Superoxide in the NTS contributes to sympathetic overactivity and baroreflex impairment in rats with CHF, suggesting that increased oxidative stress in the NTS is resoonsible for cardiovascular dysfunctions in CHF.