论文部分内容阅读
为观察延髓头端腹外侧区(rostral ventrolateral medulla,RVLM)一氧化氮(NO)在慢性心力衰竭(chronic heart failure,CHF)大鼠增强的心交感传入反射(cardiac sympathetic afferent reflex,CSAR)中的作用,实验在去压力感受器神经支配的结扎冠状动脉诱发的CHF大鼠和假手术SD大鼠进行,记录电刺激心交感传入神经中枢端前后的血压和肾交感神经活动(renal sympathetic nerve activity,RSNA)变化以评价CSAR。结果显示:(1)CHF大鼠的CSAR显著增强:(2)RVLM微量注射NO合酶(NOS)抑制剂MeTC增强对照组大鼠的CSAR但对CHF大鼠的CSAR无显著影响;(3)RVLM微量注射NO供体S-nitroso-N-acetyl-penicillamine(SNAP)抑制CHF大鼠增强的CSAR;(4)S-methyl-L-thiocitruline(MeTC)仅增强对照组大鼠基础水平的RSNA,而SNAP抑制对照组和CHF大鼠基础水平的RSNA。结果表明RVLM中内源性NO的减少是导致CHF大鼠CSAR增强的重要机制之一。
To investigate the effects of rostral ventrolateral medulla (NO) on cardiac sympathetic afferent reflex (CSAR) in rats with chronic heart failure (CHF) The experiment was performed in CHF rats and sham-operated SD rats induced by ligation of the coronary artery to governed by baroreceptor nerves, recording the effects of electrical stimulation on the sympathetic nerve activity and renal sympathetic nerve activity , RSNA) to evaluate CSAR. The results showed that: (1) CSAR was significantly increased in CHF rats: (2) microinjection of NO synthase (NOS) into RVLM increased the CSAR in control rats but did not affect CSAR in CHF rats; (3) N-acetyl-penicillamine (SNAP), an NO donor, was injected into RVLM at a dose-dependent manner. (4) S-methyl-L-thiocitruline (MeTC) only increased basal levels of RSNA in control rats, While SNAP inhibited basal levels of RSNA in control and CHF rats. The results show that the reduction of endogenous NO in RVLM is one of the important mechanisms leading to the enhancement of CSAR in CHF rats.