延髓头端腹外侧区一氧化氮与慢性心力衰竭大鼠心交感传入反射的关系

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 heartfailure,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-thiocitmline(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.

Reduced nitric oxide in the rostral ventrolateral medulla enhances cardiac sympathetic afferent reflex in rats with chronic heart failure

The purpose of this study was to determine the effect of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM)on the central integration of the cardiac sympathetic afferent reflex (CSAR) in normal rats and in rats with coronary ligationinduced chronic heart failure (CHF). Under α-chloralose and urethane anesthesia, mean arterial pressure, heart rate and renal sympathetic nerve activity (RSNA) were recorded at baseline and during elicitation of the CSAR evoked by electrical stimulation of the cardiac afferent sympathetic nerves in sino-aortic denervated and cervical vagotomized rats. A cannula was inserted into the left RVLM for microinjection of NO synthase inhibitor, S-methyl-L-thiocitruline (MeTC) or NO donor, S-nitroso-N-acetyl-penicillamine (SNAP). The CSAR was tested by electrical stimulation (5, 10, 20 and 30 Hz at 10 V for 1 ms) of the afferent cardiac sympathetic nerves. It was observed that (1) the responses of RSNA to stimulation were enhanced in rats with CHF; (2) MeTC (80nmol) potentiated the responses of RSNA to stimulation in sham rats but not in rats with CHF; (3) SNAP (50 nmol) depressed the enhanced RSNA response to stimulation in CHF rats but had no effect in sham rats; and (4) MeTC increased the baseline RSNA and MAP only in sham rats, but SNAP inhibited the baseline RSNA and MAP in both sham and CHF rats. These results indicate that reductance of NO in the RVLM is involved in the augmentation of CSAR in CHF rats.