【摘要】 既往的研究表明 ,动脉压力感受性反射 (ABR)功能下降在高血压靶器官损伤中起独立作用。为进一步研究ABR功能下降致器官损伤的可能机制 ,实验采用去窦弓神经 (SAD)大鼠作为ABR受损的动物模型 ,分别测定清醒、自由活动状态下SAD及对照的假手术组大鼠 2 4h动脉血压、心率、血压波动性 (BPV)及心率波动性 (HRV)。并采用放免法测定血浆、心脏和肾脏组织的血管紧张素Ⅱ (AngⅡ)含量。结果发现 ,SAD术后 1周大鼠的 2 4h平均收缩压 (SBP)、舒张压 (DBP)均显著高于对照组及术后 18周的慢性期SAD大鼠。SAD术后 18周 ,2 4h平均SBP、DBP及HR与假手术对照组均无显著差异 ;2 4h收缩压波动性 (SBPV)和舒张压波动性 (DBPV)均显著高于对照组大鼠。SAD大鼠术后 1周的血浆、心脏和肾脏组织的AngⅡ 含量及术后 18周的血浆AngⅡ 水平与对照组之间相比无显著差异。而在术后慢性期 (18周 ) ,SAD大鼠的心肌及肾组织AngⅡ 含量显著高于假手术对照组大鼠。在术后 18周时 ,接受慢性应激刺激的SAD大鼠 ,其血浆、心肌及肾组织中AngⅡ水平显著高于同处应激状态下的假手术对照组大鼠及未接受应激刺激的SAD大鼠。这些结果表明 ,SAD术后急性期血压增高 ,但在慢性期平均血压并无增高 ,仅BPV增高 ;慢性期心、肾组织内AngⅡ 的分泌增加 ;在慢更多还原

【Abstract】 Our previous data demonstrate that impairment of arterial baroreceptor reflex (ABR) plays an independent role in hypertension target organ damage. To elucidate the mechanisms responsible for the dysfunction of ABR associated organ damage, sinoaortic denervated (SAD) rats were used as an animal model of ABR dysfunction. Twenty four hour continuous blood pressure (SBP and DBP), blood pressure variability (BPV), heart rate (HR) and HR variability (HRV) were measured in conscious and unrestrained rats. Angiotensin Ⅱ ( AngⅡ ) in plasma, heart and kidney was assayed by raio immunological assay (RIA) 1 or 18 weeks after denervation. In short term SAD rats, twenty four hour mean SBP and DBP increased compared with that of sham operated rats and long term SAD rats. No significant difference in SBP, DBP or HR was found between long term SAD rats and sham operated ones. Compared with the sham operated rats, long term SAD rats had elevated BPV. No significant change in AngⅡ levels of caridiac and renal tissues was found in short term SAD rats. In long term SAD rats, AngⅡ level of plasma was not increased while the AngⅡ content in the heart and kidney increased. AngⅡ contents of plasma and tissues in long term SAD rats exposed to chronic stress were higher than those in the control rats. These results show (1) in short term SAD rats blood pressure increased, while in long term SAD rats 24 h mean blood pressure did not increase, although BPV elevated in long term SAD rats; (2) in long term SAD rats, secretion of AngⅡ in cardiac and renal tissues was enhanced and more AngⅡ released when the animals were exposed to chronic stress. These results suggest that elevated BPV and secretion of AngⅡ may be related to the development of organ damage induced by ABR dysfunction.更多还原