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目的 研究动脉压力反射 (ABR)功能下降加重高血压靶器官损伤的机制。方法 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 4小时动脉血压、心率、血压波动性 (BPV)及心率波动性 (HRV)。精氨酸加压素 (AVP)的测定采用放免法。结果 SAD术后 1周 ,2 4小时平均收缩压 (SBP)、舒张压 (DBP)均显著高于对照组及术后18周的慢性SAD大鼠。SAD术后 18周 ,2 4小时平均SBP、DBP及HR与假手术对照组均无显著差异 ;2 4小时SBPV、DBPV均显著高于对照组大鼠。SAD术后 1周 ,血浆AVP含量与假手术对照组大鼠相比明显升高 ;至术后 18周时 ,未接受应激的SAD大鼠与假手术大鼠的AVP含量相比无显著差异 ,慢性应激刺激状态下的SAD大鼠的血浆AVP含量显著高于对照组大鼠及未接受应激刺激的SAD大鼠。结论 ABR功能受损的慢性期平均血压无升高 ,但BPV升高 ,慢性应激可致AVP过度释放
Objective To study the mechanism of arterial baroreflex (ABR) function decline in hypertensive target organ injury. Methods Antral sinusoidal (SAD) rats were used as animal models of impaired ABR. The 24-hour arterial blood pressure, heart rate, blood pressure variability (BPV) and heart rate variability (HRV) of sham-operated and sham-operated sham-operated rats were measured respectively. Arginine vasopressin (AVP) determination using radioimmunoassay. Results The mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) at 24 hours after SAD were significantly higher than those in control group and chronic SAD rats at 18 weeks after operation. There were no significant differences in average SBP, DBP and HR between the 24-hour SAD and sham-operated control groups at 24 weeks after operation; SBPV and DBPV at 24 hours were significantly higher than those in the control group. At 1 week after SAD, plasma AVP level was significantly higher than that in sham operation control group. At 18 weeks after operation, there was no significant difference in AVP content between SAD rats and sham operated rats , And the content of AVP in SAD rats under chronic stress stimulation was significantly higher than that in control rats and SAD rats without stimulation. Conclusions There is no increase of mean blood pressure in chronic phase with impaired ABR function, but elevated BPV. Chronic stress can cause over-release of AVP