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目的探讨肾血管性高血压犬中血管紧张素Ⅱ(AngⅡ)起作用的肾内机制。方法首先以双肾双夹法(2K2C)建立肾血管性高血压犬模型(缩窄组,n=5),与假手术犬(对照组,n=5)相对照。检测两组犬术前1d和术后4、8及12个月外周血AngⅡ的水平。术后12个月,对肾组织进行HE及AngⅡ受体的免疫组化检测。结果自术后2个月,缩窄组收缩压与术前1 d及对照组比较高出约25 mmHg(P<0.01,P<0.05)。术后缩窄组的外周血AngⅡ水平与基线值及对照组比较差异无统计学意义(P>0.05);术后12个月,缩窄组犬肾组织HE染色可见部分肾小管及肾小球呈透明变性等慢性肾缺血改变,免疫组化染色可见大量AngⅡ受体表达;而对照组肾组织未见透明变性,仅有少量AngⅡ受体表达。结论由慢性缺血的肾组织在局部所产生的AngⅡ可能是肾血管性高血压犬血压升高的主要作用机制之一。
Objective To investigate the renal mechanism of angiotensin Ⅱ (Ang Ⅱ) in renovascular hypertensive dogs. Methods Renal vascular hypertensive canine model was established by 2K2C (n = 5), compared with sham-operated dogs (n = 5). The levels of AngⅡ in the peripheral blood of the two groups were detected at 1 day before operation and 4, 8 and 12 months after operation. At 12 months after operation, immunohistochemistry of HE and Ang II receptors was performed on renal tissue. Results Compared with the control group, systolic blood pressure of the constriction group was about 25 mmHg (P <0.01, P <0.05) at 2 months after operation. There was no significant difference in AngⅡ level between peripheral narrowing group and control group after operation (P> 0.05). At 12 months after operation, some renal tubules and glomeruli Acute renal ischemic changes such as transparent degeneration, immunohistochemical staining showed a large number of Ang ¢ ò receptor expression; while the control group, no clear degeneration of renal tissue, only a small amount of Ang ¢ ò receptor expression. Conclusion AngⅡ produced locally by chronic ischemic renal tissue may be one of the major mechanisms of hypertension in dogs with renal vascular hypertension.