胰激肽原酶对自发性高血压大鼠心肌纤维化及NO含量的影响

目的：探讨胰激肽原酶对自发性高血压大鼠（SHR）血压、心肌纤维化及血清一氧化氮（NO）含量的影响。方法：雄性15周龄SHR 24只，随机分成SHR组、胰激肽原酶组和卡托普利组，每组8只，另取8只雄性15周龄Wistar大鼠作为正常血压对照组。胰激肽原酶组腹腔注射（7.2 U?kg^-1?d^-1），卡托普利组灌胃给药（10 mg?kg^-1?d^-1），SHR组和正常血压对照组给0.9% NaCl溶液腹腔注射（2 mL?kg^-1?d^-1），各组均连续4周给药。实验4周后行颈动脉插管测量血压，然后处死动物，测量各组左心室重量指数（LVMI）、心肌胶原体积比例（CVF）、心肌血管周围胶原与管腔面积的比例（PVCA）及血清NO含量。结果：SHR组SBP、LVMI、CVF、PVCA增高，血清NO含量下降，与正常血压对照组比较差异均具有显著性（P<0.05）。用药4周后，胰激肽原酶组SBP、LVMI、CVF及PVCA均较SHR组显著下降，两组比较差异均具有显著性（P<0.05）；胰激肽原酶组NO含量明显升高且接近正常血压对照组水平；胰激肽原酶组除SBP外的各项指标与卡托普利组比较差异均无显著性（P>0.05）。结论：胰激肽原酶具有降低SHR血压和逆转心肌纤维化的作用，其机制可能与增加NO含量有关。

Effects of pancreatic kininogenase on myocardical fibrosis and serum nitric oxide level in spontaneously hypertensive rats

Objective To investigate the effects of pancreatic kininogenase on pressure,myocardical fibrosis and serum nitric oxide (NO) level in spontaneously hypertensive rats (SHR). Methods Twenty-four (fifteen weeks) male SHR were randomly divided into three groups:SHR group,pancreatic kininogenase group and captopril group(n=8 ),8 male Wistar kyoto rats with normal blood pressure were considered as control group. Pancreatic kininogenase was given by peritoneal injection (7.2 U·kg~ -1 ·d~ -1 ), captopril was given by intragastric administration(10 mg·kg~ -1 ·d~ -1 ), the rats in SHR group and rats with normol blood pressure in control group were treated with 0.9% NaCl(2 mL·kg~ -1 ·d~ -1 )administered through peritoneal injection. After four-week experiment, the pressure was measured in rats througth carotid artery,then the rats were sacrificed , and LVMI,CVF,PVCA and serum NO level were measured. Results In SHR group, SBP,LVMI,CVF and PVCA were higher, serum NO level was decreased obviously than those in control group (P<0.05). After treatment of pancreatic kininogenase,the serum NO level raised obviously,other indexes obviously reduced than those in SHR group (P<0.05),but except SBP,there were no significant difference compared with captopril group (P>0.05). Conclusion Pancreatic kininogenase can obviously reduce the blood pressure and reverse myocardial fibrosis,its mechanism may be concerned with the increasing of NO level in SHR.