nor-NOHA逆转自发性高血压大鼠血管重构

目的 探讨精氨酸酶抑制剂nor-NOHA对自发性高血压大鼠（SHR）血管重构的影响。方法WKY大鼠作为对照组，SHR随机分为模型组与受试组，受试组每天腹腔注射nor-NOHA(40 mg/kg)，定期测量大鼠收缩压和体质量，10周后，采用酶谱法检测心、肾及胸主动脉组织中活性MMP-2的含量，并对胸主动脉进行Tricrome- Masson，Picric-Sirius red 及Orcein组织特染观察中膜厚度（MT）、管腔内径（LD）、径腔比（M/L）、Ⅰ型和Ⅲ型胶原及弹力纤维面积百分比值等。 结果 受试组收缩压显著下降、左心室MMP-2较SHR组含量显著降低（P＜0.05)，胸主动脉的MT、M/L、Ⅰ型和Ⅲ型胶原蛋白均下降（P＜0.05)。结论 nor-NOHA可能通过抑制MMP-2活性及降低Ⅰ型和Ⅲ型胶原的合成而缓解SHR血管重构。

Effect of arginase inhibitor on the vascular remodeling in SHR

Objective To determine the role of arginase inhibitor (nor-NOHA) on vascular remodeling in SHRs. Methods WKY rats were used as the control and SHR were randomly divided into control (SHR) and treatment group(SHR-T). SHR in the treatment groups were intraperitoneally injected daily with nor-NOHA (40 mg/kg )for 10 weeks. Indirect tail-cuff systolic blood pressures and body weight were measured at given intervals. After the experiment,The thoracic aorta、left ventricular(LV) and left kidney were taken. The contents of activated MMP-2 in these organs were measured by semi-quantitative gelatine-zymography, meanwhile Media thickness (MT) , luminal diameter(LD) , ratio of media to lumen (M/L) and collagen type Ⅰ and Ⅲ, elastic fibers of thoracic aorta were measured by special Tricrome Masson, Picric-Sirius red and Orcein staining methods. Results (1) Blood pressure of treatment group was significantly lower than control groups; (2) Much more MMP-2 in LV was found in SHR group than in SHR-T group. (3 ) MT and M/L of treated group were significantly smaller than untreated control groups in thoracic aorta; Much more collagen Ⅰ and Ⅲ existing in the vascular of untreated control group compare with treated group. Conclusion nor-NOHA may relieve vascular remodeling potentially by inhibiting the activity of MMP-2 and the synthesis of collagenⅠ and Ⅲ.