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目的探讨Rho激酶抑制剂法舒地尔对肺动脉高压(PH)大鼠内皮素-1水平的干预作用。方法 32只成年Wistar大鼠均分为对照3周组(C3)、PH模型3周组(P3)、6周组(P6)及干预组(F组)。予野百合碱建模,第22日始F组予法舒地尔腹腔内注射干预。C3、P3、P6、F组大鼠分别于造模后3、6周末测定大鼠右心室收缩压(RVSP)、血浆内皮素-1(ET-1)水平,观察肺小动脉病理。结果①C3、P3、P6、F组大鼠RVSP分别为(31.2±7.6)、(43.3±8.3)、(56.9±6.9)、(47.3±6.3)mmHg。血浆ET-1分别为(1.09±0.39)、(1.83±0.29)、(2.34±0.65)、(1.90±0.33)ng.mL-1;②造模后大鼠RVSP、ET-1随时间延长而升高,法舒地尔干预后上述指标明显下降。③造模后肺小动脉平滑肌增殖,管腔狭窄,F组较P6组管腔明显增大,增殖减轻;④RVSP与ET-1存在明显正相关(r=0.721,P<0.01)。结论 Rho激酶抑制剂法舒地尔能显著降低PH大鼠血浆ET-1水平,有效降低肺动脉压力。
Objective To investigate the effect of fasudil, a Rho kinase inhibitor, on the level of endothelin-1 in rats with pulmonary hypertension (PH). Methods Thirty-two adult Wistar rats were divided into control group (C3), PH group (P3), 6 weeks group (P6) and intervention group (F group). To monocrotaline modeling, on the 22nd F group to fasudil intraperitoneal injection intervention. Rats in C3, P3, P6 and F groups were respectively subjected to right ventricular systolic pressure (RVSP) and endothelin-1 (ET-1) levels at 3 and 6 weeks after modeling to observe the pathophysiology of pulmonary arterioles. Results ① The RVSP of rats in groups C3, P3, P6 and F were (31.2 ± 7.6), (43.3 ± 8.3), (56.9 ± 6.9) and (47.3 ± 6.3) mmHg, respectively. (1.09 ± 0.39), (1.83 ± 0.29), (2.34 ± 0.65), (1.90 ± 0.33) ng.mL-1 respectively in the plasma ET-1; ②With the prolongation of RVSP and ET-1 Increased, fasudil interference after the above indicators decreased significantly. ③ The smooth muscle of pulmonary arterioles were proliferated and the stenosis was found after the model was established. The lumen of group F was significantly larger than that of group P6 and the proliferation was relieved. ④ There was a significant positive correlation between RVSP and ET-1 (r = 0.721, P <0.01). Conclusions Fasudil, a Rho kinase inhibitor, can significantly decrease the plasma ET-1 level in PH rats and decrease the pulmonary artery pressure.