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目的：观察７６４－３对野百合碱（ＭＣＴ）性肺动脉高压大鼠肺动脉胶原沉积的影响，探讨其可能的作用机制。方法：将雄性Ｗｉｓｔａｒ大鼠随机分为４组即正常组，正常给药组，ＭＣＴ对照组，ＭＣＴ给药组。给药大鼠从第１５天起，皮下注射７６４－３（４０ｍｇ／ｋｇ）１次／日。实验结束时，行血流动力学和病理形态学检查，并测定肺动脉羟脯氨酸（ＨＹＰ）和总蛋白含量。结果：ＭＣＴ性肺动脉高压大鼠肺动脉羟脯氨酸含量较正常组明显增高，平均分别为２４９．５±４９．９μｇ和１２４．２±２１．７μｇ（Ｐ＜０．００１），泡内肺肌型动脉中膜平滑肌细胞（ＳＭＣ）肥大、呈分泌型改变，细胞间胶原沉积；７６４－３能显著降低肺动脉羟脯氨酸含量（平均由２４９．５±４９．９μｇ降至１８６．８±３８．５μｇ，Ｐ＜０．０１），中膜ＳＭＣ结构逆转，胞体多细长，细胞间胶原减少。结论：７６４－３能部分抑制胶原在肺动脉壁的过度沉积，降低ＭＣＴ性肺动脉高压。而其减少胶原沉积、降低肺动脉高压的机制，很可能是通过逆转中膜ＳＭＣ表型改变
OBJECTIVE: To observe the effect of 764-3 on collagen deposition in pulmonary arteries in rats with monocrotaline (MCT) pulmonary hypertension and to explore its possible mechanism. Methods: Male Wistar rats were randomly divided into 4 groups: normal group, normal administration group, MCT control group and MCT administration group. The dosed rats were injected subcutaneously with 764-3 (40 mg/kg) once daily from the 15th day. At the end of the experiment, hemodynamic and pathological examinations were performed, and pulmonary artery hydroxyproline (HYP) and total protein levels were measured. Results: The pulmonary hydroxyproline content in MCT pulmonary hypertension rats was significantly higher than that in the normal group, with an average of 249.5±49.9 μg and 124.2±21.7 μg, respectively (P<0.001). Arterial smooth muscle cells (SMC) hypertrophy, secretory changes, collagen deposition between cells; 764-3 can significantly reduce the pulmonary artery hydroxyproline content (mean from 249.5±49.9μg to 186.8±38 (5μg, P<0.01). The structure of SMC in the media was reversed. The cell bodies were more slender and the intercellular collagen was reduced. Conclusion: 764-3 can partially inhibit the excessive deposition of collagen in the pulmonary artery wall and reduce MCT pulmonary hypertension. And its mechanism of reducing collagen deposition and reducing pulmonary hypertension may be by reversing the phenotypic changes of the mesangial SMC.