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目的：探讨苯那普利（Ｂｅｎａｚｅｐｒｉｌ，ＢＮＺ）对心衰的疗效及其神经－体液机理。方法：对３２例心衰病人（心功能Ⅱ级１９、Ⅲ级１０、Ⅳ级３），停用β受体阻滞剂和钙拮抗剂，在继续使用标准抗心衰治疗基础上，给予ＢＮＺ１０ｍｇ口服，１／ｄ，共２０～３０ｄ。给药前、后测定血浆肾素活性（ＰＲＡ）、血管紧张素Ⅱ（ＡＴ－Ⅱ）、去甲肾上腺素（ＮＥ）、肾上腺素（Ｅ）、内皮素（ＥＴ）和心钠肽（ＡＮＰ），以及ＵＣＧ左室功能和心机械图检查。结果：全组的心衰症状明显改善，运动耐量增加（Ｐ＜０．０１），左心功能（ＳＶ、ＣＯ、ＥＦ和ＰＥＰ／ＬＶＥＴ）显著改善（Ｐ＜０．０５～０．０１），其中高心病组（ｎ＝１１）的血压平均由２２．７／１３．８ｋＰａ下降至１８．８／１１．２ｋＰａ。治疗后全组的ＰＲＡ水平升高（Ｐ＜０．０５），ＡＴ－Ⅱ、ＮＥ、Ｅ、ＥＴ及ＡＮＰ水平显著降低（Ｐ＜０．０１）。结论：肯定了ＢＮＺ对心衰的疗效，并对心衰时交感系统、肾素血管紧张素系统和内皮系统激活起抑制作用。
Objective: To investigate the curative effect of Benazepril (BNZ) on heart failure and its neuro-humoral mechanism. Methods: Thirty-two patients with heart failure (cardiac function gradeⅡ, gradeⅢ, gradeⅢ, gradeⅢ), β-blockers and calcium antagonists were discontinued. On the basis of continuous treatment with standard anti-heart failure, BNZ10mg Oral, 1 / d, a total of 20 ~ 30d. The plasma levels of renin activity (PRA), angiotensin Ⅱ (AT-Ⅱ), norepinephrine (NE), epinephrine (E), endothelin (ET) and atrial natriuretic peptide (ANP) , As well as UCG left ventricular function and mechanical examination. Results: All patients’ heart failure symptoms improved significantly, exercise tolerance increased (P <0.01), left ventricular function (SV, CO, EF and PEP / LVET) Among them, the blood pressure of high heart disease group (n = 11) decreased from 22.7 / 13.8kPa to 18.8 / 11.2kPa on average. After treatment, the level of PRA increased (P <0.05) and the levels of AT-Ⅱ, NE, E, ET and ANP decreased significantly (P <0.01). CONCLUSIONS: The efficacy of BNZ on heart failure is confirmed, and the inhibition of sympathetic system, renin-angiotensin system and endothelial system activation during heart failure is also inhibited.