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Randomized Controlled Trial
. 2017 Mar;37(3):302-305.

[Effect of Shenmai Injection on Vascular Endothelial Dependence Diastolic Function in Coronary Heart Disease Patients]

[Article in Chinese]
  • PMID: 30650479
Randomized Controlled Trial

[Effect of Shenmai Injection on Vascular Endothelial Dependence Diastolic Function in Coronary Heart Disease Patients]

[Article in Chinese]
Yan Zhou et al. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2017 Mar.

Abstract

Objective To observe the effect of Shenmai Injection (SI) on vascular endothelial dependent diastolic function in coronary heart disease (CHD) patients. Methods Totally 100 recruited CHD patients were assigned to the SI group and the control group by random digit table, 50 in each group. All patients received conventional drugs for CHD, 50 in each group. Patients in the SI group were intrave- nously injected with SI, 50 mL each time, once per day for 10 days. Changes of brachial artery diameter at hyperemia and sublingual nitroglycerin were measured in all patients before treatment and at day 10 after treatment by intravascular ultrasound. Serum NO level, plasma levels of endothelin (ET) , thromboxane B₂ (TXB₂), 6-keto-PGF₁α , superoxide dismutase (SOD) were measured using biochemical assay and ELISA. Thirty non-CHD patients confirmed with coronary CT or coronary angiogram were recruited as the non-CHD group. Results Changed value of brachial artery diameter at hyperemia and after sublingual nitroglycerin were more obviously reduced in the CHD group than in the non-CHD group (P <0. 05, P <0. 01). Besides, levels of NO, 6-keto-PGF1α were lowered, levels of ET and TXB₂ were elevated (P < 0. 01). Compared with the control group, congestion of brachial artery was significantly improved, levels of NO and 6-keto-PGF₁α increased, SOD concentration was obviously elevated, plasma levels of ET and TXB₂ decreased in the SI group (all P <0. 05). Conclusion SI could directly up-regulate levels of NO and 6-keto-PGF₁α , increase SOD activity, decrease levels of ET and TXB₂ , and improve vascular endothelial dependent vasodilation.

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