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犬２１只，经左冠脉内注射麦角新硷诱发冠脉痉挛后随机静滴生理盐水（对照组）或等量盐水溶的巯甲丙脯酸（治疗组），观察１小时。心电图显示治疗组的异常ＳＴ段下降和严重室性心律失常明显少于对照组，冠脉造影显示治疗组痉挛血管支数及狭窄程度均少于和轻于对照组；左室造影和超声心电图显示治疗组的左室收缩末和舒张末容积小于对照组，ＥＦ值或△Ｄ大于对照组，ＡＡ／ＥＡ小于对照组；血流动力学参数表明治疗组左室收缩压，平均肺动脉压及心排血量均较对照组明显改善。血管紧张素Ⅰ、Ⅱ和心房肽的变化提示与巯甲丙脯酸的作用有关。肺组织病理检查表明治疗组肺血栓和肺水肿检出率少于对照组。作者认为实验性冠脉痉挛可引起急性左室收缩和舒张功能异常，用巯甲丙脯酸后可明显改善，并可减少心律失常发生。巯甲丙脯酸的作用机制可能与扩张冠脉，抑制血管紧张素转化及加强心房肽作用有关。
Twenty-one dogs were randomly divided into normal saline (control group) and captopril (saline-treated captopril) treated with ergometrine-induced left coronary artery coronary artery spasm (treatment group) for 1 hour. Electrocardiogram showed abnormal ST-segment depression and severe ventricular arrhythmia in the treatment group was significantly less than the control group, coronary angiography showed that the treatment group spastic blood vessel count and stenosis were less than and lighter than the control group; left ventricular angiography and echocardiography The left ventricular end-systolic and end-diastolic volume of the treatment group was smaller than that of the control group, the EF value or △ D was greater than that of the control group, and the AA / EA was smaller than that of the control group. The hemodynamic parameters showed that left ventricular systolic pressure, mean pulmonary artery pressure, Blood volume than the control group was significantly improved. The changes of angiotensin Ⅰ, Ⅱ and atrial natriuretic peptide are related to the effect of captopril. Pulmonary histopathological examination showed that the detection rate of pulmonary thromboembolism and pulmonary edema in the treatment group was less than that in the control group. Authors believe that experimental coronary spasm can cause acute left ventricular systolic and diastolic dysfunction, with captopril can be significantly improved, and can reduce arrhythmia. The mechanism of action of captopril may be related to the expansion of coronary arteries, inhibition of angiotensin conversion and enhancement of atrial natriuretic peptide.