Hashimoto K, Hirose M, Furukawa S, Hayakawa H, Kimura E
Jpn Heart J. 1977 Sep;18(5):679-89. doi: 10.1536/ihj.18.679.
The following parameters were studied before and after acute occlusion of the anterior descending branch of the left coronary artery in 17 dogs: bradykinin (BK) in the coronary sinus blood, heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), left ventricular max dp/dt (LV max dp/dt), and an index of myocardial contractility (LV max dp/dt/IP). BK levels increased, reaching a maximum of 30 +/- 13 ng/ml 2 min after coronary ligation, accompanied by a significant elevation of LVEDP, and lowering of the myocardial contractility index. HR and LV max dp/dt showed no significant changes. A positive correlation obtained between the level of BK and LVEDP, as well as a negative correlation between the level of BK and of both LVSP and myocardial contractility index. Pretreatment with aprotinine (Trasylol), an inhibitor of kinin forming enzyme, prevented the increase in both BK and LVEDP after coronary artery ligation and caused an elevation of myocardial contractility index. These results suggest that BK formed within ischemic myocardium exerts a negative inotropic action on the heart.
在17只犬中,研究了左冠状动脉前降支急性闭塞前后的以下参数:冠状窦血中的缓激肽(BK)、心率(HR)、左心室收缩压(LVSP)、左心室舒张末期压力(LVEDP)、左心室最大dp/dt(LV max dp/dt)以及心肌收缩性指数(LV max dp/dt/IP)。BK水平升高,在冠状动脉结扎后2分钟达到最大值30±13 ng/ml,同时LVEDP显著升高,心肌收缩性指数降低。HR和LV max dp/dt无显著变化。BK水平与LVEDP呈正相关,BK水平与LVSP及心肌收缩性指数均呈负相关。用激肽形成酶抑制剂抑肽酶(Trasylol)预处理可防止冠状动脉结扎后BK和LVEDP的升高,并使心肌收缩性指数升高。这些结果提示,缺血心肌内形成的BK对心脏发挥负性变力作用。