Bartunek J, Shah A M, Vanderheyden M, Paulus W J
Cardiovascular Center, Aalst, Belgium.
Circulation. 1997 Jan 7;95(1):90-6. doi: 10.1161/01.cir.95.1.90.
In humans, intracoronary infusion of substance P reduces left ventricular end-systolic pressure and left ventricular peak systolic pressure because of earlier onset of left ventricular relaxation induced by paracrine myocardial action of mediators released from the coronary endothelium. The present study investigated in humans the effects of beta-adrenergic stimulation, which also induces earlier left ventricular relaxation, on the left ventricular myocardial contractile response to intracoronary infusion of substance P.
Data were obtained in 13 patients after cardiac transplantation and in 3 patients with dilated nonischemic cardiomyopathy. Microtip left ventricular pressure recordings were obtained during a 5-minute intracoronary infusion of substance P (20 pmol/min) under control conditions and then repeated during concurrent intravenous administration of dobutamine. In the presence of dobutamine, intracoronary substance P caused a greater fall in left ventricular end-systolic pressure (transplantation control, -9 +/- 11 versus transplantation dobutamine, -20 +/- 18 mm Hg [P < .05]; cardiomyopathy control, -4 +/- 1 versus cardiomyopathy dobutamine, -10 +/- 3 mm Hg [P < .05]) and in left ventricular peak systolic pressure (transplantation control, -14 +/- 10 versus transplantation dobutamine, -30 +/- 22 mm Hg [P < .01]; cardiomyopathy control, -9 +/- 7 versus cardiomyopathy dobutamine, -15 +/- 6 mm Hg [P = .1]).
Dobutamine enhances the cardiodepressant effect on myocardial contractile performance of receptor-mediated coronary endothelial stimulation in transplant recipients and in patients with dilated nonischemic cardiomyopathy. This enhancement could result from a potentiating interaction of the relaxation-hastening effect exerted by beta-adrenergic stimulation and by mediators released from the coronary endothelium, such as nitric oxide.
在人类中，冠状动脉内注入P物质可降低左心室收缩末期压力和左心室收缩压峰值，这是由于冠状动脉内皮释放的介质通过旁分泌心肌作用诱导左心室更早开始舒张。本研究在人类中调查了β-肾上腺素能刺激（其也可诱导左心室更早舒张）对冠状动脉内注入P物质时左心室心肌收缩反应的影响。
数据来自13例心脏移植患者和3例扩张型非缺血性心肌病患者。在对照条件下，在冠状动脉内注入P物质（20 pmol/分钟）5分钟期间记录微尖端左心室压力，然后在同时静脉注射多巴酚丁胺期间重复记录。在多巴酚丁胺存在的情况下，冠状动脉内注入P物质导致左心室收缩末期压力下降幅度更大（移植对照组，-9±11与移植多巴酚丁胺组，-20±18 mmHg [P<.05]；心肌病对照组，-4±1与心肌病多巴酚丁胺组，-10±3 mmHg [P<.05]）以及左心室收缩压峰值下降幅度更大（移植对照组，-14±10与移植多巴酚丁胺组，-30±22 mmHg [P<.01]；心肌病对照组，-9±7与心肌病多巴酚丁胺组，-15±6 mmHg [P = 0.1]）。
多巴酚丁胺增强了移植受者和扩张型非缺血性心肌病患者中受体介导的冠状动脉内皮刺激对心肌收缩性能的负性肌力作用。这种增强可能源于β-肾上腺素能刺激和冠状动脉内皮释放的介质（如一氧化氮）所发挥的加速舒张作用之间的增效相互作用。
