Bhat A M, Sacks H, Osborne J A, Lefer A M
Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
Am Heart J. 1989 Apr;117(4):799-803. doi: 10.1016/0002-8703(89)90615-7.
The ability of BM-13505, 4-[2-(4-chlorobenzenesulfonylamino) ethyl]-benzene acetic acid), a specific thromboxane/endoperoxide receptor antagonist, to protect the myocardium against ischemia and reperfusion injury, was assessed in an anesthetized cat model. Cats were rendered ischemic by left anterior descending (LAD) coronary artery ligation for 1 1/2 hours followed by reperfusion for 4 1/2 hours. BM-13505 or its vehicle (i.e., Na2CO3) was administered intravenously 30 minutes before reperfusion at a rate of 1 mg/kg followed by 1 mg/kg/hr. BM-13505 significantly (p less than 0.001) reduced the area of ischemic tissue as a percent of total left ventricular mass and total area at risk, without altering basic hemodynamics (i.e., arterial blood pressure, heart rate, or their product) and thereby not influencing myocardial oxygen demand. The mechanism of the protective effect of the thromboxane receptor antagonist appears to be cytoprotective but may involve the prevention of neutrophil-induced cellular damage.
在麻醉猫模型中评估了特异性血栓素/内过氧化物受体拮抗剂BM - 13505（4 - [2 - (4 - 氯苯磺酰氨基)乙基] - 苯乙酸）保护心肌免受缺血和再灌注损伤的能力。通过结扎左冠状动脉前降支（LAD）使猫缺血1.5小时，随后再灌注4.5小时。在再灌注前30分钟以1mg/kg的速率静脉注射BM - 13505或其赋形剂（即碳酸钠），随后以1mg/kg/小时的速率注射。BM - 13505显著（p小于0.001）降低了缺血组织面积占左心室总质量和总危险面积的百分比，而不改变基本血流动力学（即动脉血压、心率或它们的乘积），从而不影响心肌需氧量。血栓素受体拮抗剂的保护作用机制似乎是细胞保护作用，但可能涉及预防中性粒细胞诱导的细胞损伤。
