Bitterman H, Lefer D J, Lefer A M
Proc Soc Exp Biol Med. 1987 Jul;185(3):262-6. doi: 10.3181/00379727-185-42542.
A specific inhibitor of thromboxane A2 (TxA2) synthesis, CGS-12970, a new angiotensin-converting enzyme (ACE) inhibitor, CGS-16617, and a combination of both agents were evaluated for their ability to reduce the extension of myocardial infarct size in rats. Myocardial creatine kinase (CK) loss from the left ventricular free wall (LVFW) 48 hr after left coronary artery ligation was used as an index of ischemic damage. Treatment with either CGS-12970 (4 mg/kg) or CGS-16617 (1 microgram/kg) alone did not attenuate the loss of CK from LVFW significantly, compared with animals receiving only the vehicles for these drugs. However, the combined use of both agents significantly reduced CK depletion from LFVW (P less than 0.01). These findings support the interrelated role of TxA2 and angiotensin II as mediators of myocardial ischemia and suggest that combined inhibition of their formation may be useful in the treatment of acute myocardial infarction.
对血栓素A2（TxA2）合成的特异性抑制剂CGS - 12970、新型血管紧张素转换酶（ACE）抑制剂CGS - 16617以及这两种药物的组合，评估了它们在降低大鼠心肌梗死面积扩展方面的能力。左冠状动脉结扎48小时后左心室游离壁（LVFW）的心肌肌酸激酶（CK）损失被用作缺血损伤的指标。与仅接受这些药物载体的动物相比，单独使用CGS - 12970（4毫克/千克）或CGS - 16617（1微克/千克）均未显著减轻LVFW的CK损失。然而，两种药物联合使用显著减少了LFVW的CK消耗（P小于0.01）。这些发现支持TxA2和血管紧张素II作为心肌缺血介质的相互关联作用，并表明联合抑制它们的形成可能对急性心肌梗死的治疗有用。
