Smith E F, Lefer A M, Smith J B
Can J Physiol Pharmacol. 1980 Mar;58(3):294-300. doi: 10.1139/y80-050.
The effects of thromboxane (Tx) inhibition or arachidonic acid (AA) infusion were studied in anesthetized cats during acute myocardial ischemia (MI). AA (7.2 mg kg-1 h-1) or imidazole (25 mg kg-1 h-1) infusions were initiated 30 min after occlusion of the left anterior descending coronary artery. Assessment of the degree of protection of the ischemic myocardium was made by measurement of S-T segment elevation, plasma and myocardial creatine phosphokinase (CPK) activities, and myocardial amino-nitrogen content. Assessment of Tx inhibition was performed by radioimmunoassay. Administration of imidazole inhibited the sevenfold increase in plasma thromboxane B2 (TxB2) levels occurring in MI (p less than 0.001 at 2-5 h), markedly decreased S-T segment elevations at 2-k h (p less than 0.025), significantly prevented the elevation in plasma CPK (p less than 0.05, at 4 and 5 h), the increase in TxB2 post-MI, significantly decreased (p less than 0.025) S-T segment evaluations at 2-5 h, caused a decrease in plasmaCPK levels (p less than 0.05 at 5 h), but did not prevent loss of myocardial CPK or amino-nitrogen. In summary, the administration of imidazole resulted in significant protection of the myocardium in all indices of ischemic damage measured, while AA infusion resulted in only a partial protection. The mechanism of the imidazole protection of ischemic myocardial tissue appears to be via inhibition of Tx synthesis althoug we cannot exclude a hemodynamic or cytoprotective mechanism. These results suggest that specific inhibition of Tx formation is beneficial during acute MI.
在急性心肌缺血（MI）期间，对麻醉猫进行了血栓素（Tx）抑制或花生四烯酸（AA）输注的效果研究。在左冠状动脉前降支闭塞30分钟后开始输注AA（7.2毫克/千克·小时）或咪唑（25毫克/千克·小时）。通过测量S-T段抬高、血浆和心肌肌酸磷酸激酶（CPK）活性以及心肌氨基氮含量来评估缺血心肌的保护程度。通过放射免疫测定法评估Tx抑制情况。给予咪唑可抑制MI时血浆血栓素B2（TxB2）水平升高7倍（2至5小时时p<0.001），显著降低2至5小时时的S-T段抬高（p<0.025），显著预防血浆CPK升高（4和5小时时p<0.05），MI后TxB2升高，显著降低2至5小时时的S-T段评估值（p<0.025），使血浆CPK水平降低（5小时时p<0.05），但不能防止心肌CPK或氨基氮的丢失。总之，给予咪唑在所测量的所有缺血损伤指标中均能显著保护心肌，而输注AA仅能提供部分保护。咪唑对缺血心肌组织的保护机制似乎是通过抑制Tx合成，尽管我们不能排除血流动力学或细胞保护机制。这些结果表明，在急性MI期间特异性抑制Tx形成是有益的。
