Rude R E, Tumas J, Gunst M, Kloner R A, DeBoer L W, Maroko P R
Am J Cardiol. 1983 May 1;51(8):1422-7. doi: 10.1016/0002-9149(83)90323-5.
Ortho-iodo sodium benzoate (OISB) decreases the affinity of blood for oxygen, thus enhancing potential tissue oxygen delivery. To test the hypothesis that a change in oxygen affinity would ameliorate regional myocardial ischemic injury resulting from occlusion of the left anterior descending (LAD) coronary artery, experiments were carried out in 55 anesthetized dogs which received an intravenous infusion of OISB. In Protocol I studies (n = 9), preocclusion intravenous infusion of OISB (500 mg/kg) reduced epicardial S-T segment elevation 15 minutes after coronary occlusion, while a similar volume of normal saline solution did not affect this index of ischemic damage. In Protocol II experiments, 34 dogs were randomized to either an OISB or saline group, after which the LAD was ligated, the chest closed, and the animal allowed to recover from anesthesia. Myocardial infarction (MI) size was assessed after the animal died or was killed 8 to 24 hours later, and was found to be 29% smaller in dogs receiving OISB. In 6 dogs, blood P50 (the partial oxygen pressure at which hemoglobin is 50% saturated with oxygen) was increased by OISB infusion, confirming that its administration effected a rightward shift in the oxyhemoglobin dissociation curve. Protocol III studies assessed the effects of OISB on cardiac hemodynamic function and acute myocardial ischemic damage when infusion was begun 15 minutes after LAD occlusion: average epicardial S-T segment elevation was not altered by saline solution, but decreased when OISB was infused during the last 15 minutes of myocardial ischemia. Reductions in heart rate, left ventricular dP/dt, and cardiac output were observed in 7 dogs during OISB infusion, but there were no changes in these measurements during coronary occlusion in 5 dogs receiving a constant infusion of saline solution. There were no changes in regional myocardial blood flow (microsphere technique) to either ischemic or nonischemic zones in either the saline control or OISB treatment groups. Thus, both acute myocardial ischemic injury (assessed by epicardial electrocardiographic mapping) and ultimate MI size are reduced when OISB is infused before experimental coronary artery occlusion. OISB also reduces myocardial ischemic injury when its administration is begun 15 minutes after coronary occlusion, while effecting decreases in heart rate, left ventricular contractility, and cardiac output.
邻碘苯甲酸钠（OISB）可降低血液对氧气的亲和力，从而增强潜在的组织氧输送。为了验证氧气亲和力的改变会改善因左前降支（LAD）冠状动脉闭塞导致的局部心肌缺血损伤这一假说，对55只接受OISB静脉输注的麻醉犬进行了实验。在方案I研究（n = 9）中，冠状动脉闭塞前静脉输注OISB（500 mg/kg）可降低冠状动脉闭塞15分钟后的心外膜S-T段抬高，而等量的生理盐水对此缺血损伤指标无影响。在方案II实验中，34只犬被随机分为OISB组或生理盐水组，然后结扎LAD，关闭胸腔，让动物从麻醉中恢复。在动物于8至24小时后死亡或被处死时评估心肌梗死（MI）面积，发现接受OISB的犬的MI面积小29%。在6只犬中，输注OISB可使血液P50（血红蛋白氧饱和度为50%时的氧分压）升高，证实其给药使氧合血红蛋白解离曲线向右移位。方案III研究评估了在LAD闭塞15分钟后开始输注OISB时对心脏血流动力学功能和急性心肌缺血损伤的影响：生理盐水未改变平均心外膜S-T段抬高，但在心肌缺血的最后15分钟输注OISB时则降低。在7只犬输注OISB期间观察到心率、左心室dP/dt和心输出量降低，但在5只持续输注生理盐水的犬冠状动脉闭塞期间这些测量值无变化。生理盐水对照组或OISB治疗组的缺血区或非缺血区的局部心肌血流量（微球技术）均无变化。因此，在实验性冠状动脉闭塞前输注OISB时，急性心肌缺血损伤（通过心外膜心电图标测评估）和最终的MI面积均减小。当在冠状动脉闭塞后第15分钟开始给予OISB时，也可减轻心肌缺血损伤，同时使心率、左心室收缩力和心输出量降低。
