Purine metabolite accumulation during myocardial ischemia: adenosine pretreatment versus brief ischemia.
Purine metabolite accumulation during myocardial ischemia: adenosine pretreatment versus brief ischemia.
复制标题
心肌缺血期间嘌呤代谢物的积累：腺苷预处理与短暂缺血。
DOI：
10.1007/bf00796210
复制
发表时间：
1997
影响因子：
9.5
通讯作者：
VanWylen,DG
中科院分区：
文献类型：
--
作者：
Manthei,SA;VanWylen,DG
经过短暂缺血预处理的心脏的特点是，在随后的长时间缺血期间，细胞嘌呤代谢产物的产生率降低。本研究的目的是确定短暂的外源腺苷预处理是否可以模拟这种现象。将未经治疗的麻醉犬 (n=7) 长时间缺血期间间质液 (ISF) 嘌呤代谢物的积累与短暂缺血预处理组（缺血预处理组；n=9）、用 1.5 μmol/min 冠状动脉内腺苷预处理组 (n=7) 进行比较。通过闭塞左冠状动脉前降支 (LAD) 5 分钟，然后再灌注 10 分钟来实现缺血预适应。腺苷治疗组接受 10 分钟的冠状动脉内腺苷注射，然后恢复 10 分钟。所有动物均接受 60 分钟 LAD 闭塞，然后再灌注 60 分钟。通过心脏微透析评估 ISF 腺苷和腺苷代谢物的变化，使用透析液浓度作为 ISF 水平的指标。缺血预处理降低了长时间缺血期间透析液腺苷和总嘌呤积累的速率。尽管两种剂量的外源腺苷涵盖了缺血预处理中观察到的ISF腺苷的增加，但两种剂量的腺苷均不能减弱长时间缺血期间嘌呤代谢物积累的速率。我们得出的结论是，外源腺苷预处理无法模拟缺血引起的嘌呤流出减少，这是经过短暂缺血预处理的肌细胞的特征。
Hearts preconditioned by brief ischemia are characterized by a reduced rate of cellular purine metabolite production during subsequent prolonged ischemia; the purpose of this study was to determine if transient exogenous adenosine pretreatment can mimic this phenomenon. The accumulation of interstitial fluid (ISF) purine metabolites during prolonged ischemia in untreated anesthetized dogs (n=7) was compared to that in a group pretreated with brief ischemia (ischemic preconditioned group; n=9), a group pretreated with 1.5 μmoles/min intracoronary adenosine (n=7). Ischemic preconditioning was achieved by a 5 min period of left anterior descending coronary artery (LAD) occulusion followed by 10 min of reperfusion. The adenosine-treated groups were subjected to 10 min of intracoronary adenosine followed by 10 min of recovery. All animals were exposed to 60 min LAD occlusion followed by 60 min reperfusion. The changes in ISF adenosine and adenosine metabolites were assessed by cardiac microdialysis, using dialysate concentrations as indices of ISF levels. Ischemic preconditioning decreased the rate of dialysate adenosine and total purine accumulation during the prolonged ischemia. Although the two doses of exogenous adenosine bracketed the increase in ISF adenosine seen with ischemic preconditioning, neither adenosine dose was able to attenuate the rate of purine metabolite accumulation during prolonged ischemia. We conclude that exogenous adenosine pretreatment is unable to mimic the reduced ischemia-induced purine efflux that is characteristic of myocytes pretreated with brief ischemia.