Role of calcium overload on coronary arterial stunning caused by myocardial ischemia reperfusion

短暂性心肌缺血可减弱药理学上的冠状动脉血管扩张，提示在短暂性心肌缺血后降低冠脉灌注压的过程中冠脉血流量(CBF)减少。为了验证这个想法，研究人员对32只狗进行了研究。在逐步降低冠脉灌流压10毫米汞柱的过程中，测量冠状动脉左前降支的CBF。在对照组，当冠脉灌流压力为100-70毫米汞柱时，脑血流量、短轴缩短率(FS)和乳酸摄取率(LER)未见降低。冠脉结扎10min后30min，腺苷(2mug/kg/min，ic)和罂粟碱(60mug/kg/min，ic)的CBF反应分别减弱34%和26%，而FS、LER和基础CBF恢复正常。冠脉灌流压在80-50毫米汞柱之间时，CBF和END/EPI流量比缺血前分别下降9%和35%。冠脉灌流压=80-50毫米汞柱时，FS和LER均减弱(P&lt；0.01)(冠脉灌流压=70毫米汞柱时FS：9.8；正负；1.2vs.20.6&lt；正负1.2%，LER：-18.5；正负；6.8vs.26.7&lt；+-3.6%)。因此，我们得出结论，短暂性缺血主要损害心肌内膜血流的自动调节，并在冠脉灌流受压时引起心肌收缩和代谢功能障碍。

Transient myocardial ischemia attenuates pharmacological coronary vasodilation, suggesting attenuation of colonary blood flow(CBF) during reduction of coronary perfusion pressure after transient ischemia. To test this idea, 32 dogs were studied. CBF of the left anterior descending coronary artery was measured during stepwise reduction of coronary perfusion pressure by 10mmHg. In the control, reductions of CBF,fractional shortening(FS) and lactate extraction ratio (LER) were not observed during coronary perfusion pressure=100-70mmHg. Thirty min after 10 min of coronary occlusion, CBF response to adenosine (2mug/kg/min, ic) and papaverine (60mug/kg/min, ic) were attenuated by 34<plus-minus>9 and 26<plus-minus>7%, respectively, although FS,LER and basal CBF returned to control. During reduction of coronary perfusion pressure between 80-50mmHg, CBF and End/Epi flow ratio decreased by 9<plus-minus>5 and 35<plus-minus>9%, respectively, compared with the pre-ischemic condition. Both FS and LER were attenuated (p<.01) at coronary perfusion pressure=80-50mmHg (FS : 9.8<plus-minus>1.2 vs.20.6<plus-minus>1.2%, LER : -18.5<plus-minus>6.8 vs.26.7<plus-minus>3.6% at coronary perfusion pressure=70mmHg). Thus we conclude that transient ischemia mainly impairs autoregulation of endomyocadial flow, and causes myocardial contractile and metabolic dysfunction when coronary perfusion pres