Kitakaze M, Takashima S, Funaya H, Minamino T, Node K, Shinozaki Y, Mori H, Hori M
First Department of Medicine, Osaka University School of Medicine, Japan.
Am J Physiol. 1997 May;272(5 Pt 2):H2071-8. doi: 10.1152/ajpheart.1997.272.5.H2071.
We tested the hypothesis that myocardial extracellular acidosis during early reperfusion limits infarct size. The left anterior descending coronary artery was perfused with blood through a bypass tube in dogs. We occluded the bypass tube for 40 (protocol I; n = 24 hearts) and 90 min (protocol II; n = 36 hearts). In protocols I and II, we infused one group of hearts with HCl (60 micrograms.kg-1.min-1) for 60 min after the onset of reperfusion (the metabolic acidosis group), and another group of hearts were ventilated with 3 liters of 70% O2-30% CO2 mixed with room air 10 min before the onset of reperfusion for 70 min (the respiratory acidosis group). pH in the coronary venous blood and myocardial pH during reperfusion in the metabolic and respiratory acidosis groups were lower than those in the control groups. Infarct sizes in the metabolic (16.4 +/- 2.5 and 22.3 +/- 2.5%) and respiratory (16.7 +/- 2.6 and 22.3 +/- 2.5%) acidosis groups in protocols I and II, respectively, were smaller than those in the control groups (33.1 +/- 3.0 and 40.6 +/- 4.1%, respectively). Thus we conclude that temporary acidosis during reperfusion limits infarct size.
我们验证了早期再灌注期间心肌细胞外酸中毒限制梗死面积的假说。通过犬的搭桥管向其左前降支冠状动脉灌注血液。我们分别将搭桥管闭塞40分钟(方案I;24颗心脏)和90分钟(方案II;36颗心脏)。在方案I和II中,一组心脏在再灌注开始后60分钟内输注盐酸(60微克·千克⁻¹·分钟⁻¹)(代谢性酸中毒组),另一组心脏在再灌注开始前10分钟用3升70%氧气-30%二氧化碳与室内空气混合气体通气70分钟(呼吸性酸中毒组)。代谢性和呼吸性酸中毒组再灌注期间冠状静脉血pH值和心肌pH值均低于对照组。在方案I和II中,代谢性酸中毒组(分别为16.4±2.5%和22.3±2.5%)和呼吸性酸中毒组(分别为16.7±2.6%和22.3±2.5%)的梗死面积均小于对照组(分别为33.1±3.0%和40.6±4.1%)。因此我们得出结论,再灌注期间的短暂酸中毒限制梗死面积。