Samaja M, Motterlini R, Allibardi S, Brenna L, Casalini S, Santoro F, Grossi A
Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi, Milano.
Cardiologia. 1992 Sep;37(9):651-4.
The events associated to myocardial ischemia result from 2 overlapping phenomena due to reduced blood flow (ischemia) and reduced O2 supply (hypoxemia). To distinguish these effects, 2 groups of isolated rat hearts were perfused through the aorta (Langendorff's method) with Krebs-Henseleit buffer, and were exposed for 20 min to hypoxemia or ischemia, matched in terms of the O2 supply (10% of baseline), with continuous monitoring of cardiac contractility, O2 uptake and lactate production. The developed pressure and the O2 uptake were similar in hypoxemic and ischemic hearts; heart rate, end-diastolic pressure and lactate production rate were higher in hypoxemia than in ischemia; the recovery from hypoxemia was less than that from ischemia, despite the same O2 supplies; treatment with superoxide dismutase and catalase, scavengers of the O2 derived free radicals, during hypoxemia, allowed hypoxemic hearts to recover as ischemic hearts. Therefore, the main determinant of the reperfusion injury is to be attributed to the low O2 supply rather than to the low coronary flow; part of the injury is due to free radicals; a substantial portion is mediated by the energy demand during the stress which was higher in hypoxemia than in ischemia.
与心肌缺血相关的事件是由血流减少(缺血)和氧气供应减少(低氧血症)这两种重叠现象导致的。为区分这些影响,将两组离体大鼠心脏通过主动脉(Langendorff法)用Krebs-Henseleit缓冲液灌注,并使其暴露于低氧血症或缺血状态20分钟,两组的氧气供应(基线的10%)相匹配,同时持续监测心脏收缩力、氧气摄取和乳酸生成。低氧血症心脏和缺血心脏的发育压力和氧气摄取相似;低氧血症时的心率、舒张末期压力和乳酸生成率高于缺血时;尽管氧气供应相同,但低氧血症后的恢复情况不如缺血后;在低氧血症期间用超氧化物歧化酶和过氧化氢酶(氧衍生自由基清除剂)治疗,可使低氧血症心脏像缺血心脏一样恢复。因此,再灌注损伤的主要决定因素应归因于低氧供应而非低冠脉血流;部分损伤是由自由基引起的;相当一部分损伤是由应激期间的能量需求介导的,低氧血症时的能量需求高于缺血时。