Maskal S L, Cohen N M, Hsia P W, Wechsler A S, Damiano R J
Medical College of Virginia, Virginia Commonwealth University, Richmond, USA.
J Thorac Cardiovasc Surg. 1995 Oct;110(4 Pt 1):1083-95. doi: 10.1016/s0022-5223(05)80178-3.
Cardioplegic solutions that arrest the heart at or near the resting membrane potential may provide better myocardial protection than standard depolarizing hyperkalemic cardioplegia by reducing both metabolic demand and harmful transmembrane ion fluxes. This hypothesis was investigated in an isolated, blood-perfused, rabbit heart Langendorff model during 30 minutes of normothermic global ischemia. Hyperpolarized cardiac arrest induced by aprikalim, an opener of adenosine triphosphate-dependent potassium channels, was compared with hyperkalemic depolarized arrest and with unprotected global ischemia. Left ventricular pressure was recorded over a wide range of balloon volumes before ischemia and 30 minutes after reperfusion. End-diastolic pressure versus balloon volume data were fitted to a two-coefficient exponential relationship. Changes in the diastolic compliance of the left ventricle were assessed by comparison of preischemic and postischemic coefficients within each cardioplegia group. Postischemic recovery of developed pressure was used to assess changes in left ventricular systolic function. The tissue water content of each heart was also determined. Myocardial protection with aprikalim resulted in better postischemic recovery of developed pressure (90% +/- 9%) than either protection with hyperkalemic cardioplegia (73% +/- 11%) or no protection (62% +/- 9%). Myocardial tissue water content in hearts protected with hyperkalemic cardioplegia (77.4% +/- 1.4%) was less than the tissue water content of either unprotected hearts (79.4% +/- 1.2%) or hearts protected with aprikalim (78.7% +/- 0.9%). Despite these differences, neither hyperkalemic cardioplegia (p = 0.15) nor aprikalim cardioplegia (p = 0.30) was associated with a significant postischemic decrease in ventricular compliance. By contrast, unprotected global ischemia was associated with a significant decrease in ventricular compliance (p < 0.001).
能使心脏停搏于静息膜电位或接近静息膜电位的心脏停搏液，可能通过降低代谢需求和有害的跨膜离子通量，比标准的去极化高钾心脏停搏液提供更好的心肌保护。在一个离体的、血液灌注的兔心脏Langendorff模型中，在30分钟常温全心缺血期间对这一假设进行了研究。将由三磷酸腺苷依赖性钾通道开放剂阿普卡林诱导的超极化心脏停搏与高钾去极化停搏及未保护的全心缺血进行比较。在缺血前及再灌注后30分钟，在很宽的球囊容积范围内记录左心室压力。舒张末期压力与球囊容积数据拟合为双系数指数关系。通过比较每个心脏停搏液组缺血前后的系数，评估左心室舒张顺应性的变化。用缺血后收缩压的恢复来评估左心室收缩功能的变化。还测定了每个心脏的组织含水量。与高钾心脏停搏液保护（73%±11%）或未保护（62%±9%）相比，阿普卡林心肌保护导致缺血后收缩压更好的恢复（90%±9%）。高钾心脏停搏液保护的心脏（77.4%±1.4%）的心肌组织含水量低于未保护心脏（79.4%±1.2%）或阿普卡林保护心脏（78.7%±0.9%）的组织含水量。尽管存在这些差异，但高钾心脏停搏液（p = 0.15）和阿普卡林心脏停搏液（p = 0.30）均与缺血后心室顺应性的显著降低无关。相比之下，未保护的全心缺血与心室顺应性的显著降低相关（p < 0.001）。
