Perrault L P, Menasché P, Bel A, de Chaumaray T, Peynet J, Mondry A, Olivero P, Emanoil-Ravier R, Moalic J M
Department of Cardiovascular Surgery, Hôpital Lariboisière, Paris, France.
J Thorac Cardiovasc Surg. 1996 Nov;112(5):1378-86. doi: 10.1016/s0022-5223(96)70155-1.
Ischemic preconditioning is now established as an effective means of reducing infarct size. However, it remains uncertain whether preconditioning can improve the myocardial protection afforded by cardioplegia. The present study was designed to address this issue.
After the institution of cardiopulmonary bypass, 10 patients were preconditioned with 3 minutes of aortic crossclamping followed by 2 minutes of reperfusion before the onset of retrograde continuous warm cardioplegic arrest. Ten case-matched patients served as controls. Three blood samples were drawn simultaneously from the radial artery and the coronary sinus before bypass, at the end of the 5-minute preconditioning protocol or after 5 minutes of bypass in control patients, and at the end of cardioplegic arrest. These samples were assayed for creatine kinase MB isoenzyme and lactate. Right atrial biopsy specimens taken at the same time points were processed by Northern blotting for the expression of messenger ribonucleic acid of both c-fos and heat shock protein 70.
At the end of arrest, the release of creatine kinase MB from the myocardium was markedly greater in preconditioned patients than in the controls. The transmyocardial lactate gradient was shifted toward production in the preconditioned group (+0.22 +/- 0.13 mmol/L) and toward extraction in the control group (-0.06 +/- 0.21 mmol/L). Molecular biology data did not suggest a protective effect of preconditioning. There were no clinical adverse events related to preconditioning.
Preconditioning does not enhance cardioplegic protection and might even be deleterious. These results do not dismiss its use in cardiac operations. They rather emphasize the need for identifying pharmacologic mediators that could safely and effectively duplicate the cardioprotective effects of ischemic preconditioning.
缺血预处理现已被确认为减少梗死面积的有效手段。然而，预处理是否能改善心脏停搏液提供的心肌保护作用仍不确定。本研究旨在解决这一问题。
在建立体外循环后，10例患者在逆行持续温血心脏停搏开始前，先进行3分钟主动脉交叉阻断，随后再灌注2分钟进行预处理。10例匹配病例作为对照。在体外循环前、5分钟预处理方案结束时或对照患者体外循环5分钟后以及心脏停搏结束时，同时从桡动脉和冠状窦采集三份血样。检测这些样本中的肌酸激酶同工酶MB和乳酸。在相同时间点采集的右心房活检标本通过Northern印迹法检测c-fos和热休克蛋白70信使核糖核酸的表达。
在心脏停搏结束时，预处理患者心肌中肌酸激酶MB的释放明显高于对照组。预处理组心肌乳酸跨壁梯度向生成方向移动（+0.22±0.13 mmol/L），而对照组则向摄取方向移动（-0.06±0.21 mmol/L）。分子生物学数据未提示预处理具有保护作用。未出现与预处理相关的临床不良事件。
预处理不能增强心脏停搏液的保护作用，甚至可能有害。这些结果并不否定其在心脏手术中的应用。相反，它们强调需要确定能够安全有效地复制缺血预处理心脏保护作用的药物介质。
