Fremes S E, Zhang J, Furukawa R D, Mickle D A, Weisel R D
Division of Cardiovascular Surgery, University of Toronto, Ontario, Canada.
J Thorac Cardiovasc Surg. 1995 Aug;110(2):293-301. doi: 10.1016/S0022-5223(95)70225-3.
Adenosine pretreatment has been shown to be beneficial in several models of ischemia-reperfusion. We wished to evaluate whether adenosine pretreatment is cardioprotective for prolonged cardiac storage and whether the presence of adenosine in the storage media affects the results. Isolated rodent hearts were obtained from Sprague-Dawley rats, mounted on a Langendorff apparatus, instrumented with an intraventricular balloon, and ventricularly paced at 300 beats/min. Four groups of hearts were studied in a 2 x 2 factorial experiment (n = 8 to 12 per group). Hearts were subjected to normal perfusion or to solution supplemented with adenosine 50 mumol/L for 10 minutes followed by adenosine-free perfusion for 10 minutes. Hearts then were stored for 8 hours at 0 degrees C in either University of Wisconsin solution (adenosine 5 mmol/L) or St. Thomas' Hospital II solution (adenosine free). Adenosine pretreatment increased tissue levels of adenosine triphosphate before storage (p = 0.04). Nonfunction was less common after storage (1/19 versus 6/20 hearts, p < 0.05), and diastolic function was better preserved in the adenosine groups in the reperfusion phase (p = 0.01). The beneficial effects of adenosine pretreatment were independent of which storage solution was used. Developed pressure was increased (p < 0.05) and release of creatine kinase and lactate dehydrogenase was reduced (p < 0.0001) in hearts treated with University of Wisconsin solution compared with those treated with St. Thomas' Hospital solution. These studies suggest that adenosine pretreatment improves recovery after prolonged hypothermic storage and that the presence of adenosine in the preservation solution does not alter the results. The experiments provide further evidence that extended myocardial protection is better enhanced with University of Wisconsin solution than with St. Thomas' Hospital II solution.
腺苷预处理已被证明在几种缺血再灌注模型中是有益的。我们希望评估腺苷预处理对延长心脏保存是否具有心脏保护作用，以及保存介质中腺苷的存在是否会影响结果。从Sprague-Dawley大鼠获取离体心脏，安装在Langendorff装置上，插入心室内球囊，并以300次/分钟的频率进行心室起搏。在2×2析因实验中研究了四组心脏（每组n = 8至12）。心脏接受正常灌注或用50μmol/L腺苷补充的溶液灌注10分钟，然后进行无腺苷灌注10分钟。然后将心脏在0℃下于威斯康星大学溶液（腺苷5 mmol/L）或圣托马斯医院II溶液（无腺苷）中保存8小时。腺苷预处理增加了保存前组织中的三磷酸腺苷水平（p = 0.04）。保存后无功能的情况较少见（1/19对6/20心脏，p < 0.05），并且在再灌注阶段腺苷组的舒张功能得到更好的保留（p = 0.01）。腺苷预处理的有益效果与使用哪种保存溶液无关。与用圣托马斯医院溶液处理的心脏相比，用威斯康星大学溶液处理的心脏的收缩压升高（p < 0.05），肌酸激酶和乳酸脱氢酶的释放减少（p < 0.0001）。这些研究表明，腺苷预处理可改善长时间低温保存后的恢复情况，并且保存溶液中腺苷的存在不会改变结果。实验提供了进一步的证据，即威斯康星大学溶液比圣托马斯医院II溶液能更好地增强延长的心肌保护作用。
