McCully J D, Uematsu M, Parker R A, Levitsky S
Division of Cardiothoracic Surgery and Biometrics Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass 02215, USA.
J Thorac Cardiovasc Surg. 1998 Jul;116(1):154-62. doi: 10.1016/S0022-5223(98)70254-5.
The purpose of this study was to determine the effect of an intracoronary bolus injection of adenosine used in concert with ischemic preconditioning on postischemic functional recovery and infarct size reduction in the rabbit heart and to compare adenosine-enhanced ischemic preconditioning with ischemic preconditioning and magnesium-supplemented potassium cardioplegia.
New Zealand White rabbits (n = 36) were used for Langendorff perfusion. Control hearts were perfused at 37 degrees C for 180 minutes; global ischemic hearts received 30 minutes of global ischemia and 120 minutes of reperfusion; magnesium-supplemented potassium cardioplegic hearts received cardioplegia 5 minutes before global ischemia; ischemic preconditioned hearts received 5 minutes of zero-flow global ischemia and 5 minutes of reperfusion before global ischemia; adenosine-enhanced ischemic preconditioned hearts received a bolus injection of adenosine just before the preconditioning. To separate the effects of adenosine from adenosine-enhanced ischemic preconditioning, a control group received a bolus injection of adenosine 10 minutes before global ischemia.
Infarct volume in global ischemic hearts was 32.9% +/- 5.1% and 1.03% +/- 0.3% in control hearts. The infarct volume decreased (10.23% +/- 2.6% and 7.0% +/- 1.6%, respectively; p < 0.001 versus global ischemia) in the ischemic preconditioned group and control group, but this did not enhance postischemic functional recovery. Magnesium-supplemented potassium cardioplegia and adenosine-enhanced ischemic preconditioning significantly decreased infarct volume (2.9% +/- 0.8% and 2.8% +/- 0.55%, respectively; p < 0.001 versus global ischemia, p = 0.02 versus ischemic preconditioning and p = 0.05 versus control group) and significantly enhanced postischemic functional recovery.
Adenosine-enhanced ischemic preconditioning is superior to ischemic preconditioning and provides equal protection to that afforded by magnesium-supplemented potassium cardioplegia.
本研究旨在确定冠状动脉内推注腺苷联合缺血预处理对兔心脏缺血后功能恢复及梗死面积缩小的影响,并比较腺苷增强缺血预处理与缺血预处理及镁补充钾停搏液的效果。
选用36只新西兰白兔进行Langendorff灌注。对照心脏在37℃灌注180分钟;全心缺血心脏经历30分钟全心缺血和120分钟再灌注;镁补充钾停搏液心脏在全心缺血前5分钟接受停搏液;缺血预处理心脏在全心缺血前接受5分钟零流量全心缺血和5分钟再灌注;腺苷增强缺血预处理心脏在预处理前即刻接受腺苷推注。为区分腺苷与腺苷增强缺血预处理的作用,一个对照组在全心缺血前10分钟接受腺苷推注。
全心缺血心脏的梗死体积为32.9%±5.1%,对照心脏为1.03%±0.3%。缺血预处理组和对照组的梗死体积均减小(分别为10.23%±2.6%和7.0%±1.6%;与全心缺血相比,p<0.001),但这并未增强缺血后功能恢复。镁补充钾停搏液和腺苷增强缺血预处理显著减小梗死体积(分别为2.9%±0.8%和2.8%±0.55%;与全心缺血相比,p<0.001,与缺血预处理相比,p = 0.02,与对照组相比,p = 0.05),并显著增强缺血后功能恢复。
腺苷增强缺血预处理优于缺血预处理,且提供与镁补充钾停搏液同等的保护作用。