ADENOSINE CARDIOPLEGIA - REDUCING REPERFUSION INJURY OF THE ISCHEMIC MYOCARDIUM

被引:10
作者
BOEHM, DH
HUMAN, PA
VONOPPELL, U
OWEN, P
REICHENSPURNER, H
OPIE, LH
ROSE, AG
REICHART, B
机构
[1] Department of Pathology, University of Cape Town Medical School, Cape Town
关键词
CARDIOPLEGIA; ADENOSINE; BABOON; REPERFUSION INJURY; ISCHEMIA;
D O I
10.1016/1010-7940(91)90108-V
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hyperkalaemia-induced hypopolarization of the sarcolemnal membrane during standard crystalloid cardioplegic arrest potentiates calcium influx during reperfusion and is associated with depletion of high-energy phosphate reserves. Adenosine has been shown to induce fast cardiac arrest whilst preserving membrane hyperpolarization in an isolated rat heart model [14]. In this study we compared the efficacy of adenosine, both as an arresting agent and as an ultrastructural, haemodynamic and high-energy phosphate preserving agent, in an in situ global ischemia model in the baboon with St. Thomas' Hospital solution No. 2 (ST2; n = 8) and with Krebs-Henseleit buffer (KHB; n = 7). The addition of 10 mM adenosine to the non-cardioplegic KHB (ADO; n = 8) improved haemodynamic recovery significantly in terms of cardiac index (91.6% +/- 7.2 vs 59.9% +/- 9.9) and stroke volume index (101.6% +/- 8.9 vs 55.6% +/- 10.0) and was not statistically distinguishable from the ST2 with regard to cardiac index (91.6% +/- 7.2 vs 94.8% +/- 5.8), stroke volume index (101.6% +/- 8.9 vs 114.0% +/- 8.3) or left ventricular dP/dt (73.1% +/- 9.9 vs 87.0% +/- 12.4). Adenosine triphosphate was best preserved with ADO (103.5% +/- 21.1 vs 67.9% +/- 9.3 and 48.5% +/- 8.7) although this was not statistically significant. This suggests therefore that the mechanism of cardioprotection by adenosine occurs by means other than its role as high-energy phosphate precursor.
引用
收藏
页码:542 / 545
页数:4
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