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

来源：

EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY | 1991年 / 5卷 / 10期

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

页码：542 / 545

页数：4

共 15 条

[1]

Babbitt D.G., Virmani R., Forman M.B., Intracoronary adenosine administered after reperfusion limits vascular injury after prolonged ischemia in the canine model, Circulation, 80, pp. 1388-1399, (1989)

[2]

Bolling S.F., Bies L.E., Gallagher K.P., Bove E.L., Enhanced myocardial protection with adenosine, Ann Thorac Surg, 47, pp. 809-815, (1989)

[3]

Buckberg G.D., Strategies and logic of cardioplegic delivery to prevent, avoid, and reverse ischemic and reperfusion damage, J Thorac Cardiovasc Surg, 93, pp. 127-139, (1987)

[4]

Cronstein B.N., Levin R.I., Belanoff J., Weissmann G., Hirschhorn R., Adenosine: An endogenous inhibitor of neutrophilme- diated injury to endothelial cells, J Clin Invest, 78, pp. 760-770, (1986)

[5]

Cronstein B.N., Kramer S.B., Weissmann G., Hirschhorn R., Adenosine: A physiological modulator of superoxide anion generation by human neutrophils, J Exp Med, 158, pp. 1160-1177, (1983)

[6]

De Jong J.W., Van Der Meer P., Van Loon H., Owen P., Opie L.H., Adenosine as adjunct to potassium cardioplegia: Effect on function, energy metabolism and electrophysiology, J Thorac Cardiovasc Surg, 100, pp. 445-454, (1990)

[7]

Ferguson T.B., Smith P.K., Lofland G.K., Holman W.L., Helms M.A., Cox J.L., The effects of cardioplegic potassium concentration and myocardial temperature on electrical activity in the heart during elective cardioplegic arrest, J Thorac Cardiovasc Surg, 92, pp. 755-765, (1986)

[8]

Jynge P., Hearse D.J., Feuvray D., Mahalu W., Cankovic-Darra- Cott S., O'Brien K., Braimbridge M.V., The St. Thomas’ Hospital cardioplegic solution, Scand J Thorac Cardiovasc Surg, 30, (1981)

[9]

Lamprecht W., Transchold I., Adenosine 5'-Triphosphate Determination with Hexokinase and Glucose-6-Phosphate Dehydrogenase, 4, pp. 2101-2110, (1974)

[10]

Ledingham S., Katayama O., Lachno D., Patel N., Yacoub M., Beneficial effect of adenosine during reperfusion following prolonged cardioplegic arrest, Cardiovasc Res, 24, pp. 247-253, (1990)

← 1 2 →