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(Circulation. 2005;112:I-184 – I-189.)
© 2005 American Heart Association, Inc.

Myocardial Protection and Vascular Biology

Molecular Indices of Apoptosis After Intermittent Blood and Crystalloid Cardioplegia

Jun Feng, MD, PhD; Cesario Bianchi, MD, PhD; Jennifer L. Sandmeyer, BS; Jianyi Li, MD; Frank W. Sellke, MD

From the Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass.

Correspondence to Dr Frank W. Sellke, Division of Cardiothoracic Surgery, BIDMC, LMOB 2A, 110 Francis St, Boston, MA 02215. E-mail fsellke{at}caregroup.harvard.edu

Background— We investigated whether intermittent blood and crystalloid cardioplegia differentially affect myocardial apoptosis and apoptosis gene-related proteins.

Methods and Results— Rabbit hearts were perfused with Krebs-Henseleit buffer on a Langendorff apparatus. Control hearts (n=6) were perfused for 120 minutes without cardioplegic ischemia. Hearts were arrested for 60 minutes with warm (37°C) crystalloid cardioplegia (iW-CCP) (n=8) or with warm blood cardioplegia (iW-BCP) (n=8) administered intermittently. In cold (0 to 4°C) groups, hearts were arrested for 60 minutes with cold crystalloid cardioplegia (iC-CCP; n=8) or with cold blood cardioplegia (iC-BCP; n=6) administered intermittently. The hearts were reperfused for 30 minutes with Krebs-Henseleit buffer. iC-BCP significantly preserved the recovery of left ventricular and microvascular function compared with the other 3 experimental groups. There were no significant differences in total protein levels of caspase 3, Bcl-2, Bad, and Bax among the groups. iC-BCP significantly induced greater phosphorylation of Bad (5.6±0.8-fold) as compared with the other 3 groups (3.4±0.6-fold in iC-CCP, P<0.05; 2.5±0.3 in iW-BCP, P<0.05; and 1.4±0.2 in iW-CCP, P<0.01). iC-BCP induced less caspase 3 activation and apoptosis than the other 3 groups.

Conclusions— iC-BCP is superior to the other cardioplegic solutions in increasing the phosphorylation of Bad, inhibiting the activation of caspase 3, and preventing apoptosis. These effects of iC-BCP were associated with preserved left ventricular function and endothelium-dependent relaxation of coronary microvessels.

Key Words: apoptosis • cardioplegia • microcirculation • reperfusion • transplantation