Cor Vasa 2004, 45(1):24-28

The importance of post-reperfusion myocardial tissue apoptosis in cardiac surgery

Robert Wagner*, Pavel Piler, Radek Horváth, Jaroslav Benedík, Petr Adámek, Jiří Černošek, Alžběta Sirotková
Centrum kardiovaskulární a transplantační chirurgie, Brno, Česká republika

Aim:
To assess the clinical importance of the phenomenon of apoptosis following ischemia-reperfusion caused by cardioplegic myocardial arrest in cardiac surgery and its modulation by sevofluran.

Method:
A prospective clinical trial in 40 patients (20 + 20) undergoing standard off-pump cardiac surgery procedure in extracorporeal circulation (Capiox membrane oxygenator, St. Thomas' cold cardioplegia, normothermia with local cooling). One group was receiving sevofluran, an inhaled anesthetic enhancing myocardial resistance to ischemia, throughout the procedure. Myocardial tissue specimens (3× 3 mm) were removed from the right atrial auricle prior to and after cardiopulmonary bypass (myocardial ischemia/reperfusion times were 45/25 minutes on average). To determine pro- and antiapoptotic stimuli, the degree of mRNA expresion for the membrane receptors Fas/Fas-L, TNFr, and mitochondrial Bax/Bcl-2, and/or their ratios were assessed. Detection and quantification of specific mRNA was made using the technique of real time polymerase chain reaction (RT-PCR) (ABI Prism 7000 Sequence Detection System) in duplex reaction with an internal standard (GAPDH). The differences in mRNA expression before and after ischemia/reperfusion were considered significant for p < 0.05.

Results:
Changes occurred in all the genes studied; however, the differences were only significant in the control group. Reperfusion was followed by downregulation of Fas/Fas-L, TNFr, Bax and upregulation of antiapoptotic Bcl-2 with a change in the ratio to 0,98-0,92, that is, overall, an increase in resistance to apoptosis. In the sevofluran group, reperfusion was followed by stagnation in Fas/Fas-L, a small decrease in TNFr, and a change in the Bax/Bcl-2 proapoptotic ratio (0.97-1.01).

Conclusion:
Ischemia-reperfusion injury induced by cardioplegic myocardial arrest is not likely to cause a clinically relevant loss of cells by apoptosis. On the contrary, the standard procedure of myocardial protection in cardiac surgery-heart arrest by cold cardioplegic solution-enhances the resistance to apoptosis. In our study, sevofluran did not enhance resistance to apoptosis, rather, a proapoptotic tendency was seen.

Keywords: Apoptosis; Cardioplegic myocardial arrest; Reperfusion; Sevofluran

Published: January 1, 2004  Show citation

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Wagner R, Piler P, Horváth R, Benedík J, Adámek P, Černošek J, Sirotková A. The importance of post-reperfusion myocardial tissue apoptosis in cardiac surgery. Cor Vasa. 2004;45(1):24-28.
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