[Protective effects of propofol preconditioning on cardiopulmonary bypass-induced apoptosis: report of 40 cases].
OBJECTIVE
To investigate the protective effects of propofol preconditioning on cardiopulmonary bypass (CPB)-induced apoptosis and its possible mechanism.


METHODS
Forty patients undergoing CPB were randomly divided into 2 equal groups: propofol preconditioning group (Group P, pre-treated with propofol 2 mg/kg pre-operatively and 5 mg.kg(-1).h(-1) intra-operatively) and control group (Group C, pre-treated with midazolam 0.2 mg/kg pre- and 0.1 mg.kg(-1).h(-1) intra-operatively). Specimens of right auricle tissue were taken before and after CPB to undergo HE staining and electron microscopy to observe the changes of mitochondria. TUNEL technique was used to detect the apoptotic cells and the apoptotic index (AI) was calculated. Avidin biotin complex method was used to detect the expression of caspase-9 and caspase-3.


RESULTS
The rate of spontaneous restoration of beats of Group P was 65%, significantly higher than that of Group C (30%, P < 0.05). The amount used of dobutamine within 12 h post-operatively of Group P was 4.6 +/- 1.1 microg.kg(-1).h(-1), significantly lower than that of Group C (7.8 +/- 1.0 microg.kg(-1).h(-1), P < 0.05). The ICU stay time of Group P was 40 +/- 6 h. significantly shorter than that of Group C (58 +/- 7 h, P < 0.05). The specimens taken after CPB showed that in comparison with Group C the mitochondria were relatively intact with clear ridges and intermembrane spaces in Group P. The AI after CPB of Group C was (19.3 +/- 3.5)%, significantly higher than that before CPB [(7.1 +/- 1.4)%, P < 0.05] and the corresponding level of Group P [(10.9 +/- 1.4)%, P < 0.05]. The expression levels of Caspace-9 and Caspace-3 after CPO of Group C were both significantly higher than those before CPB (both P < 0.05), and the corresponding levels of Group P (both P < 0.05).


CONCLUSIONS
Propofol preconditioning significantly inhibits CPB-induced cardiomyocyte apoptosis and the mechanism is associated with protecting the mitochondria and down-regulating the expression of caspase-9 and caspases-3.
Zhu
Shao-Jun
SJ
Department of Anesthesiology, First Affiliated Hospital of College of Medicine, Zhejiang University, Hangzhou, China.
Han
Wei-Li
WL
Zhu
Sheng-Mei
SM
Zhou
Yan-Feng
YF
D000368:Aged; D018686:Anesthetics, Intravenous / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D002315:Cardiopulmonary Bypass; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D005260:Female; D006801:Humans; D020287:In Situ Nick-End Labeling; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D015742:Propofol / Q000627:therapeutic use*
D018686:Anesthetics, Intravenous; D053148:Caspase 3; D053453:Caspase 9; D015742:Propofol