General anesthesia with thoracic epidural anesthesia in the cardiopulmonary bypass surgery reduces apoptosis by upregulating antiapoptotic protein Bcl-2.
OBJECTIVE
The aim of the paper was to investigate whether thoracic epidural anesthesia (TEA) together with general anaesthesia (GA) play a role on apoptosis in humans before cardiopulmonary bypass (CPB), before aortic cross clamp (ACC) and at 15 min after ACC release (after ischemia and reperfusion).


METHODS
Eighty patients scheduled for elective CABG were randomized to receive either GA group (n: 40) or TEA+GA group (n: 40). The right atrial biopsy samples were taken before CPB, before ACC and at 15 min after ACC release from all patients. Human heart tissues were obtained from patients of TEA+GA group and GA group. The number of Bcl-2 positive cardiomyocytes was counted in multiple tissue sections of biopsies of 80 patients using light microscopy (magnification x 40) with an ocular micrometer system (Olympus).


RESULTS
In the TEA+GA group, the Bcl-2 positive cardiomyocytes were distinctly statistically increased compared to the GA group (P<0.001). In addition, the intensity of the immunostaining was also increased in the TEA+GA compared with the GA group. The number of immunoreactive cardiomyocytes is as follows: before CPB, TEA+GA group 396+/-61, GA group 92+/-41, before ACC, TEA+GA group 333+/-47, GA group 94+/-18, at 15 min after ACC release, TEA+GA group 346+/-68.8, GA group 85+/-9.5. There were statistically significant differences between groups, (P<0.001). Between groups, at 4 h and at 24 h after the end of CPB, in the TEA+GA group, the CI was significantly higher than GA group respectively; (3.4+/-0.8 L/min/m(2) vs 2.5+/-0.8 L/min/m(2); P<0.001), (3.8+/-1.1 L/min/m(2) vs 3.1+/-1.1 L/min/m(2); P<0.008). Within groups, at 4 and 24 h after the end of CPB, in the TEA+GA group, the CI was significantly higher than baseline values, respectively, (3.4+/-0.8 L/min/m(2) vs 2.4+/-0.7 L/min/m(2); P<0.001), (3.8+/-1.1 L/min/m(2) vs 2.4+/-0.7 L/min/m(2); P<0.001). Whereas no difference was found in the GA group respectively, (2.6+/-0.8 L/min/m(2) vs. 2.5+/-0.8 L/min/m(2); P>0.05), (2.6+/-0.8 L/min/m(2) vs. 3.1+/-1.1 L/min/m(2); P>0.05). The number of patients showing ventricular fibrillation (VF), atrial fibrillation or heart block after release of the ACC was 11 of 40 (27.5%) in the TEA+GA group versus 25 of 40 (62.5%) in the GA group. The number of patients showing VF after release of ACC was 9 out of 20 patients (22.5%) in the TEA+GA group which was significantly lower than in the GA group (21 of 40 patients 52.5%); (P<0.006). Sinus rhythm after release of ACC, in the TEA+GA group was observed in 29 of 40 patients (72.5%) and was significantly higher than in the GA group (15 of 40 patients 37.5%); (P<0.002).


CONCLUSIONS
The result of the present study indicate that TEA plus GA in coronary surgery had preserved cardiac function during intraoperative and postoperative period by means of reduced apoptosis, improved hemodynamic function and reduced arrhythmias after release of the ACC.
Kiliçkan
L
L
Department of Anesthesiology and Reanimation, Kocaeli University School of Medicine, Kocaeli, Turkey. leventkilickan@hotmail.com
Gonca
S
S
Dalçik
C
C
Dalçik
H
H
Solak
M
M
Bayindir
O
O
Süzer
K
K
Omay
O
O
Calikan
E
E
D000368:Aged; D000767:Anesthesia, Epidural; D000768:Anesthesia, General; D017209:Apoptosis; D001281:Atrial Fibrillation / Q000209:etiology / Q000503:physiopathology; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D002452:Cell Count; D003131:Combined Modality Therapy; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D005260:Female; D006327:Heart Block / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D013525:Surgical Instruments; D016896:Treatment Outcome; D015854:Up-Regulation; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology
D019253:Proto-Oncogene Proteins c-bcl-2