PubMed · 12740970
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Mardi Gomberg-Maitland, Jonathan L Halperin. 2003-05-08. Off-pump coronary bypass surgery.. https://pubmed.ncbi.nlm.nih.gov/12740970/
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OBJECTIVE: To study the intervention of reduced glutathione for neutrophil activation in the process of extracorporeal circulation. METHOD: 20 congenital heart disease children aged from 6 to 12 years were selected randomly, divided into control group and interventional group, patients of interventional group were added reduced glutathione (30 mg/kg) in priming fluid, then phlebotomized on the time of 24 hours before operation, 20 minutes after CPB, rewarming, the end of CPB, 4 hours after operation, 24 hours after operation. After separated neutrophil, we distilled nuclear protein and mensurated the activation of nuclear factor-kappaB by EMSA, assayed the expression of ICAM-1. by immunohistochemistry. RESULTS: Neutrophil nuclear factor-kappaB has been activated on the time of 20 minutes after CPB, arrives at the top on the time of rewarming, and resumes 24 hours after operation; ICAM-1 expresses on the time of rewarming, arrives at the top 4 hours after operation in control group. The data of interventional group is lower than the control group. CONCLUSION: Neutrophil nuclear factor-kappaB is activated and ICAM-1 is expressed in the process of extracorporeal circulation and play an important role in the inflammatory response happening in extracorporeal circulation, which could be relieved by reduced glutathione.
PURPOSE: Myocardial tumor necrosis factor alpha (TNF) production and nuclear factor kappa B (NF-kappaB) activation has been demonstrated in chronic heart failure and experimental models of acute ischemia-reperfusion injury. Further, a cause and effect relationship has been established between these events and cardiomyocyte apoptosis following such conditions. It remains unknown, however, whether the myocardial injury associated with coronary artery bypass surgery (CAB) results in myocardial NF-kappaB activation and TNF production. We hypothesized that CAB with cardiopulmonary bypass ("on-pump") activates human myocardial NF-kappaB and increases TNF in the heart. METHODS: Patients, 18 to 65 years of age, scheduled for elective cardiac surgery but without other preexisting disease were considered eligible for the study. Biopsies of human myocardium were obtained before and after cardiopulmonary bypass and myocardial TNF levels were determined by ELISA and cytotoxicity assay, and NF-kappaB activation was determined by electrophoretic mobility shift assay (n = 6 patients). NF-kappaB activation was quantitated with gel densitometry. RESULTS: The clinical characteristics of the study patients were as follows (means +/- SEM): mean age (y) 50.0 +/- 5.7, male 6 (100%), cardiopulmonary bypass time (min) 107 +/- 37.7, cross-clamp time (min) 68 +/- 17.6, number of CAB 3.0 +/- 1.1, and length of hospital stay (d) 4.8 +/- 0.9. Before CAB, myocardial TNF-alpha levels were 251 +/- 22 pg/g and 33 +/- 9 U/g, as determined by ELISA and cytotoxicity assay, respectively. Following CAB, human myocardial TNF-alpha levels increased to 892 +/- 71 pg/g (P = 0.0008) and 141 +/- 11 U/g (P = 0.0042), as determined by ELISA and cytotoxicity assay, respectively. Before CAB, the ratio of bound to unbound NF-kappaB DNA was 0.009 +/- 0.0007 and after CAB the ratio was 0.24 +/- 0.01 (P < 0.0001). CONCLUSIONS: This study represents the initial demonstration that coronary artery bypass grafting results in an activation of NF-kappaB and an increase of TNF in the heart.
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