Retrograde Autologous Priming as a Safe and Easy Method to Reduce Hemodilution and Transfusion Requirements during Cardiac Surgery.

BACKGROUND: During the last decades many efforts have been made to reduce transfusion requirements and adverse clinical effects during cardiopulmonary bypass (CPB). The minimal extracorporeal circulation (MECC) system and the technique of retrograde autologous priming (RAP) of a conventional CPB circuit have been associated with decreased hemodilution. Our study aimed to compare conventional CPB (cCPB), RAP, and the ROCsafe MECC (Terumo Europe N.V., Leuven, Belgium) system in elective coronary artery bypass patients. PATIENTS AND METHODS: Data were retrospectively collected on three cohorts of 30 adult CPB patients. Patients were operated using cCPB, RAP, and the ROCsafe MECC system. RESULTS: The three groups were comparable in demographic data. The priming volume in the ROCsafe and RAP group was significantly less compared with the conventional priming group (p <0.05). The mean time of extracorporeal circulation and aortic cross-clamp time (p <0.05) were significantly shorter in the ROCsafe group. The levels of hemoglobin (Hb) and hematocrit (Hct) during CPB and postoperatively showed significant differences between the three groups (p < 0.05) and resulted in significantly higher blood transfusion requirements (p < 0.05). Lactate, serum creatinine, troponin, and creatine kinase-myocardial band (CK-MB) levels did not differ significantly among the three groups (p >0.05). There was also no statistically significant difference in ventilation time, intensive care unit (ICU) stay, overall hospital stay, and postoperative complications (p >0.05). CONCLUSION: In conclusion, RAP is compared with cCPB and MECC a safe and low-cost technique in reducing the priming volume of the CPB system, causes less hemodilution, and reduces the need for intra- and postoperative blood transfusion.

The basal levels of 8-oxoG and other oxidative modifications in intact mitochondrial DNA are low even in repair-deficient (Ogg1(-/-)/Csb(-/-)) mice.

Mitochondrial DNA (mtDNA) is assumed to be highly prone to damage by reactive oxygen species (ROS) because of its location in close proximity to the mitochondrial electron transport chain. Accordingly, mitochondrial oxidative DNA damage has been hypothesized to be responsible for various neurological diseases, ageing and cancer. Since 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most frequent oxidative base modifications, is removed from the mitochondrial genome by the glycosylase OGG1, the basal levels of this lesion are expected to be highly elevated in Ogg1(-/-) mice. To investigate this hypothesis, we have used a mtDNA relaxation assay in combination with various repair enzymes (Fpg, MutY, endonuclease III, endonuclease IV) to determine the average steady-state number of oxidative DNA modifications within intact (supercoiled) mtDNA from the livers of wild-type mice and those deficient in OGG1 and/or the Cockayne syndrome B (CSB) protein for mice aged up to 23 months. The levels of all types of oxidative modifications were found to be less than 12 per million base pairs, and the difference between wild-type and repair-deficient (Ogg1(-/-)/Csb(-/-)) mice was not significant. Thus, the increase of 8-oxoG caused by the repair deficiency in intact mtDNA is not much higher than in the nuclear DNA, i.e., not more than a few modifications per million base pairs. Based on these data, it is hypothesized that the load of oxidative base modifications in mtDNA is efficiently reduced during replication even in the absence of excision repair.