ABSTRACT
OBJECTIVE: During cardiopulmonary bypass (CPB), gaseous microemboli (GME) that originate from the extracorporeal circuit are released into the arterial blood stream of the patient. Gaseous microemboli may contribute to adverse outcome after cardiac surgery with CPB. Possibly, air may be collected in the right atrium during induction of anesthesia and released during CPB start. The aim of this study was to assess if the GME load entering the venous line of the CPB circuit could be reduced by training of anesthesia personal in avoiding air introduction during administration of intravenous medication. METHODS: In 94 patients undergoing coronary artery bypass grafting with CPB, GME number and volume were measured intraoperatively with a bubble counter (BCC300). The quantity and the relationship between GME number and volume in the venous and arterial line were determined in 2 periods before and after education of the anesthesiologists and nurses. RESULTS: In the venous line no significant differences were observed between numbers and volumes of GME between groups. Comparing patients with low versus high GME load, showed significantly more patients from the intervention group in the low GME-load group, namely 29 versus 18. Administration of medication by anesthesia was confirmed as a clear cause of GME/air-introduction into the venous circulation. Scavenging properties of the CPB circuit including the oxygenator showed a 99.9% reduction of GME. CONCLUSIONS: A wide spread of GME generation during perfusion was present with no difference in generation of GME between groups. Lower GME load observed in patients (intervention group) and examples of air introduction during drug administration suggest that air introduced by anesthesia contributes to the GME load during CPB. Scavenging properties of the CPB circuit contribute very much to patient safety regarding reduction of venous air. Awareness and education create the possibilities for further reduction of GME during cardiopulmonary bypass.
ABSTRACT
INTRODUCTION: This study aimed to determine whether, as in osteoarthritis, increased levels of interleukin-6 (IL-6) are present in the synovial fluid of patients with symptomatic cartilage defects and whether this IL-6 affects cartilage regeneration as well as the cartilage in the degenerated knee. METHODS: IL-6 concentrations were determined by ELISA in synovial fluid and in conditioned media of chondrocytes regenerating cartilage. Chondrocytes were obtained from donors with symptomatic cartilage defects, healthy and osteoarthritic donors. The effect of IL-6 on cartilage regeneration and on metabolism of the resident cartilage in the knee was studied by both inhibition of endogenous IL-6 and addition of IL-6, in a regeneration model and in osteoarthritic explants in the presence of synovial fluid, respectively. Readout parameters were DNA and glycosaminoglycan (GAG) content and release. Differences between controls and IL-6 blocked or supplemented samples were determined by univariate analysis of variance using a randomized block design. RESULTS: Synovial fluid of patients with symptomatic cartilage defects contained more IL-6 than synovial fluid of healthy donors (P = 0.001) and did not differ from osteoarthritic donors. IL-6 production of osteoarthritic chondrocytes during cartilage regeneration was higher than that of healthy and defect chondrocytes (P < 0.001). Adding IL-6 increased GAG production by healthy chondrocytes and decreased GAG release by osteoarthritic chondrocytes (P < 0.05). Inhibition of IL-6 present in osteoarthritic synovial fluid showed a trend towards decreased GAG content of the explants (P = 0.06). CONCLUSIONS: Our results support a modest anabolic role for IL-6 in cartilage matrix production. Targeting multiple cytokines, including IL-6, may be effective in improving cartilage repair in symptomatic cartilage defects and osteoarthritis.
