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- Arnestad, J P, et al.
(author)
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Removal of activated complement from shed blood: comparison of high- and low-dilutional haemofiltration.
- 1998
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In: Acta anaesthesiologica Scandinavica. - 0001-5172. ; 42:7, s. 811-5
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Journal article (peer-reviewed)abstract
- BACKGROUND: Perioperative blood salvage is associated with release of inflammatory mediators. Depending on type of processing, the complement system is activated to some extent in the final blood product. The aim of the present study was to evaluate a haemofiltration technique concerning complement system activation and whether the volume of added saline will have an influence on the elimination of activated complement during processing. METHODS: Sixteen patients undergoing total hip arthroplasty received wound blood salvaged intraoperatively with a haemofiltration technique. Saline was added to the reservoir for washing in a ratio of 1:1 or 5:1 of estimated blood volume. Samples for determination of the anaphylatoxins C3a and C5a, and the terminal SC5b-9 complement complex (TCC) were drawn from the patients, the collected blood, the ultrafiltrate and the processed blood. RESULTS: Increased concentrations of C3a, C5a and TCC were found in aspirated and processed blood. Haemofiltration did not reduce the concentrations of these factors, except that of C3a in the group where saline was added in a ratio of 5:1. There were no increased concentrations of C3a, C5a or TCC in the patient plasma after reinfusion. No differences in blood pressure, heart rate, pH, arterial oxygen tension, arterial carbon dioxide tension, or base excess were found in association with reinfusion of the blood. CONCLUSION: Collected shed blood washed through haemofiltration contained moderately elevated concentrations of C3a, C5a and TCC. Reinfusion of the blood neither led to increased systemic concentrations of complement activation products, nor to disturbances in haemodynamic or biochemical parameters.
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| 2. |
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| 3. |
- Gong, J, et al.
(author)
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Tubing loops as a model for cardiopulmonary bypass circuits : both the biomaterial and the blood-gas phase interfaces induce complement activation in an in vitro model.
- 1996
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In: Journal of Clinical Immunology. - 0271-9142 .- 1573-2592. ; 16:4, s. 222-223
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Journal article (peer-reviewed)abstract
- We describe here a model for the study of blood/surface and blood/air interaction as encountered in cardiopulmonary bypass (CPB) circuits. Polyethylene tubing was filled with serum or blood and closed end to end into loops whereby the volume of the remaining air bubble was inversely varied with respect to that of the fluid. The loops were rotated vertically in a water bath at 37 degrees C. The profiles of C3a, iC3, and TCC generation were similar to those observed at surgery, involving CPB. Soluble heparin and heparan sulfate inhibited both C3a and TCC formation, but surface-conjugated heparin had only a minor effect. Binding of C3 and/or C3 fragments to the heparin surface was much reduced compared to the amine matrix to which heparin was linked, but compared with the polyethylene surface the effect was less pronounced. These data suggest that, in addition to the biomaterial surface, the blood-gas interface seems to play an important role in the activation of complement and that this activation is inhibitable by high concentrations of soluble glucose aminoglycans.
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| 4. |
- Nordang, Leif, et al.
(author)
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Complement activation in sudden deafness.
- 1998
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In: Archives of Otolaryngology - Head & Neck Surgery. - 0886-4470 .- 1538-361X. ; 124:6, s. 633-6
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Journal article (peer-reviewed)abstract
- OBJECTIVE: To test whether complement activation is associated with sudden deafness.DESIGN: Plasma samples obtained from patients in the acute phase of sudden deafness were analyzed for complement activation measured by C3bc levels and terminal complement complex. Comparisons were made with plasma samples from healthy controls.PATIENTS: Twenty-five adult patients with unilateral sudden deafness. The criteria for inclusion were symptoms of hearing loss for not longer than 14 days and a hearing loss of 35 dB or more measured at entry.RESULTS: Levels of C3bc were higher in patients compared with controls (P<.001). There were no differences in the formation of terminal complement complex in patients and controls.CONCLUSIONS: The elevated levels of C3bc in patients with sudden deafness indicate an activation of the first part of the complement cascade and therefore suspected inflammatory causes. Measurements of C3bc levels might identify patients with sudden deafness who would benefit from treatment with anti-inflammatory drugs.
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