Pro-inflammatory cytokines in elective flap surgery.

BACKGROUND: Surgical trauma releases inflammatory mediators such as pro-inflammatory cytokines. In this prospective, controlled, randomized trial we investigated the release of pro-inflammatory cytokines and monocyte/macrophage activation in patients scheduled for breast reconstruction after mastectomy. Patients were allocated to one of three surgical procedures, differing in complexity and in the need for implants used for reconstruction. METHODS: Thirty mastectomized women underwent delayed breast reconstruction with the lateral thoracodorsal flap (LTD), the latissimus dorsi flap (LD), or the pedicled transverse rectus abdominis muscle flap (TRAM). Blood samples for TNF, IL-6, IL-8, neopterin, C-reactive protein (CRP), and leukocyte determination were drawn pre-operatively, 24 h, and 2 weeks post-operatively. RESULTS: All groups had significantly elevated IL-6 levels 24 h after surgery. The levels were significantly higher in the TRAM group compared to the LTD and LD groups. IL-8 levels were increased in all groups 2 weeks after surgery (P < 0.05), the LTD (83 pg/mL) and LD (84 pg/mL) group having higher mean IL-8 levels than the TRAM patients (48 pg/mL) (ns). TNF and leukocyte counts were within the normal range. CRP levels were elevated in all groups one day after surgery (P < 0.05). CONCLUSION: Flap procedures for breast reconstruction stimulate the pro-inflammatory response. IL-6 levels were highest in patients with TRAM operations, being the most extensive procedure studied, whereas the highest IL-8 levels were seen in women with a saline filled silicone implant suggesting immunomodulation by foreign material. Although all three investigated procedures are major operations in the field of plastic surgery, according to the inflammatory response to trauma they should be regarded as minor procedures.

Release of PMN elastase, TGF-beta1 and neopterin during blood storage; unfiltered versus filtered blood.

Release of inflammatory mediators from blood cells during prestorage leukocyte filtration may result in recipient immune suppression. To investigate the effects of prestorage leukocyte filtration on the quality of blood components, twenty-four blood units were collected from healthy donors and randomised into 3 groups. Eight units were stored as whole blood, eight units were separated into plasma, red blood cells (RBC) and buffy coat and eight units were collected and filtered through the ASAHI RZ 2000 leukocyte filter and separated into plasma and RBC. The units were stored for 35 days. Samples were collected weekly for analyses of polymorphonuclear elastase (PMN elastase), transforming growth factor-beta1 (TGF-beta1) and neopterin. PMN elastase and neopterin increased during storage of whole blood and RBC. From the beginning and throughout storage, PMN elastase was increased in filtered plasma as compared with unfiltered plasma. Filtration per se did not influence the neopterin concentration in plasma or RBC. TGF-beta1 increased in plasma and RBC during storage. In filtered plasma, an elevation of the TGF-beta1 concentration was observed from the start of storage. The TGF-beta1 levels were higher in filtered plasma compared with unfiltered plasma. Prestorage leukocyte filtration increased the release of PMN elastase and TGF-beta1 in plasma and RBC.

Sympathetic activation and inflammatory response in patients with subarachnoid haemorrhage.

OBJECTIVE: The aim of this study was to evaluate the correlation between sympathetic nervous activation and the immune response in patients following subarachnoid haemorrhage (SAH). DESIGN AND SETTING: Clinical study in a neurosurgical intensive care unit. PATIENTS AND PARTICIPANTS: Fourteen patients with acute non-traumatic SAH were included. Fifteen healthy, age-matched volunteers served as controls for measurement of catecholamine spillover. INTERVENTION: Blood sampling for C3a, C5b-9, IL-6, IL-8 and norepinephrine kinetic determination was made within 48 h, at 72 h and on the 7th-10th day after the SAH. MEASUREMENTS AND RESULTS: SAH patients exhibited a profound increase in the rate of norepinephrine spillover to plasma at 48 h, 72 h and 7-10 days after the insult, 3-4 times that in healthy individuals. The plasma levels of C3a, IL-6 and C5b-9 were significantly elevated at 48 h, at 72 h and 7-10 days after the SAH, but the plasma level of IL-6 decreased significantly 7-10 days after the SAH. There was no relationship between the magnitude of sympathetic activation and the levels of inflammatory markers. CONCLUSIONS: Following SAH a pronounced activation of the sympathetic nervous system and the inflammatory system occurs. The lack of significant association between the rate of spillover of norepinephrine to plasma and the plasma levels of inflammatory markers indicates that the two processes, sympathetic activation and the immune response, following SAH are not quantitatively linked. In spite of a persistent high level of sympathetic activation the plasma level of IL-6 decreased significantly one week after SAH.

Activation of the complement system by different autologous transfusion devices: an in vitro study.

BACKGROUND: The aim of the present investigation was to study whether autologous transfusion devices activate the complement system and whether complement-activated blood is more vulnerable to further activation during processing. STUDY DESIGN AND METHODS: Forty-eight blood units were randomized to be processed by one of three different salvage systems: Group 1 underwent whole blood filtration (hemofiltration) (n=16); Group 2 underwent continuous processing, saline washing, and centrifugation (CATS, Fresenius AG ) (n=16); and Group 3 underwent saline washing and centrifugation (Cell-Saver, Haemonetics Corp.) (n=16). Eight blood units for each system were activated with cobra venom factor (CVF) at a concentration of 0.2 U per mL whole blood before processing. C activation was studied by determinations of C4d, Bb, C3a, and SC5b-9. Samples were drawn from whole blood, processed blood, and the waste bags. RESULTS: The concentrations of Bb, C3a, and SC5b-9 in whole blood after activation with CVF were significantly elevated compared to blood that was not activated (p < 0.01). Processed blood from hemofiltration contained significantly higher levels of complement-split products than techniques that use washing and centrifugation. The concentrations of SC5b-9 in blood processed by hemofiltration were higher in the experiments with CVF activation (p < 0.05). CONCLUSION: The tested autologous transfusion systems did not themselves activate the complement system, and complement-activated blood was not more vulnerable to further activation during processing. A blood-salvaging technique that used washing and centrifugation reduced elevated concentrations of complement-split products, whereas hemofiltration did not.