Supplemental oxygen reduces serotonin levels in plasma and platelets during colorectal surgery and reduces postoperative nausea and vomiting.

BACKGROUND AND OBJECTIVE: it has been shown that supplemental oxygen reduces the incidence of postoperative nausea and vomiting (PONV) in patients undergoing colon surgery. Serotonin is a potent trigger of PONV. Theoretically, supplemental oxygen decreases gut ischaemia during surgery and in this way minimizes the release of serotonin. We investigated the release of serotonin during and after colorectal surgery with normal and supplemental oxygen administration. METHODS: patients (n = 53) undergoing colon surgery were randomly assigned to one of two intraoperative ventilation regimens: group A (n = 30) received 80% oxygen and 20% nitrogen mixed with desflurane and group B (n = 23) received 30% oxygen and 70% nitrogen mixed with desflurane. To verify oxygenation status, we measured the arterial oxygen partial pressure (pO2) by blood gas analysis and the intramuscular tissue oxygenation using a polarographic microoxygen sensor (Licox, GMS, Mielkendorf, Germany). Serotonin levels in plasma and in platelets were measured using high-performance liquid chromatography (HPLC) before the beginning of surgery (T0), at the end of surgery (T1), and 2 h (T2), 8 h (T3) and 24 h (T4) postoperatively. PONV was assessed in the early (0-4 h) and overall (0-24 h) postoperative period by an anaesthesiologist unaware of patients' treatment regime. RESULTS: at T1, T2 and T3, serotonin levels were significantly (T1 '80% group' 80 ± 68.2 vs. '30% group' 147 ± 130.5; T2 '80% group' 78.4 ± 61 vs. '30% group' 139 ± 103; T3 '80% group' 76.2 ± 49.5 vs. '30% group' 124 ± 73.7; P < 0.05) reduced in the '80% oxygen group'. Patients in the '80% group' showed a significantly higher pO2 and subcutaneous tissue oxygenation (ptO2). The overall incidence of PONV was significantly reduced in the '80% oxygen group' ('80% group' 7% vs. '30% group' 35%). CONCLUSION: an inspired oxygen fraction of 0.8 reduces serotonin levels significantly and decreases PONV significantly in patients undergoing colon surgery.

The complement receptor 1, CR1 (CD35), mediates inhibitory signals in human T-lymphocytes.

The modulation the specific, adaptive immune response by complement, particularly of by complement C3, is mainly attributed to its interaction with complement receptors on B-lymphocytes. The function of complement receptors on T-lymphocytes, in contrast, is less well understood, although expression of the complement receptor (CR)1 and CR3 on T-cells has been described years ago. In the present study we investigated the effect of antibodies to CR1 on T-cell lines and peripheral T-cells of healthy donors, respectively. Antibodies to CR1 profoundly inhibited the proliferation of the T-cells; of note is, that exogenously added interleukin 2, though enhancing proliferation, did not overcome the inhibitory effect mediated by anti-CR1. While anti-CR1 had no effect on the activation of the immediate early genes c-jun or c-fos nor on the early increase of gamma interferon- or interleukin 2-specific RNA, the protein synthesis of those cytokines was inhibited. Moreover, synthesis of the proliferating cell nuclear antigen (PCNA) was reduced as was the expression of cyclins, particularly of cyclin A and cyclin D3. Taken together, the data indicate that triggering CR1 inhibits proliferation of T-lymphocytes by a mechanism operating downstream of the initial signalling events.