Application of an autotransfusion pressure control system in blood salvage.

OBJECTIVE: This study was performed to evaluate the effect of a homemade autotransfusion pressure-control system on the regulation of negative pressure and to clarify the influence of different negative pressures on the recovered erythrocytes. METHODS: Fifty patients were randomly divided into five groups, and five different suction-generated negative pressures were applied. Before suction, 6 mL of blood was collected from the surgical field; after suction, 6 mL of blood was collected from the blood storage tank. The hemoglobin, hematocrit, mean corpuscular volume, newly generated standardized plasma free hemoglobin, and change in the hemolysis rate of erythrocytes before and after suction were compared. Additionally, the erythrocyte morphology was observed. RESULTS: The hemoglobin and hematocrit were significantly different before and after suction in all five groups. As the suction pressure increased, gradual increases were noted in the number of abnormal erythrocytes in the field of view, the newly generated standardized plasma free hemoglobin, and the change in the hemolysis rate. CONCLUSIONS: The destruction rate of erythrocytes increased as the suction-generated negative pressure increased. When using a pressure-control system, a negative pressure of <200 mmHg should be applied to reduce the damage to the autotransfused blood.

Sevoflurane inhibits the migration and invasion of colorectal cancer cells through regulating ERK/MMP-9 pathway by up-regulating miR-203.

Surgery resection is the primary treatment for colorectal cancer (CRC) patients with the risk of cancer dissemination and metastasis. Sevoflurane is one inhalational anesthesia which regulates migration and invasion in varying cancers. However, the effect of sevoflurane on CRC cells and its mechanism remain poorly understood. In this study, SW620 and HCT116 cells were treated with different concentrations of sevoflurane for 6 h in vitro. We measured the effect of sevoflurane on cell survival, migration and invasion by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide or trans-well assays. Moreover, we explored the interaction between sevoflurane and miR-203 and Roundabout1 (Robo1) as well as the extracellular signal-regulated kinase (ERK) and matrix metalloproteinase-9 (MMP-9) pathway. Results showed that sevoflurane inhibited cell migration and invasion in SW620 and HCT116 cells in a concentration dependent manner. Moreover, different concentrations of sevoflurane suppressed the phosphorylation of ERK. miR-203 expression was impaired while sevoflurane reversed the expression of miR-203 in CRC cells. In addition, inhibition of miR-203 attenuated the inhibitory effect of sevoflurane on cell migration, invasion and phosphorylated ERK level. Notably, MMP-9, as a downstream of ERK, was involved in sevoflurane-mediated processes in CRC cells. Besides, Robo1 was indicated as a target of miR-203 and inhibited by sevoflurane treatment. These results indicated that sevoflurane suppressed cell migration and invasion through regulating ERK/MMP-9 pathway via miR-203/Robo1 in CRC cells, indicating important clinical implications for anesthetic agents to prevent metastasis in CRC.