Red blood cells are damaged by intraoperative blood salvage via Ca2+-dependent and -independent mechanisms
Autor: | Kang Du, Da-Ming Gou, Shan-Shan Zuo, Wen-Tong Meng, Qin Huang, Xin-Yi Liao, Haiying Wang, Jie Zhang |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
business.industry Intraoperative blood salvage Spherocyte medicine.medical_treatment hemic and immune systems General Medicine Phosphatidylserine 030226 pharmacology & pharmacy General Biochemistry Genetics and Molecular Biology Andrology 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine chemistry Annexin Ionomycin Medicine General Pharmacology Toxicology and Pharmaceutics business Incubation |
Zdroj: | Life Sciences. 227:114-121 |
ISSN: | 0024-3205 |
DOI: | 10.1016/j.lfs.2019.03.036 |
Popis: | Aims Intraoperative blood salvage (IBS) is associated with shortened lifespan of red blood cells (RBCs). This study aims to examine how salvaged RBCs are compromised during IBS. Main methods Thirty patients who underwent vertebra surgery with IBS were included in the study. To examine possible mechanisms of IBS-induced injury, both fresh and salvaged RBCs from each patient were mixed with plasma, the Ca2+ ionophore ionomycin or mannitol-adenine-phosphate (MAP) solution (n = 10 patients per condition). Binding of Fluo-3 and/or Annexin V by RBCs was measured. Key findings The percentage of Fluo-3-binding RBCs in salvaged samples was 2.83 ± 0.76%, which increased to 15.34 ± 5.99% after 48-h incubation in plasma. These percentages were significantly higher than those observed with fresh RBCs (P Significance Our results suggest that IBS induces a postponed RBC damage by inducing spherocyte formation, which likely reflects Ca2+ entry induced by energy exhaustion, as well as by exposing phosphatidylserine on the RBC surface, which likely occurs via Ca2+ entry and via Ca2+-independent pathways. |
Databáze: | OpenAIRE |
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