A hypotonic storage solution did not prolong the viability of RBCs.

BACKGROUND: Hypotonic storage solutions and WBC filtration are both reported to improve RBC viability. This study tested the ability of an investigational hypotonic storage solution (AS-24, Medsep Corp.) to extend the viability of liquid-stored RBCs to 8 weeks. STUDY DESIGN AND METHODS: In a pair of crossover trials, 11 RBC units, WBC-reduced by filtration and stored in AS-24 for 8 weeks, were compared with units from the same donors that were stored for 6 weeks in AS-3, and 13 RBC units, WBC-reduced by filtration and stored in AS-3 for 8 weeks, were compared with units from the same donors that were stored for 6 weeks in AS-3. Viability was measured by the (51)Cr/(99m)Tc double-isotope method. RESULTS: RBC viability at 8 weeks averaged 64 +/- 3 percent in the AS-24 units and 67 +/- 2 percent in the AS-3 units. It was equal at 77 +/- 3 percent and 77 +/- 2 percent after 6 weeks' storage in AS-3 in both trials. CONCLUSIONS: Prestorage WBC reduction and storage in AS-24 did not extend RBC viability to 8 weeks. The improved viability previously demonstrated with storage of dilute suspensions of RBCs in hypotonic solutions is probably caused by factors other than the hypotonicity.

The effects of phosphate, pH, and AS volume on RBCs stored in saline-adenine-glucose-mannitol solutions.

BACKGROUND: RBC ATP concentrations are the most important correlate of RBC viability. Tests were performed to determine whether increased AS volume, pH, and phosphate content increased stored RBC ATP concentrations. STUDY DESIGN AND METHODS: In three studies, packed RBCs were pooled in groups of 3 or 4 units and realiquoted as combined units to reduce intradonor differences. Pooled units were stored in the licensed ASs, AS-1 or AS-5, which contain saline, adenine, glucose, and mannitol (SAGM), or in experimental ASs (EASs) containing SAGM and disodium phosphate. Ten pools were stored in AS-1 at RBC concentrations equivalent to 100, 200, or 300 mL of AS. Six pools were stored in 100, 200, 300, or 400 mL volumes of EAS-61. Ten pools were stored in 100 mL of AS-5, 200 mL of EAS-61, or 300 mL of EAS-64. RBC ATP concentration and other measures of RBC metabolism and function were measured weekly. RESULTS: RBC ATP concentrations decreased sooner with storage in increasing volumes of AS-1. In EAS-61 and EAS-64, RBC ATP concentrations initially increased and stayed elevated longer with increasing AS volume. CONCLUSIONS: The addition of disodium phosphate to SAGM AS increases the RBC ATP concentrations. Reducing storage Hct appears to have a separate beneficial effect in reducing hemolysis.

The viability of autologous human red cells stored in additive solution 5 and exposed to 25 degrees C for 24 hours.

BACKGROUND: No data exist on the viability of red cells (RBCs) stored in modern additive solution systems and allowed to warm above 10 degrees C. STUDY DESIGN AND METHODS: In a randomized crossover study, 3 units of blood were collected at least 8 weeks apart from 11 volunteer donors and stored in additive solution 5 (AS-5). Of 3 units from each volunteer, 1 was stored for 6 weeks at 4 degrees C, 1 for 5 weeks at 4 degrees C except for 24 hours at 25 degrees C on Day 14, and 1 for 5 weeks at 4 degrees C except for 24 hours at 25 degrees C on Day 28. Units were sampled periodically during storage; at the end of storage, viability was measured by the 99mTc/51 Cr double-label method. RESULTS: RBC viability was not significantly different in the storage protocols. Less than 1 percent of stored cells hemolyzed. RBC ATP concentrations at the end of storage correlated with viability and were approximately equal in the warmed units after 30 days' storage and the conventionally stored units after 42 days. CONCLUSIONS: The data suggest that RBCs stored in AS-5 and allowed to warm to 25 degrees C for 24 hours lose about 12 days of their shelf life.

Adhesion of human basophils, eosinophils, and neutrophils to interleukin 1-activated human vascular endothelial cells: contributions of endothelial cell adhesion molecules.

Cytokines such as interleukin 1 (IL-1) promote adhesiveness in human umbilical vein endothelial cells for leukocytes including basophils, eosinophils, and neutrophils, and induce expression of adherence molecules including ICAM-1 (intercellular adhesion molecule-1), ELAM-1 (endothelial-leukocyte adhesion molecule-1), and VCAM-1 (vascular cell adhesion molecule-1). In the present study, blocking monoclonal antibodies (mAb) recognizing ICAM-1, ELAM-1, and VCAM-1 have been used to compare their roles in IL-1-induced adhesion of human basophils, eosinophils, and neutrophils. IL-1 treatment of endothelial cell monolayers for 4 hours induced a four- to eight-fold increase in adhesion for each cell type. Treatment of endothelial cells with either anti-ICAM-1 or anti-ELAM-1 mAb inhibited IL-1-induced adherence of each cell type. In contrast, treatment with anti-VCAM-1 mAb inhibited basophil and eosinophil (but not neutrophil) adhesion, and was especially effective in blocking eosinophil adhesion. The effects of these mAb were at least additive. Indirect immunofluorescence and flow cytometry demonstrated expression of VLA-4 alpha (very late activation antigen-4 alpha, a counter-receptor for VCAM-1) on eosinophils and basophils but not on neutrophils. These data document distinct roles for ICAM-1, ELAM-1, and VCAM-1 during basophil, eosinophil, and neutrophil adhesion in vitro, and suggest a novel mechanism for the recruitment of eosinophils and basophils to sites of inflammation in vivo.