A comparison of biochemical and functional alterations of rat and human erythrocytes stored in CPDA-1 for 29 days: implications for animal models of transfusion.
Animal models of transfusion are employed in many research areas yet little is known about the storage-related changes occurring in the blood used in these studies. This study assessed storage-related changes in red blood cell (RBC) biochemistry, function and membrane deformability in rat and human packed RBCs when stored in CPDA-1 at 4 degrees C over a 4-week period. Human blood from five volunteers and five bags of rat RBC concentrates (five donor rats per bag) were collected and stored at 4 degrees C. RBC function was assessed by post-transfusion viability and the ability to regenerate adenosine triphosphate (ATP) and 2,3-diphosphoglycerate (DPG) when treated with a rejuvenation solution. Membrane deformability was determined by a micropipette aspiration technique. ATP in rat RBCs declined more rapidly than human RBCs; after 1 week rat ATP fell to the same level as human cells after 4 weeks of storage (rat, 2.2 +/- 0.2 micromol g(-1) Hb; human, 2.5 +/- 0.3 micromol g(-1) Hb). Baseline DPG concentrations were similar in rat and human RBCs (16.2 +/- 2.3 micromol g(-1) Hb and 13.7 +/- 2.4 micromol g(-1) Hb) and declined very rapidly in both species. Human RBCs fully regenerated ATP and DPG when treated with a rejuvenation solution after 4 weeks of storage. Rat RBCs regenerated ATP but not DPG. Post-transfusion viability in rat cells was 79%, 26% and 5% after 1, 2 and 4 weeks of storage, respectively. In rats, decreased membrane deformability became significant (- 54%) after 7 days. Human RBC deformability decreased significantly by 34% after 4 weeks of storage. The rejuvenation solution restored RBC deformability to control levels in both species. Our results indicate that rat RBCs stored for 1 week in CPDA-1 develop a storage lesion similar to that of human RBCs stored for 4 weeks and underscores significant species-specific differences in the structure and metabolism of these cells.
d'Almeida
M S
MS
Department of Hematology, London Health Sciences Centre, the AC Burton Vascular Biology Laboratory and the Department of Pharmacology and Toxicology, University of Western Ontario, London, Ontario, Canada.
Jagger
J
J
Duggan
M
M
White
M
M
Ellis
C
C
Chin-Yee
I H
IH
D019794:2,3-Diphosphoglycerate / Q000378:metabolism; D000225:Adenine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D001793:Blood Preservation / Q000009:adverse effects / Q000379:methods*; D001803:Blood Transfusion / Q000379:methods; D002470:Cell Survival; D002951:Citrates / Q000494:pharmacology*; D015925:Cryopreservation / Q000379:methods; D004907:Erythrocyte Deformability; D004912:Erythrocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D008297:Male; D023421:Models, Animal; D010710:Phosphates / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013045:Species Specificity; D013997:Time Factors
C034876:CPDA solutions; D002951:Citrates; D010710:Phosphates; D019794:2,3-Diphosphoglycerate; D000255:Adenosine Triphosphate; D005947:Glucose; D000225:Adenine