Persistent injury-associated anemia in aged rats

Academic Article


  • Background Hypercatecholaminemia and bone marrow dysfunction have been implicated in the pathophysiology of persistent-injury associated anemia. The elderly may be vulnerable to this phenomenon due to high basal and peak catecholamine levels, impaired erythroid progenitor growth, and baseline anemia. We hypothesized that aged F344-BN rats subjected to severe trauma and chronic stress would have persistent injury-associated anemia. Methods Male F344-BN rats age 25 months were randomly allocated to: naïve (n = 8), lung contusion (LC, n = 9), LC followed by daily chronic restraint stress (LC/CS, n = 9), LC followed immediately by hemorrhagic shock (LCHS, n = 8), and LCHS followed by daily CS (LCHS/CS, n = 8). Urine norepinephrine was measured on days one and seven. Locomotor testing was performed on day five. Bone marrow cellularity, hematopoietic progenitor growth, and peripheral blood hemoglobin levels were assessed at sacrifice on day seven. Data are presented as mean ± standard deviation, *p < 0.05 vs. naïve. Results Norepinephrine levels (ng/mL) were significantly elevated one day after LCHS (420 ± 239* vs. naïve: 97 ± 71) and LCHS/CS (375 ± 185*), and remained significantly elevated on day seven for LCHS/CS (359 ± 99*), but not LCHS (212 ± 130). On locomotor testing, groups subjected to CS traveled shorter distances at lower velocities and spent less time in the center of the cage. Colony forming units-erythroid (colonies/plate), representing late erythroid progenitors, were significantly decreased after LC/CS (40 ± 1* vs. naïve: 47 ± 4), LCHS (40 ± 1*), and LCHS/CS (38 ± 3*). LCHS/CS animals had significantly lower hemoglobin (g/dL) than naïve animals (13.3 ± 1.3* vs. naïve: 15.2 ± 0.9). Conclusions Persistent injury-associated anemia occurs in aged rats. Further research is needed to determine whether the pathophysiology of this phenomenon differs from that of younger rats, and to translate these findings to elderly trauma patients.
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  • Loftus TJ; Kannan KB; Carter CS; Plazas JM; Mira JC; Brakenridge SC; Leeuwenburgh C; Efron PA; Mohr AM
  • Start Page

  • 63
  • End Page

  • 68
  • Volume

  • 103