Tyler J Loftus1, Kolenkode B Kannan2, Christy S Carter3, Jessica M Plazas4, Juan C Mira5, Scott C Brakenridge6, Christiaan Leeuwenburgh7, Philip A Efron8, Alicia M Mohr9. 1. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States. Electronic address: Tyler.Loftus@surgery.ufl.edu. 2. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States. Electronic address: Kolenkode.Kannan@surgery.ufl.edu. 3. University of Florida Health, Institute on Aging, Gainesville, FL, United States. Electronic address: Cartercs@ufl.edu. 4. University of Florida, Gainesville, FL, United States. Electronic address: JessicaMPlazas@ufl.edu. 5. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States. Electronic address: Juan.Mira@surgery.ufl.edu. 6. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States. Electronic address: Scott.Brakenridge@surgery.ufl.edu. 7. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States; University of Florida Health, Institute on Aging, Gainesville, FL, United States. Electronic address: CLeeuwen@ufl.edu. 8. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States. Electronic address: Philip.Efron@surgery.ufl.edu. 9. University of Florida Health, Department of Surgery and Sepsis and Critical Illness Research Center, Gainesville, FL, United States. Electronic address: Alicia.Mohr@surgery.ufl.edu.
Abstract
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 25months 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.
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 25months 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 traumapatients.
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