Erythropoiesis in Multiply Injured Patients

Robinson, Yohan; Hostmann, Arwed; Matenov, Alexander; Ertel, Wolfgang; Oberholzer, Andreas

doi:10.1097/01.ta.0000240969.13891.9b

Cited by 42 publications

(45 citation statements)

References 78 publications

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“…Akt also regulates the availability of ATP for the cells because activation of Akt maintains cell survival by allowing cells to continuously import glucose and prevent cells from ATP depletion (20, 41). Because regional hypoxia occurs following trauma-hemorrhage (42, 43), the traumahemorrhage-induced hypoxia produces an unfavorable environment for the production of ATP. Furthermore, the decreased phospho-Akt may exacerbate the ATP depletion, thus resulting in impaired phagocytosis following trauma-hemorrhage.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of the Salutary Effects of Estrogen on Kupffer Cell Phagocytic Capacity following Trauma-Hemorrhage: Pivotal Role of Akt Activation

Hsieh

Nickel

Chen

et al. 2009

The Journal of Immunology

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Kupffer cells are macrophages in the liver whose major role is to clear circulating pathogens. Decreased phagocytic capacity of Kupffer cells may result in severe systemic infection. We tested the hypothesis that the depressed Kupffer cell phagocytic capacity following trauma-hemorrhage is enhanced by estrogen administration and this occurs due to maintenance of Fc receptor expression and cellular ATP content via the activation of Akt. Male C3H/HeN mice were subjected to sham operation or trauma-hemorrhage and sacrificed 2 h thereafter. Estrogen, with or without an estrogen receptor antagonist (ICI 182,780), a PI3K inhibitor (Wortmannin), or vehicle, was injected during resuscitation. Kupffer cell phagocytic capacity was tested in vivo. The expression of Fc receptors, of Akt phosphorylation, of p38 MAPK phosphorylation, of DNA binding activity of NF-κB and ATP content of Kupffer cells were also determined. Trauma-hemorrhage suppressed Kupffer cell phagocytosis by decreasing Fc receptor expression and Akt activation; however, it induced p38 MAPK activation and increased NF-κB activity. Cellular ATP levels were also decreased following trauma-hemorrhage. Administration of estrogen following trauma-hemorrhage increased phospho-Akt levels and normalized all the parameters described as well as plasma levels of TNF-α, IL-6, and IL-10. Coadministration of ICI 182,780 or Wortmannin abolished the beneficial effects of estrogen in improving the phagocytic capacity of Kupffer cells following trauma-hemorrhage. Thus, activation of Akt plays a crucial role in mediating the salutary effect of estrogen in restoring trauma-hemorrhage-induced suppression of Kupffer cell phagocytosis.

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Section: Discussionmentioning

confidence: 99%

Mechanism of the Salutary Effects of Estrogen on Kupffer Cell Phagocytic Capacity following Trauma-Hemorrhage: Pivotal Role of Akt Activation

Hsieh

Nickel

Chen

et al. 2009

The Journal of Immunology

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“…After blood loss, an individual's total blood volume and red blood cell (RBC) mass decrease; therefore, oxygen carrying capacity of the blood is reduced. Decreased blood volume accompanied by decreased red cell volume may result from surgery, through donation, or because of injury (18). The body will restore total blood volume within 3 days after donation, initially through plasma expansion, which occurs within the first week after donation (17).…”

Section: Introductionmentioning

confidence: 99%

Time Course for Recovery of Peak Aerobic Power After Blood Donation

Judd

Cornish²,

Barss³

et al. 2011

Journal of Strength and Conditioning Research

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Peak aerobic power (VO2peak) is decreased after blood donation, but the time course for full recovery is unknown. We measured VO2peak and exercise time to fatigue before and weekly for 4 weeks after 450-ml blood donation at a blood donor clinic, to determine the time course of recovery. Twelve moderately active individuals (2 women, 10 men; 24.3 ± 5.2 years) of average aerobic fitness (based on their VO2peak relative to normative values) completed VO2peak exercise tests before donation, the day after donation, and at weekly intervals for 4 weeks after donation. VO2peak was determined by an incremental exercise test on a cycle ergometer. At baseline, mean absolute and relative VO2peak values were 4.06 ± 0.92 L·min(-1) and 46.6 ± 7.0 ml·kg(-1)·min(-1), respectively. VO2peak was significantly decreased on day 1 (3.85 ± 0.89 L·min(-1); 44.0 ± 6.5 ml·kg(-1)·min(-1)) and during week 2 (3.91 ± 0.97 L·min(-1); 44.5 ± 7.2 ml·kg(-1)·min(-1)) after blood donation (p < 0.05), and recovered at week 3 after donation. Time to fatigue and peak heart rate were not significantly affected by blood donation. We conclude that blood donation causes a significant decrease in VO2peak for between 2 and 3 weeks. The practical application of this study is that aerobic power in people of average fitness will be decreased, up to 3 weeks after donating blood. Despite this, there is no effect of blood donation on performance as measured by time to fatigue during an incremental test on a cycle ergometer.

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“…Inflammation, infection, and injury also profoundly alter erythropoiesis and generally result in anemia. The pathogenesis behind alterations in erythropoiesis involves multiple factors, including cytokine-mediated erythroid apoptosis, a blunted BM response to erythropoietin, reduced iron availability, suppression of erythroid progenitor cell proliferation, and BM egress of erythroid progenitor cells (34,40,50,51). Infection and inflammation also modulate the numbers of platelets.…”

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confidence: 99%

Infection withAnaplasma phagocytophilumInduces Multilineage Alterations in Hematopoietic Progenitor Cells and Peripheral Blood Cells

et al. 2009

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Infection withHematopoietic lineage assessment demonstrated that there was loss of erythrocytes and B lymphocytes from the BM along with increased granulopoiesis. These changes were accompanied by splenomegaly due to lymphoid hyperplasia and increased hematopoiesis, most notably erythropoiesis. These changes largely mimic well-described inflammation and endotoxin-mediated effects on the BM and spleen; however, the numbers of peripheral blood neutrophils appear to be independently modulated as granulocytic hyperplasia does not result in neutrophilia. Our findings highlight a well-conserved series of events that we demonstrate can be instigated by an LPS-negative pathogen in the absence of an endotoxin-mediated acute proinflammatory response.

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Erythropoiesis in Multiply Injured Patients

Cited by 42 publications

References 78 publications

Mechanism of the Salutary Effects of Estrogen on Kupffer Cell Phagocytic Capacity following Trauma-Hemorrhage: Pivotal Role of Akt Activation

Mechanism of the Salutary Effects of Estrogen on Kupffer Cell Phagocytic Capacity following Trauma-Hemorrhage: Pivotal Role of Akt Activation

Time Course for Recovery of Peak Aerobic Power After Blood Donation

Infection withAnaplasma phagocytophilumInduces Multilineage Alterations in Hematopoietic Progenitor Cells and Peripheral Blood Cells

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