β-Adrenergic blockade during systemic inflammation: Impact on cellular immune functions and survival in a murine model of sepsis

Schmitz, Daniel; Wilsenack, Klaus; Lendemanns, Sven; Schedlowski, Manfred; Oberbeck, Reiner

doi:10.1016/j.resuscitation.2006.07.001

Cited by 73 publications

(51 citation statements)

References 32 publications

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“…In fact, recent Wndings of altered cytokine release following catecholamine administration during the early phase after trauma in humans (Batistaki et al 2008) and modulation of IL-6 (that was increased in the present study) release with -adrenergic blockade in septic mice (Schmitz et al 2007) provide further support for catecholamines' involvement in inXammation. Furthermore, epinephrine has been shown to enhance platelet-neutrophil adhesion and adhesion molecule expression (Schmitz et al 2007). Collectively, these observations suggest that a sustained post-exercise rise in catecholamines may be related to an exercise-induced inXammatory response.…”

Section: Discussionsupporting

confidence: 75%

Physiological and performance adaptations of elite Greco-Roman wrestlers during a one-day tournament

et al. 2010

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The aim of this study was to determine the effects of a simulated one-day Greco-Roman wrestling tournament on selected performance and inflammatory status indices. Twelve competitive wrestlers (22.1 ± 1.3 years) completed five matches according to the official Olympic wrestling tournament regulations following a ~6% weight loss. Performance measurements, muscle damage assessment, and blood sampling were performed before and following each match. Performance and inflammatory markers were not affected by weight loss. Mean wrestling heart rate reached ~85% of maximal and lactate concentration exceeded 17 mM. Fatigue rating demonstrated a progressive rise (P < 0.05) throughout the tournament, peaking in match 4. Performance demonstrated a progressive deterioration (P < 0.05) throughout the tournament, especially in the last two matches (P < 0.05), with upper-body measures exhibiting a greater decline (P < 0.05) and remaining below baseline (P < 0.05) until the end of the tournament. Muscle damage markers increased during the course of the tournament with upper limbs affected more. Creatine kinase activity, CRP levels, IL-6 concentration, and leukocyte counts increased (P < 0.05) progressively throughout the tournament, peaking in the last two matches. Cortisol, epinephrine and norepinephrine increased (P < 0.05) after each match, but testosterone declined (P < 0.05) progressively, reaching a nadir before the last match. This inflammatory response was accompanied by a marked increase (p < 0.05) in lipid peroxidation, protein oxidation, and antioxidant status markers indicating the development of oxidative stress. These results suggest that a one-day wrestling tournament may induce significant physiological demands on wrestlers that may adversely affect their performance and inflammatory status especially during the later stages of the tournament.

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Section: Discussionsupporting

confidence: 75%

Physiological and performance adaptations of elite Greco-Roman wrestlers during a one-day tournament

et al. 2010

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“…All mice were individually housed following surgery and given access to water until euthanization. Because sepsis acutely decreases food consumption, food was withheld from all mice in the acute sepsis study so that the nutritional status was identical across groups (46); hence, observed differences in protein synthesis and signal transduction are not due to differences in the nutritional state of the mice. The 24-h survival rate did not differ between genotypes, as survival was 100% in septic WT mice and 93% in septic REDD1 mice.…”

Section: Animalsmentioning

confidence: 99%

Disruption of REDD1 gene ameliorates sepsis-induced decrease in mTORC1 signaling but has divergent effects on proteolytic signaling in skeletal muscle

Steiner¹,

Crowell

Kimball³

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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Steiner JL, Crowell KT, Kimball SR, Lang CH. Disruption of REDD1 gene ameliorates sepsis-induced decrease in mTORC1 signaling but has divergent effects on proteolytic signaling in skeletal muscle. Am J Physiol Endocrinol Metab 309: E981-E994, 2015. First published October 20, 2015 doi:10.1152/ajpendo.00264.2015.-Sepsis-induced skeletal muscle atrophy and weakness are due in part to decreased mTORC1-mediated protein synthesis and increased proteolysis via the autophagy-lysosomal system and ubiquitin-proteasome pathway. The REDD1 (regulated in development and DNA damage-1) protein is increased in sepsis and can negatively regulate mTORC1 activity. However, the contribution of REDD1 to the sepsis-induced change in muscle protein synthesis and degradation has not been determined. Sepsis was produced by cecal ligation and puncture in female REDD1Ϫ/Ϫ or wild-type (WT) mice, and end points were assessed 24 h later in gastrocnemius; time-matched, pair-fed controls of each genotype were included. Sepsis increased REDD1 protein 300% in WT mice, whereas REDD1 was absent in REDD1 Ϫ/Ϫ mice despite unaltered PDK1, PP2A, or TSC2 expression. Sepsis increased autophagy as indicated by decreased ULK1 Ser 757 phosphorylation and p62 abundance and increased LC3B-II/I in WT mice, whereas these changes were absent in septic REDD1 Ϫ/Ϫ mice. Conversely, REDD1 deletion did not prevent the sepsis-induced decrease in IGF-I mRNA or the concomitant increase in IL-6, TNF␣, MuRF1, and atrogin1 mRNA expression. Lastly, 5-day survival in a separate set of septic mice did not differ between WT and REDD1 Ϫ/Ϫ mice. These data highlight the central role of REDD1 in regulating both protein synthesis and autophagy in skeletal muscle during sepsis. rgulated in development and DNA damage-1; mechanistic target of rapamycin complex 1; protein synthesis; autophagy; cecal ligation and puncture; proteolysis; critical illness SKELETAL MUSCLE ATROPHY IS A DEBILITATING CONSEQUENCE of sepsis and critical illness that increases the length of hospitalization and mortality (19). Loss of muscle mass and strength during sepsis results from the prolonged imbalance between rates of protein synthesis and degradation caused by several factors, including increased proinflammatory cytokine signaling, anabolic resistance, and excess glucocorticoids (1,32,48). Protein synthesis is controlled predominantly by the mechanistic (a.k.a. mammalian) target of rapamycin complex 1 (mTORC1), which phosphorylates 70-kDa ribosomal protein S6 kinase-1 (S6K1) and eukaryotic initiation factor (eIF) 4E-binding protein-1 (4E-BP1) to increase translation initiation and peptide chain elongation within muscle (13,25). mTORC1 represents a central regulatory factor in the integration of various metabolic signals, including those induced by energy stress [AMP-activated protein kinase (AMPK), regulated in development and DNA damage-1 (REDD-1)] and growth factors (insulin/Akt). Upon activation of the insulin or insulin-like growth factor (IGF)-I receptor and the phosphoinositide 3-kinase signaling...

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“…Another study demonstrated that administration of selective b1-adrenergic blocker provided protective effects on various organs [3,5], and was probably capable of improving the outcomes of septic hosts if initiated before septic insult [6]. In contrast, administration of the nonselective b-adrenergic receptor antagonist, propranolol, increased mortality when administered before or within 48 h of septic insult [7]. Collectively, selective blockade of the b1-adrenoreceptor may have beneficial effects in sepsis, although the exact mechanism remains to be elucidated.…”

mentioning

confidence: 99%

Beta-1 blocker improves survival of septic rats through preservation of gut barrier function

et al. 2011

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β-Adrenergic blockade during systemic inflammation: Impact on cellular immune functions and survival in a murine model of sepsis

Cited by 73 publications

References 32 publications

Physiological and performance adaptations of elite Greco-Roman wrestlers during a one-day tournament

Physiological and performance adaptations of elite Greco-Roman wrestlers during a one-day tournament

Disruption of REDD1 gene ameliorates sepsis-induced decrease in mTORC1 signaling but has divergent effects on proteolytic signaling in skeletal muscle

Beta-1 blocker improves survival of septic rats through preservation of gut barrier function

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