Literature DB >> 22846938

Is the sympathetic system involved in shock-induced gut and lung injury?

Gregg M Baranski1, Ziad C Sifri, Kristen M Cook, Walter D Alzate, David H Livingston, Alicia M Mohr.   

Abstract

BACKGROUND: β-blockade (BB) has been shown to prevent bone marrow (BM) dysfunction after trauma and hemorrhagic shock (HS). The impact of the sympathetic system and the role of BB on shock-induced distant organ injury is not known. This study will determine if BB has systemic effects and can diminish gut and lung injury after trauma and HS.
METHODS: Male Sprague-Dawley rats were subjected to lung contusion (LC) followed by 45 minute of HS. Animals (n = 6 per group) were then randomized to either receive propranolol (LCHS + BB) immediately after resuscitation or not (LCHS). Gut permeability was evaluated in by diffusion of Mr 4,000 of fluorescein dextran (FD4) from a segment of small bowel into peripheral blood. Villous injury and lung injury were graded histologically by a blinded reader. Plasma-mediated effects of BB were evaluated in vitro by an assessment of BM progenitor growth.
RESULTS: Animals undergoing LCHS had significantly higher plasma levels of FD4 compared with control animals (mean [SEM], 2.8 [0.4] µg/mL vs. 0.8 [0.2] µg/mL). However, animals receiving BB had a significant reduction in plasma FD4 compared with the LCHS group. With the use of BB after LCHS, both ileal and lung injury scores were similar to control. In addition, BM progenitor growth was inhibited by the addition of LCHS plasma, and LCHS + BB plasma showed no inhibition of BM progenitor growth.
CONCLUSION: Propranolol can protect against the detrimental effects of trauma and HS on gut permeability, villous, and lung injury. The effects of BB are likely systemic and appear to be mediated through plasma. BB likely blunts the exaggerated sympathetic response after shock and injury. Propranolol's reduction of both BM dysfunction and distant organ injury further demonstrates the importance of the sympathetic nervous system and its role in potentiating end organ dysfunction after severe trauma.

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Year:  2012        PMID: 22846938      PMCID: PMC4297311          DOI: 10.1097/TA.0b013e31825a785a

Source DB:  PubMed          Journal:  J Trauma Acute Care Surg        ISSN: 2163-0755            Impact factor:   3.313


  37 in total

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4.  Hemorrhage and resuscitation induce delayed inflammation and pulmonary dysfunction in mice.

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7.  Effects of catecholamines on kinase activation in lung neutrophils after hemorrhage or endotoxemia.

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8.  Multiple organ failure in trauma patients.

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9.  Bone marrow failure following severe injury in humans.

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10.  Hemorrhagic shock.

Authors:  Marie-Jocelyne Martel; Katherine Jane MacKinnon; Marc-Yvon Arsenault; Elias Bartellas; Michael C Klein; Carolyn A Lane; Ann E Sprague; Ann Kathleen Wilson
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2.  Do all β-blockers attenuate the excess hematopoietic progenitor cell mobilization from the bone marrow following trauma/hemorrhagic shock?

Authors:  Latha V Pasupuleti; Kristin M Cook; Ziad C Sifri; Walter D Alzate; David H Livingston; Alicia M Mohr
Journal:  J Trauma Acute Care Surg       Date:  2014-04       Impact factor: 3.313

Review 3.  Altered Neuroendocrine Immune Responses, a Two-Sword Weapon against Traumatic Inflammation.

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