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

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

doi:10.1097/ta.0b013e31825a785a

Cited by 6 publications

(5 citation statements)

References 36 publications

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“…However, plasma from LCHS + β2B or LCHS + β3B animals improved BM HPC colony growth, suggesting that both β2B and β3B have protective systemic effects. Baranski et al 18 showed similar improvement in HPC colony growth with LCHS plasma of animals given with propranolol.…”

Section: Discussionmentioning

confidence: 81%

“…3,18 While HPC mobilization and homing play a role in tissue repair at the sites of injury, 2 an excessive release of HPCs with a corresponding decrease in BM cellularity may contribute to persistent BM dysfunction. In this study, when β2B and β3B were administered after LCHS, there was a significant increase in BM cellularity after 3 hours, and this protection of BM cellularity was maintained at 7 days after injury.…”

Section: Discussionmentioning

confidence: 99%

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Do all β-blockers attenuate the excess hematopoietic progenitor cell mobilization from the bone marrow following trauma/hemorrhagic shock?

Pasupuleti

Cook

Sifri

et al. 2014

Journal of Trauma and Acute Care Surgery

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BACKGROUND Severe injury results in increased mobilization of hematopoietic progenitor cells (HPC) from the bone marrow (BM) to sites of injury, which may contribute to persistent BM dysfunction after trauma. Norepinephrine is a known inducer of HPC mobilization, and nonselective β-blockade with propranolol has been shown to decrease mobilization after trauma and hemorrhagic shock (HS). This study will determine the role of selective β-adrenergic receptor blockade in HPC mobilization in a combined model of lung contusion (LC) and HS. METHODS Male Sprague-Dawley rats were subjected to LC, followed by 45 minutes of HS. Animals were then randomized to receive atenolol (LCHS + β1B), butoxamine (LCHS + β2B), or SR59230A (LCHS + β3B) immediately after resuscitation and daily for 6 days. Control groups were composed of naive animals. BM cellularity, %HPCs in peripheral blood, and plasma granulocyte-colony stimulating factor levels were assessed at 3 hours and 7 days. Systemic plasma-mediated effects were evaluated in vitro by assessment of BM HPC growth. Injured lung tissue was graded histologically by a blinded reader. RESULTS The use of β2B or β3B following LCHS restored BM cellularity and significantly decreased HPC mobilization. In contrast, β1B had no effect on HPC mobilization. Only β3B significantly reduced plasma G-CSF levels. When evaluating the plasma systemic effects, both β2B and β3B significantly improved BM HPC growth as compared with LCHS alone. The use of β2 and β3 blockade did not affect lung injury scores. CONCLUSION Both β2 and β3 blockade can prevent excess HPC mobilization and BM dysfunction when given after trauma and HS, and the effects seem to be mediated systemically, without adverse effects on subsequent healing. Only treatment with β3 blockade reduced plasma G-CSF levels, suggesting different mechanisms for adrenergic-induced G-CSF release and mobilization of HPCs. This study adds to the evidence that therapeutic strategies that reduce the exaggerated sympathetic stimulation after severe injury are beneficial and reduce BM dysfunction.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Do all β-blockers attenuate the excess hematopoietic progenitor cell mobilization from the bone marrow following trauma/hemorrhagic shock?

Pasupuleti

Cook

Sifri

et al. 2014

Journal of Trauma and Acute Care Surgery

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“…The effects of norepinephrine are protective from lung injury but maybe contribute to the generalized immunosuppression in severe trauma. Meanwhile, Beta-blockade of propranolol can protect against the detrimental effects of trauma on lungs by blunting the exaggerated sympathetic response after shock and injury 83 . Also, the activation of adrenergic receptors and releasing of CA play an important role in traumatic infections 84 , 85 .…”

Section: The Dynamic Regularity Of Neuroendocrine Immune Network In Tmentioning

confidence: 99%

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

Yang

Gao

et al. 2017

Int. J. Biol. Sci.

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During the occurrence and development of injury (trauma, hemorrhagic shock, ischemia and hypoxia), the neuroendocrine and immune system act as a prominent navigation leader and possess an inter-system crosstalk between the reciprocal information dissemination. The fundamental reason that neuroendocrinology and immunology could mix each other and permeate toward the field of traumatology is owing to their same biological languages or chemical information molecules (hormones, neurotransmitters, neuropeptides, cytokines and their corresponding receptors) shared by the neuroendocrine and immune systems. The immune system is not only modulated by the neuroendocrine system, but also can modulate the biological functions of the neuroendocrine system. The interactive linkage of these three systems precipitates the complicated space-time patterns for the courses of traumatic inflammation. Recently, compelling evidence indicates that the network linkage pattern that initiating agents of neuroendocrine responses, regulatory elements of immune cells and effecter targets for immune regulatory molecules arouse the resistance mechanism disorders, which supplies the beneficial enlightenment for the diagnosis and therapy of traumatic complications from the view of translational medicine. Here we review the alternative protective and detrimental roles as well as possible mechanisms of the neuroendocrine immune responses in traumatic inflammation.

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“…(82) In a rodent model of lung contusion and hemorrhagic shock with and without propranolol administration, lung injury scores were significantly attenuated three hours after injury in the propranolol treatment group. (83) Baranski et al hypothesized that the improvement in lung injury scores was related to either the systemic effects of propranolol or a reduction in gut permeability. (83) …”

Section: Pulmonary Dysfunctionmentioning

confidence: 99%

“…(83) Baranski et al hypothesized that the improvement in lung injury scores was related to either the systemic effects of propranolol or a reduction in gut permeability. (83) …”

Section: Pulmonary Dysfunctionmentioning

confidence: 99%

β-Blockade use for Traumatic Injuries and Immunomodulation

Loftus

Efron

Moldawer

et al. 2016

Shock

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Sympathetic nervous system activation and catecholamine release are important events following injury and infection. The nature and timing of different pathophysiologic insults have significant effects on adrenergic pathways, inflammatory mediators, and the host response. Beta adrenergic receptor blockers (β-blockers) are commonly used for treatment of cardiovascular disease but recent data suggests that the metabolic and immunomodulatory effects of β-blockers can expand their use. β-blocker therapy can reduce sympathetic activation and hypermetabolism as well as modify glucose homeostasis and cytokine expression. It is the purpose of this review to examine either the biologic basis for proposed mechanisms or to describe current available clinical evidence for the use of β-blockers in traumatic brain injury (TBI), spinal cord injury (SCI), hemorrhagic shock, acute traumatic coagulopathy, erythropoietic dysfunction, metabolic dysfunction, pulmonary dysfunction, burns, immunomodulation, and sepsis.

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

Cited by 6 publications

References 36 publications

Do all β-blockers attenuate the excess hematopoietic progenitor cell mobilization from the bone marrow following trauma/hemorrhagic shock?

Do all β-blockers attenuate the excess hematopoietic progenitor cell mobilization from the bone marrow following trauma/hemorrhagic shock?

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

β-Blockade use for Traumatic Injuries and Immunomodulation

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