Hemorrhage and resuscitation: immunological aspects

Ih, Chaudry; Ayala, Alfred; Ertel, Wolfgang; Stephan, Rabie N.

doi:10.1152/ajpregu.1990.259.4.r663

Cited by 91 publications

(82 citation statements)

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“…The THS model in this article is a fixed pressure method. however, the procedures can be used with either a fixed pressure or fixed volume hemorrhage approach, and the animal can remain in ThS for 0.5-3 h, which has excellent potential for the investigation of pathophysiological conditions in mice [2]. Our ThS model could also be an important model for studying cellular communication patterns and the responses of systems such as hormonal and inflammatory mediator systems, and danger signals, as it elicits distinct responses that differ from other forms of shock [7,15].…”

Section: Discussionmentioning

confidence: 99%

Establishment of an Experimental Mouse Model of Trauma-Hemorrhagic Shock

et al. 2012

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This study established an experimental mouse model of trauma-hemorrhagic shock (THS). THS-induced mice (C57BL/6J, n=33) were subjected to femoral fracture, ischemia for 90 min, and resuscitation for 15 min. The sham-operated mice (C57BL/6J, n=33) underwent the same anesthetic and surgical procedures, but neither trauma-hemorrhage nor fluid resuscitation were performed. Mean arterial pressure (MAP) and microvascular tissue perfusion over the small intestine, liver, and left kidney were longitudinally measured in all mice. Blood was collected for analysis at baseline and 3, 6, 12, and 24 h post resuscitation, and the small intestine, liver, and left kidney were resected for hematoxylin and eosin staining 24 h post resuscitation. Compared with the sham group, MAP and microvascular tissue perfusion over the small intestine, liver, and left kidney were all significantly reduced in the THS group at the end of hemorrhage. Following resuscitation, no significant differences were observed between the groups. THS induction was associated with significantly increased plasma concentrations of Cr, AST, CPK, IL-6, IL-10, and TNF-α from the baseline values by two-to three-fold after the hemorrhage phase, and THS-induced mice demonstrated significantly increased histological injury scores. The rapid drop in MAP and microvascular tissue perfusion observed following THS induction, and the gradual recovery post resuscitation, reflects the successful establishment of a THS experimental mouse model.

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Section: Discussionmentioning

confidence: 99%

Establishment of an Experimental Mouse Model of Trauma-Hemorrhagic Shock

et al. 2012

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“…Not surprisingly, cytokines play a major role in the body's response to T/HS and TBI [107,109]. Major cytokines that participate in the response to trauma include tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-2, IL-6, IL-8 [20,24,25], IL-4 [26] and recently IL -18 www.ljm.org.ly [27]. On the other hand, the cytokine IL-10 counteracts the effects of the pro-inflammatory cytokines IL-1, IL-6 and TNF-α in various contexts [28], including severe hemorrhagic shock [29].…”

Section: Trauma and The Immune Response From A Clinical Perspectivementioning

confidence: 99%

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Namas¹,

Ghuma²,

Hermus

et al. 2008

Libyan Journal of Medicine

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Abstract; Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

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“…Hemorrhagic shock produces multiple abnormalities in immunological functions, resulting in immunodeficiency and a subsequent increased susceptibility to sepsis 1 . Tissue hypoxia that occurs after hemorrhagic shock produces changes in cellular organic metabolism 2 , and induces the release of proinflammatory cytokines, such as interleukins one and six (IL-1 and IL-6) and tumor necrosis α factor (TNF-α), into the plasma.…”

Section: Introductionmentioning

confidence: 99%

Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide

et al. 2016

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PURPOSE:To investigate changes in the serum concentration and renal expression of IL-1 and TNF-α cytokines in rats that received sevoflurane and glibenclamide prior to hemorrhage. METHODS:Two groups of sevoflurane-anesthetized Wistar rats (n=10): G1 (control) and G2 (glibenclamide, 1 µg/g i.v.); hemorrhage of 30% blood volume (10% every 10 min), with replacement using Ringer solution, 5 ml/kg/h. Serum concentrations of IL-1 and TNF-α were studied in the first hemorrhage (T1) and 50 min later (T2), renal expression, at T2. RESULTS:In serum, G1 TNF-α (pg/mL) was T1=178.6±33.5, T2=509.2±118.8 (p<0.05); IL-1 (pg/mL) was T1=148.8±31.3, T2=322.6±115.4 (p<0.05); in G2, TNF-α was T1=486.2±83.6, T2=261.8±79.5 (p<0.05); IL-1 was T1=347.0±72.0, T2= 327.3±90.9 (p>0.05). The expression of TNF-α and IL-1 in the glomerular and tubular cells was significantly higher in the G2 group. CONCLUSIONS:Hemorrhage and glibenclamide elevated TNF-α and IL-1 concentrations in serum and kidneys. High levels of TNF-α already present before the hemorrhage in the glibenclamide group may have attenuated the damages found in the kidneys after the ischemia event.Key words: Hemorrhage. Glyburide. Cytokines. Kidney. Rats. Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide

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Hemorrhage and resuscitation: immunological aspects

Cited by 91 publications

References 0 publications

Establishment of an Experimental Mouse Model of Trauma-Hemorrhagic Shock

Establishment of an Experimental Mouse Model of Trauma-Hemorrhagic Shock

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide

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