Plasma and myocardial visfatin expression changes are associated with therapeutic hypothermia protection during murine hemorrhagic shock/resuscitation

David G. Beiser, Huashan Wang, Jing Li, Xu Wang, Violeta Yordanova, Anshuman Das, Tamara Mirzapoiazova, Joe GN Garcia, Susan A. Stern, Terry L. Vanden Hoek

Research output: Contribution to journalArticle

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Abstract

Aim: Cytokine production during hemorrhagic shock (HS) could affect cardiac function during the hours after resuscitation. Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD+) salvage pathway. We developed a mouse model of HS to study the effect of therapeutic hypothermia (TH) on hemodynamic outcomes and associated plasma and tissue visfatin content. Methods: Mice were bled and maintained at a mean arterial pressure (MAP) of 35 mmHg. After 30 min, animals (n=52) were randomized to normothermia (NT, 37 ± 0.5 °C) or TH (33 ± 0.5 °C) followed by rewarming at 60 min following resuscitation. After 90 min of HS (S90), mice were resuscitated and monitored for 180 min (R180). Visfatin, interleukin 6 (IL-6), keratinocyte-derived chemokine (KC), tumor necrosis factor-alpha (TNF-α), and myoglobin were measured by ELISA. Results: Compared to NT, TH animals exhibited improved R180 survival (23/26 [88.5%] vs. 13/26 [50%]; p=0.001). Plasma visfatin, IL-6, KC, and TNF-α increased by S90 in both groups (p< 0.05). TH attenuated S90 plasma visfatin and, after rewarming, decreased R180 plasma IL-6, KC, and myoglobin (p< 0.05) relative to NT. Heart and gut KC increased at S90 while IL-6 increases were delayed until R180 (p< 0.05). NT produced sustained elevations of myocardial KC but decreased visfatin by R180, effects abrogated by TH (p< 0.05). Conclusions: In a mouse model of HS, TH improves hemodynamics and alters plasma and tissue proinflammatory cytokines including the novel cytokine visfatin. TH modulation of cytokines may attenuate cardiac dysfunction following HS.

Original languageEnglish (US)
Pages (from-to)742-748
Number of pages7
JournalResuscitation
Volume81
Issue number6
DOIs
StatePublished - Jun 2010
Externally publishedYes

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Nicotinamide Phosphoribosyltransferase
Induced Hypothermia
Hemorrhagic Shock
Resuscitation
Cytokines
Interleukin-6
Rewarming
Myoglobin
NAD
Tumor Necrosis Factor-alpha
Hemodynamics
Arterial Pressure
Enzyme-Linked Immunosorbent Assay
keratinocyte-derived chemokines
Enzymes

Keywords

  • CXCL1
  • Cytokine
  • Hemorrhagic shock
  • Inflammation
  • Interleukin-6
  • Keratinocyte-derived chemokine
  • Nampt
  • Pre-B-cell colony-enhancing factor
  • Resuscitation
  • Temperature
  • Tumor necrosis factor-alpha
  • Visfatin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Emergency
  • Emergency Medicine

Cite this

Plasma and myocardial visfatin expression changes are associated with therapeutic hypothermia protection during murine hemorrhagic shock/resuscitation. / Beiser, David G.; Wang, Huashan; Li, Jing; Wang, Xu; Yordanova, Violeta; Das, Anshuman; Mirzapoiazova, Tamara; Garcia, Joe GN; Stern, Susan A.; Vanden Hoek, Terry L.

In: Resuscitation, Vol. 81, No. 6, 06.2010, p. 742-748.

Research output: Contribution to journalArticle

Beiser, David G. ; Wang, Huashan ; Li, Jing ; Wang, Xu ; Yordanova, Violeta ; Das, Anshuman ; Mirzapoiazova, Tamara ; Garcia, Joe GN ; Stern, Susan A. ; Vanden Hoek, Terry L. / Plasma and myocardial visfatin expression changes are associated with therapeutic hypothermia protection during murine hemorrhagic shock/resuscitation. In: Resuscitation. 2010 ; Vol. 81, No. 6. pp. 742-748.
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abstract = "Aim: Cytokine production during hemorrhagic shock (HS) could affect cardiac function during the hours after resuscitation. Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD+) salvage pathway. We developed a mouse model of HS to study the effect of therapeutic hypothermia (TH) on hemodynamic outcomes and associated plasma and tissue visfatin content. Methods: Mice were bled and maintained at a mean arterial pressure (MAP) of 35 mmHg. After 30 min, animals (n=52) were randomized to normothermia (NT, 37 ± 0.5 °C) or TH (33 ± 0.5 °C) followed by rewarming at 60 min following resuscitation. After 90 min of HS (S90), mice were resuscitated and monitored for 180 min (R180). Visfatin, interleukin 6 (IL-6), keratinocyte-derived chemokine (KC), tumor necrosis factor-alpha (TNF-α), and myoglobin were measured by ELISA. Results: Compared to NT, TH animals exhibited improved R180 survival (23/26 [88.5{\%}] vs. 13/26 [50{\%}]; p=0.001). Plasma visfatin, IL-6, KC, and TNF-α increased by S90 in both groups (p< 0.05). TH attenuated S90 plasma visfatin and, after rewarming, decreased R180 plasma IL-6, KC, and myoglobin (p< 0.05) relative to NT. Heart and gut KC increased at S90 while IL-6 increases were delayed until R180 (p< 0.05). NT produced sustained elevations of myocardial KC but decreased visfatin by R180, effects abrogated by TH (p< 0.05). Conclusions: In a mouse model of HS, TH improves hemodynamics and alters plasma and tissue proinflammatory cytokines including the novel cytokine visfatin. TH modulation of cytokines may attenuate cardiac dysfunction following HS.",
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author = "Beiser, {David G.} and Huashan Wang and Jing Li and Xu Wang and Violeta Yordanova and Anshuman Das and Tamara Mirzapoiazova and Garcia, {Joe GN} and Stern, {Susan A.} and {Vanden Hoek}, {Terry L.}",
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T1 - Plasma and myocardial visfatin expression changes are associated with therapeutic hypothermia protection during murine hemorrhagic shock/resuscitation

AU - Beiser, David G.

AU - Wang, Huashan

AU - Li, Jing

AU - Wang, Xu

AU - Yordanova, Violeta

AU - Das, Anshuman

AU - Mirzapoiazova, Tamara

AU - Garcia, Joe GN

AU - Stern, Susan A.

AU - Vanden Hoek, Terry L.

PY - 2010/6

Y1 - 2010/6

N2 - Aim: Cytokine production during hemorrhagic shock (HS) could affect cardiac function during the hours after resuscitation. Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD+) salvage pathway. We developed a mouse model of HS to study the effect of therapeutic hypothermia (TH) on hemodynamic outcomes and associated plasma and tissue visfatin content. Methods: Mice were bled and maintained at a mean arterial pressure (MAP) of 35 mmHg. After 30 min, animals (n=52) were randomized to normothermia (NT, 37 ± 0.5 °C) or TH (33 ± 0.5 °C) followed by rewarming at 60 min following resuscitation. After 90 min of HS (S90), mice were resuscitated and monitored for 180 min (R180). Visfatin, interleukin 6 (IL-6), keratinocyte-derived chemokine (KC), tumor necrosis factor-alpha (TNF-α), and myoglobin were measured by ELISA. Results: Compared to NT, TH animals exhibited improved R180 survival (23/26 [88.5%] vs. 13/26 [50%]; p=0.001). Plasma visfatin, IL-6, KC, and TNF-α increased by S90 in both groups (p< 0.05). TH attenuated S90 plasma visfatin and, after rewarming, decreased R180 plasma IL-6, KC, and myoglobin (p< 0.05) relative to NT. Heart and gut KC increased at S90 while IL-6 increases were delayed until R180 (p< 0.05). NT produced sustained elevations of myocardial KC but decreased visfatin by R180, effects abrogated by TH (p< 0.05). Conclusions: In a mouse model of HS, TH improves hemodynamics and alters plasma and tissue proinflammatory cytokines including the novel cytokine visfatin. TH modulation of cytokines may attenuate cardiac dysfunction following HS.

AB - Aim: Cytokine production during hemorrhagic shock (HS) could affect cardiac function during the hours after resuscitation. Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD+) salvage pathway. We developed a mouse model of HS to study the effect of therapeutic hypothermia (TH) on hemodynamic outcomes and associated plasma and tissue visfatin content. Methods: Mice were bled and maintained at a mean arterial pressure (MAP) of 35 mmHg. After 30 min, animals (n=52) were randomized to normothermia (NT, 37 ± 0.5 °C) or TH (33 ± 0.5 °C) followed by rewarming at 60 min following resuscitation. After 90 min of HS (S90), mice were resuscitated and monitored for 180 min (R180). Visfatin, interleukin 6 (IL-6), keratinocyte-derived chemokine (KC), tumor necrosis factor-alpha (TNF-α), and myoglobin were measured by ELISA. Results: Compared to NT, TH animals exhibited improved R180 survival (23/26 [88.5%] vs. 13/26 [50%]; p=0.001). Plasma visfatin, IL-6, KC, and TNF-α increased by S90 in both groups (p< 0.05). TH attenuated S90 plasma visfatin and, after rewarming, decreased R180 plasma IL-6, KC, and myoglobin (p< 0.05) relative to NT. Heart and gut KC increased at S90 while IL-6 increases were delayed until R180 (p< 0.05). NT produced sustained elevations of myocardial KC but decreased visfatin by R180, effects abrogated by TH (p< 0.05). Conclusions: In a mouse model of HS, TH improves hemodynamics and alters plasma and tissue proinflammatory cytokines including the novel cytokine visfatin. TH modulation of cytokines may attenuate cardiac dysfunction following HS.

KW - CXCL1

KW - Cytokine

KW - Hemorrhagic shock

KW - Inflammation

KW - Interleukin-6

KW - Keratinocyte-derived chemokine

KW - Nampt

KW - Pre-B-cell colony-enhancing factor

KW - Resuscitation

KW - Temperature

KW - Tumor necrosis factor-alpha

KW - Visfatin

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