Suppression of cytokine-induced neutrophil accumulation in rat mesenteric venules in vivo by general anesthesia

Lloyd S Miller, Y. Morita, U. Rangan, S. Kondo, M. G. Clemens, G. B. Bulkley

Research output: Contribution to journalArticle

Abstract

Most studies of neutrophil-endothelial interactions in vivo necessarily require the use of general anesthetic agents which are well known to be immunosuppressive. By using whole-mount preparations of the rat mesoappendix, we were able to study tumor necrosis factor alpha (TNF-α) induced neutrophil adhesion to the mesenteric venular endothelium in vivo without necessarily using general anesthesia. TNF-α significantly increased venular-neutrophil accumulation in a dose-dependent manner; accumulation was markedly increased at 1, 2, and 4 h, but returned to baseline after 24 h. After these preliminary dose-response and time-course studies, we evaluated the influence of standard clinically effective doses of several commonly used anesthetic agents (thiopental, pentobarbital, ketamine, α-chloralose, methoxyflurane, and halothane) on the extent of neutrophil-venular accumulation induced 2 h after intraperitoneal injection of 0.4 mg/kg TNF-α, compared to unanesthetized rats. All general anesthetics tested, with the exception of methoxyflurane, significantly suppressed this response. In most cases this suppression was striking (from 60 to 85%) such that a statistically significant proinflammatory response was obscured. Although methoxyflurane also tended to suppress this response to TNF-α, it was the only agent that allowed the response to be clearly seen. Because anesthesia markedly suppresses cytokine-induced neutrophil-venular adhesion, this model should provide an important complementary technique to the classical in vivo microcirculatory approaches which do necessarily require general anesthesia.

Original languageEnglish (US)
Pages (from-to)147-154
Number of pages8
JournalInternational journal of microcirculation, clinical and experimental / sponsored by the European Society for Microcirculation
Volume16
Issue number3
StatePublished - May 1996

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Venules
General Anesthesia
Methoxyflurane
Neutrophils
Cytokines
Tumor Necrosis Factor-alpha
General Anesthetics
Anesthetics
Chloralose
Thiopental
Ketamine
Halothane
Pentobarbital
Immunosuppressive Agents
Intraperitoneal Injections
Reaction Time
Endothelium
Anesthesia

Keywords

  • Esterase staining
  • Immunosuppression
  • Microvasculature
  • Tumor necrosis factor alpha

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology

Cite this

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title = "Suppression of cytokine-induced neutrophil accumulation in rat mesenteric venules in vivo by general anesthesia",
abstract = "Most studies of neutrophil-endothelial interactions in vivo necessarily require the use of general anesthetic agents which are well known to be immunosuppressive. By using whole-mount preparations of the rat mesoappendix, we were able to study tumor necrosis factor alpha (TNF-α) induced neutrophil adhesion to the mesenteric venular endothelium in vivo without necessarily using general anesthesia. TNF-α significantly increased venular-neutrophil accumulation in a dose-dependent manner; accumulation was markedly increased at 1, 2, and 4 h, but returned to baseline after 24 h. After these preliminary dose-response and time-course studies, we evaluated the influence of standard clinically effective doses of several commonly used anesthetic agents (thiopental, pentobarbital, ketamine, α-chloralose, methoxyflurane, and halothane) on the extent of neutrophil-venular accumulation induced 2 h after intraperitoneal injection of 0.4 mg/kg TNF-α, compared to unanesthetized rats. All general anesthetics tested, with the exception of methoxyflurane, significantly suppressed this response. In most cases this suppression was striking (from 60 to 85{\%}) such that a statistically significant proinflammatory response was obscured. Although methoxyflurane also tended to suppress this response to TNF-α, it was the only agent that allowed the response to be clearly seen. Because anesthesia markedly suppresses cytokine-induced neutrophil-venular adhesion, this model should provide an important complementary technique to the classical in vivo microcirculatory approaches which do necessarily require general anesthesia.",
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T1 - Suppression of cytokine-induced neutrophil accumulation in rat mesenteric venules in vivo by general anesthesia

AU - Miller, Lloyd S

AU - Morita, Y.

AU - Rangan, U.

AU - Kondo, S.

AU - Clemens, M. G.

AU - Bulkley, G. B.

PY - 1996/5

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N2 - Most studies of neutrophil-endothelial interactions in vivo necessarily require the use of general anesthetic agents which are well known to be immunosuppressive. By using whole-mount preparations of the rat mesoappendix, we were able to study tumor necrosis factor alpha (TNF-α) induced neutrophil adhesion to the mesenteric venular endothelium in vivo without necessarily using general anesthesia. TNF-α significantly increased venular-neutrophil accumulation in a dose-dependent manner; accumulation was markedly increased at 1, 2, and 4 h, but returned to baseline after 24 h. After these preliminary dose-response and time-course studies, we evaluated the influence of standard clinically effective doses of several commonly used anesthetic agents (thiopental, pentobarbital, ketamine, α-chloralose, methoxyflurane, and halothane) on the extent of neutrophil-venular accumulation induced 2 h after intraperitoneal injection of 0.4 mg/kg TNF-α, compared to unanesthetized rats. All general anesthetics tested, with the exception of methoxyflurane, significantly suppressed this response. In most cases this suppression was striking (from 60 to 85%) such that a statistically significant proinflammatory response was obscured. Although methoxyflurane also tended to suppress this response to TNF-α, it was the only agent that allowed the response to be clearly seen. Because anesthesia markedly suppresses cytokine-induced neutrophil-venular adhesion, this model should provide an important complementary technique to the classical in vivo microcirculatory approaches which do necessarily require general anesthesia.

AB - Most studies of neutrophil-endothelial interactions in vivo necessarily require the use of general anesthetic agents which are well known to be immunosuppressive. By using whole-mount preparations of the rat mesoappendix, we were able to study tumor necrosis factor alpha (TNF-α) induced neutrophil adhesion to the mesenteric venular endothelium in vivo without necessarily using general anesthesia. TNF-α significantly increased venular-neutrophil accumulation in a dose-dependent manner; accumulation was markedly increased at 1, 2, and 4 h, but returned to baseline after 24 h. After these preliminary dose-response and time-course studies, we evaluated the influence of standard clinically effective doses of several commonly used anesthetic agents (thiopental, pentobarbital, ketamine, α-chloralose, methoxyflurane, and halothane) on the extent of neutrophil-venular accumulation induced 2 h after intraperitoneal injection of 0.4 mg/kg TNF-α, compared to unanesthetized rats. All general anesthetics tested, with the exception of methoxyflurane, significantly suppressed this response. In most cases this suppression was striking (from 60 to 85%) such that a statistically significant proinflammatory response was obscured. Although methoxyflurane also tended to suppress this response to TNF-α, it was the only agent that allowed the response to be clearly seen. Because anesthesia markedly suppresses cytokine-induced neutrophil-venular adhesion, this model should provide an important complementary technique to the classical in vivo microcirculatory approaches which do necessarily require general anesthesia.

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