TY - JOUR
T1 - Deep anesthesia worsens outcome of rats with inflammatory responses
AU - Inoue, Kei
AU - Suzuki, Takeshi
AU - Igarashi, Toru
AU - Minamishima, Shizuka
AU - Seki, Hiroyuki
AU - Kosugi, Shizuko
AU - Katori, Nobuyuki
AU - Morisaki, Hiroshi
PY - 2016/3/21
Y1 - 2016/3/21
N2 - Objective: We tested the hypothesis that deep anesthesia with sevoflurane, known as a potent immunomodulator, for 4 h would worsen the 24-h outcomes of rats through modulation of the inflammatory responses. Methods: Forty-nine male Wistar rats, administered low dose of lipopolysaccharide (0.5 mg/kg) intravenously to elicit moderate inflammatory responses mimicked mild surgical stress, underwent one minimum alveolar concentration (MAC) or 2 MAC sevoflurane anesthesia for 4 h. The 24-h survival rate, arterial blood gases, plasma interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations, and rate of T lymphocyte apoptosis in spleen were evaluated. We further examined the effects of hypotension and TNF-α discharge on the survival rate. Results: The survival rate in 2 MAC group was significantly lower accompanied with decreased base excess and increased level of cytokines (IL-6, TNF-α) compared to 1 MAC group. The apoptosis rate did not differ between the two groups. Neither norepinephrine infusion to restore hypotension nor administration of anti-TNF-α antibody improved the outcome in the 2 MAC group. Conclusions: Deep anesthesia with sevoflurane even for a short-term period augments the release of inflammatory cytokines evoked by inflammatory insults like surgical stress, impairs the acid–base balance, and subsequently deteriorates the outcomes.
AB - Objective: We tested the hypothesis that deep anesthesia with sevoflurane, known as a potent immunomodulator, for 4 h would worsen the 24-h outcomes of rats through modulation of the inflammatory responses. Methods: Forty-nine male Wistar rats, administered low dose of lipopolysaccharide (0.5 mg/kg) intravenously to elicit moderate inflammatory responses mimicked mild surgical stress, underwent one minimum alveolar concentration (MAC) or 2 MAC sevoflurane anesthesia for 4 h. The 24-h survival rate, arterial blood gases, plasma interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations, and rate of T lymphocyte apoptosis in spleen were evaluated. We further examined the effects of hypotension and TNF-α discharge on the survival rate. Results: The survival rate in 2 MAC group was significantly lower accompanied with decreased base excess and increased level of cytokines (IL-6, TNF-α) compared to 1 MAC group. The apoptosis rate did not differ between the two groups. Neither norepinephrine infusion to restore hypotension nor administration of anti-TNF-α antibody improved the outcome in the 2 MAC group. Conclusions: Deep anesthesia with sevoflurane even for a short-term period augments the release of inflammatory cytokines evoked by inflammatory insults like surgical stress, impairs the acid–base balance, and subsequently deteriorates the outcomes.
KW - Cytokine
KW - Inflammation
KW - Outcome
KW - Sevoflurane
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U2 - 10.1007/s00011-016-0940-3
DO - 10.1007/s00011-016-0940-3
M3 - Article
C2 - 27001561
AN - SCOPUS:84961768981
SN - 1023-3830
SP - 1
EP - 9
JO - Inflammation Research
JF - Inflammation Research
ER -