The beta‐adrenoceptor antagonist propranolol counteracts anti‐inflammatory effects of isoflurane in rat endotoxemia

Boost, Kim Alexander; Flondor, Michael; Hofstetter, Christian; Platacis, I.; Stegewerth, Klaus; Hoegl, Sandra; Nguyen, Tai D.; Mühl, Heiko; Zwißler, Bernhard

doi:10.1111/j.1399-6576.2007.01363.x

Cited by 33 publications

(24 citation statements)

References 39 publications

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“…The only theoretical limitation we see with the intranasal challenge is that it requires light isoflurane anaesthesia. It has been suggested that isoflurane may have an anti-inflammatory effect [22,23]. However, the duration of the isoflurane anaesthesia was very short in our protocol.…”

Section: Discussionmentioning

confidence: 60%

Comparison of Aerosol and Intranasal Challenge in a Mouse Model of Allergic Airway Inflammation and Hyperresponsiveness

Swedin

Ellis

Kemi

et al. 2010

Int Arch Allergy Immunol

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Background: The aim was to optimize antigen challenge for induction of airway hyperresponsiveness (AHR) and inflammation in BALB/c mice sensitized to ovalbumin (OVA). Comparisons were made between mice challenged with OVA either as an aerosol or intranasally. The protocol that induced maximal AHR in BALB/c mice was thereafter tested in C57BL/6 mice. Method: Methacholine responsiveness was measured using the flexiVent® system to assess AHR. Inflammatory responses were investigated by histology and cell counts in bronchoalveolar lavage (BAL) fluid. Results: 48 h after challenge with 1 or 6% OVA aerosols, there were similar increments in AHR and BAL cells, predominantly eosinophils. When comparing the effect of 1% OVA aerosol on AHR and cell infiltration at 24 and 48 h after challenge, the responses were similar. At 24 h, intranasal OVA administration (20–200 µg) caused a dose-dependent increase in AHR. BAL cells were increased by all intranasal OVA doses and to a greater extent than after 1% OVA aerosol challenge but without any dose dependency. Histological examination confirmed that there was an increase of eosinophils in lung tissue following either challenge. In C57BL/6 mice, baseline tissue elastance was the only functional outcome that was increased after intranasal OVA challenge. Even though the AHR response was negligible in C57BL/6 mice, a similar infiltration of BAL cells was observed in both strains. Conclusion: Intranasal challenge was more effective than aerosol challenge at inducing both AHR and airway inflammation in BALB/c mice. Although intranasal challenge caused airway inflammation in C57BL/6 mice, this strain is not optimal for studying AHR.

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Section: Discussionmentioning

confidence: 60%

Comparison of Aerosol and Intranasal Challenge in a Mouse Model of Allergic Airway Inflammation and Hyperresponsiveness

Swedin

Ellis

Kemi

et al. 2010

Int Arch Allergy Immunol

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“…Isofl urane decreases the phagocytotic capacity of human alveolar macrophages during surgery [55]. An in vivo study using rat endotoxemia showed that the inhalation of isofl urane reduced the release of the proinfl ammatory cytokine, IL-1β in bronchoalveolar lavage fl uid (BALF) [56]. This fi nding suggests an inhibitory effect of isofl urane on proinfl ammatory cytokine release from alveolar macrophages, because the main source cells of proinfl ammatory cytokines in BALF in endotoxemia are alveolar macrophages.…”

Section: Monocyte and Macrophage Functionsmentioning

confidence: 95%

Anesthetics, immune cells, and immune responses

2008

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General anesthesia accompanied by surgical stress is considered to suppress immunity, presumably by directly affecting the immune system or activating the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Along with stress such as surgery, blood transfusion, hypothermia, hyperglycemia, and postoperative pain, anesthetics per se are associated with suppressed immunity during perioperative periods because every anesthetic has direct suppressive effects on cellular and neurohumoral immunity through influencing the functions of immunocompetent cells and inflammatory mediator gene expression and secretion. Particularly in cancer patients, immunosuppression attributable to anesthetics, such as the dysfunction of natural killer cells and lymphocytes, may accelerate the growth and metastases of residual malignant cells, thereby worsening prognoses. Alternatively, the anti-inflammatory effects of anesthetics may be beneficial in distinct situations involving ischemia and reperfusion injury or the systemic inflammatory response syndrome (SIRS). Clinical anesthesiologists should select anesthetics and choose anesthetic methods with careful consideration of the clinical situation and the immune status of critically ill patients, in regard to long-term mortality, morbidity, and the optimal prognosis.

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“…In humans, isoflurane may decrease phagocytic activity of human alveolar macrophages during surgery (21). In endotoxemic rats, isoflurane also inhibits the release from macrophages of TNF-a in plasma, and IL-I~both in plasma and bronchoalveolar lavage fluid (BALF) (22), an effect which seems to be counteracted from propranolol.…”

Section: Volatile Anestheticsmentioning

confidence: 99%

Immunological Modifications Induced from Products Used during the Perioperative Period

Cardinale

Mastrototaro

Cappiello

et al. 2011

Int J Immunopathol Pharmacol

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Anesthetics and other products used during the perioperative period may influence immune function not only merely by reducing the HPA-axis stress response but also by directly modulating innate and adaptive immune responses. Most of the literature on the immune effects of anesthetics has been derived from in vitro or animal studies, due to the number of confounding variables in “real life” surgical settings. These immunosuppressive effects might not normally have clinical consequences for an immune-competent patient, but may act as important modifiers in postoperative morbidity and mortality. Furthermore, some inhibitory effects on neutrophil functions may provide a therapeutically beneficial effect under specific surgical clinical conditions, such as ischemia-reperfusion injury.

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The beta‐adrenoceptor antagonist propranolol counteracts anti‐inflammatory effects of isoflurane in rat endotoxemia

Abstract: Our results indicate for the first time, that blockade of beta-adrenoceptors counteracts the anti-inflammatory effects of isoflurane in endotoxemic rats.

Cited by 33 publications

References 39 publications

Comparison of Aerosol and Intranasal Challenge in a Mouse Model of Allergic Airway Inflammation and Hyperresponsiveness

Comparison of Aerosol and Intranasal Challenge in a Mouse Model of Allergic Airway Inflammation and Hyperresponsiveness

Anesthetics, immune cells, and immune responses

Immunological Modifications Induced from Products Used during the Perioperative Period

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