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68 (1.44�C1.79) and 1.66 (1.60�C1.68) versus 0.20 (0.18�C0.29) ml cmH2O?1 kg?1, respectively, P http://en.wikipedia.org/wiki/YES1 the HV25-sham group, P http://www.selleckchem.com/products/azd9291.html This highlights the role of SP in lung cytokine upregulation induced by high-pressure ventilation. In addition, although ineffective during HV40, vagotomy or NK-1 receptor blockade prevented the lung injury induced by HV25, nearly suppressing the variations in lung mechanics, lung weight and MPO present in the HV25-sham group. The mechanisms of HV-induced cytokine release are only suspected. The lung stretch induces a mechanical disruption of the alveolar�Ccapillary barrier, causing an intense pulmonary oedema (Dreyfuss et al. 1985). The direct contact between the basement membrane and the circulating immunocompetent cells might be responsible for their activation (Dreyfuss & Saumon, 1998). This may have contributed to increasing the lung cytokine production and MPO activity in our HV40 and HV25 ventilation models. We limited our study to the measurements of IL-1�� and IL-6 lung cytokines because http://www.selleckchem.com/products/carfilzomib-pr-171.html both cytokines have been shown to respond strongly to the ventilation of previously healthy lungs (Tremblay et al. 1997, 2002; Br��geon et al. 2002, 2004; Chu et al. 2004; Frank et al. 2008). Moreover, these cytokines are released within the first 60�C120 min of HV (Stuber et al. 2002; Rich et al. 2003), a delay that corresponds to the duration of our experiments. Also, some reports have suggested that both IL-1�� and IL-6 might be involved in vagally mediated pro-inflammatory neuro-immune interactions (Lotz et al. 1988; Linard et al. 2005; Yu et al. 2007). Vagally mediated neuro-immune interactions result from complex mechanisms since pro- as well as anti-inflammatory pathways coexist in the same nerve, both being possibly affected by vagotomy. Among mediators contained in the vagus nerve, neurokinins (afferent fibres) are known to be potent inducers of inflammation (Barnes, 1986) but acetylcholine can also worsen lung inflammation (Lutz & Sulkowski, 2004; McQueen et al. 2007). The involvement of multiple vagal pro-inflammatory mediators may explain why vagotomy was more effective on lung cytokines than on SP reduction in our study.