Background/Aims: Lipopolysaccharide (LPS) pretreatment has a strong neuroprotective effect on cerebral ischaemia/reperfusion injury (IRI), but the mechanism has not been fully elucidated to date. This study investigated the effect of LPS pretreatment on the pathway mediated by endoplasmic reticulum (ER) stress–CCAAT/enhancer-binding protein- homologous protein (CHOP) and the role of this pathway on cerebral ischaemia/reperfusion (I/R)-induced inflammation and apoptosis. Methods: Healthy male BALB/c mice were randomised into four groups as follows: sham operation group (sham group, n=30); LPS group (BALB/c mice treated with LPS, n=30); ischaemia/reperfusion group (I/R group, n=30) and I/R+LPS group (BALB/c mice treated with LPS before ischaemia, n=30). The mice were pre-treated with LPS (0.2 mg/kg) intra-peritoneally for three days prior to cerebral ischaemia. After 24 hours, the neurological deficit score, TTC staining and TUNEL assay were used to assess the neuroprotective effect of the LPS pretreatment against cerebral IRI. To assess whether the ER stress-CHOP pathway participated in the LPS-pretreatment neuroprotective mechanism, the expression levels of related proteins (GRP78, CHOP, caspase-12 and caspase-3) from the ischaemic cortical penumbra were detected via a western blot analysis. An immunohistochemical study was used to detect the expression and location of CHOP in the cortical penumbra. To further assess the protective effect of the LPS pretreatment, the concentrations of inflammatory factors (TNF-α, IL-6, IL-1β and IL-10) in the cortical penumbra were measured by ELISA, and ER stress-CHOP pathway inflammation-related caspase-11 was analysed through western blot analysis. Results: As demonstrated by the experiments, the pretreatment with LPS significantly reduced the neurological deficit score and the infarct size of cerebral IRI. The expression levels of ER stress-CHOP pathway related proteins (GRP78, CHOP, caspase-12 and caspase-3) from the cortical penumbra were significantly decreased by LPS, as well as the level of apoptosis in the cells in the brain. Immunohistochemistry showed that the expression of CHOP significantly decreased after the LPS pretreatment. Furthermore, the concentrations of inflammatory factors (TNF-α, IL-1β, IL-6) were reduced after the LPS pretreatment, whereas the anti-inflammatory cytokine IL-10 was upregulated. In addition, ER stress-CHOP pathway inflammation-related caspase-11 expression was significantly suppressed after the pretreatment with LPS. Conclusions: LPS pretreatment significantly ameliorates the effects of cerebral IRI by inhibiting inflammation and apoptosis, and the potential mechanism of the neuroprotective effect may be associated with the ER stress-CHOP mediated signalling pathway.

Objective:To investigate the effect of epidural anesthesia combined with inhalation or intravenous anesthesia on intrapulmonary shunt and oxygenation in patients undergoing long term single lung ventilation.Methods:Eighty patients, aged 35-75, American Society of Anesthesiology (ASA) classification of I-III, undergoing thoracic surgery with one lung ventilation more than three hour, were randomly divided into propofol group (group Pro), propofol combined with epidural anesthesia group (group Pro+Epi), isoflurane group (group Iso) and isoflurane combined with epidural anesthesia group (group Iso+ Epi), 20 patients in each group. Arterial blood and mixed venous blood were taken for blood gas analysis, and hemodynamic data were recorded at following time points: before induction in supine position (T1), 30min after bilateral lung ventilation (T2), 15min after one lung ventilation (T3), 30min after one lung ventilation (T4), 60min after one lung ventilation (T5), 180min after one lung ventilation (T6), intrapulmonary shunt (Qs/Qt) was calculated according to the correlation formula.Results:Qs/Qt values at T2-6 in four groups were significantly higher than that of T1, and Qs/Qt values at T3-6 was significantly higher than that of T2 (P< 0.05); PaO2 at T2-6 were significantly higher than that of T1, with PaO2 at T3-6 were significantly lower than T2 (P< 0.05). Between groups, Qs/Qt values in group Iso were significantly higher than that of group Pro, Pro+Epi and Iso+Epi at T3-5 (P< 0.05). There was no significant difference in PaO2 between groups (P> 0.05). CI at T3-6 in group Iso and Iso+Epi were significantly higher than that of T1 (P<0.05), and were significantly higher than that of propofol group (P<0.05). MAP at T3-6 in group Pro+Epi and Iso+Epi were significantly lower than that at T1 (P <0.05). Heart rate at T4-6 in group Iso were significantly higher than T1, and higher than group Pro and group Iso+Epi (P <0.05).Conclusion:One lung ventilation may predispose to increase of intrapulmonary shunt and decrease in arterial partial pressure of oxygen; isoflurane inhalation anesthesia is more likely to cause intrapulmonary shunt, but no changes in arterial partial pressure of oxygen.