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Models of inflammation, oxidative stress, hyperoxia and hypoxia have demonstrated that magnesium sulfate (MgSO4), a commonly used drug in obstetrics, has neuroprotective potential. In the present study, the effects of MgSO4 treatment on inflammation, oxidative stress and fetal brain histopathology were evaluated in an experimental rat model following sevoflurane (Sv) exposure during the mid-gestational period. Rats were randomly divided into groups: C (control; no injections or anesthesia), Sv (exposure to 2.5% Sv for 2 h), MgSO4 (administered 270 mg/kg MgSO4 intraperitoneally) and Sv + MgSO4 (Sv administered 30 min after MgSO4 injection). Inflammatory and oxidative stress markers were measured in the serum and neurotoxicity was investigated histopathologically in fetal brain tissue. Short-term mid-gestational exposure to a 1.1 minimum alveolar concentration of Sv did not significantly increase the levels of any of the measured biochemical markers, except for TNF-α. Histopathological evaluations demonstrated no findings suggestive of pathological apoptosis, neuroinflammation or oxidative stress-induced cell damage. MgSO4 injection prior to anesthesia caused no significant differences in biochemical or histopathological marker levels compared to the C and Sv groups. The present study indicated that short-term exposure to Sv could potentially be considered a harmless external stimulus to the fetal brain. [ABSTRACT FROM AUTHOR]

In this study, we aimed to investigate the effects of chronic sleep deprivation on mucociliary clearance, which is the primary defence mechanism of the upper airway tract and nasal mucosal histology. Forty‐two Wistar Albino rats (250‐300 g), 8 or 12 weeks old, were randomly assigned into three groups as follows. The first sleep‐deprivation group consisted of 14 rats (A), another 14 of them were assigned to platform group (B), and the remaining 14 were included to the home cage control group (C). For the two deprivation groups (A and B), the modified multiple platform method (MMPM) was used to induce sleep deprivation for 21 days. Tc‐99m MAA rhinoscintigraphy was performed to assess mucociliary clearance and the nasal histopathological changes of the sacrificed rats were also examined. Mucociliary clearance was significantly higher in sleep deprivation (A) and deprivation control (B) groups than the control group (C) (p =.037). The ratio of columnar ciliary was significantly higher in group A and B than in the control group (p =.003). The transitional epithelial ratio in groups A and B was also significantly increased compared with group C (p =.04). The control group's squamous epithelial ratio was increased compared to the sleep‐deprived groups (p =.003). There was a significantly increased inflammatory response in the ciliated columnar epithelium in groups A and B compared to group C (p =.02). For the first time in the literature, we demonstrated that chronic sleep deprivation has caused a significant increase in mucociliary clearance speed and in the number of ciliary cells. [ABSTRACT FROM AUTHOR]