No abstract

Dexmedetomidine may be used in patients with TBI without risk of affecting brain oxygenation.

In CFNB under ultrasound guidance, using the catheter perpendicular to the nerve technique can shorten the time of catheter insertion while providing a similar quality of analgesia after total knee arthroplasty as compared with the catheter parallel to the nerve technique.

This study aims to examine the impact of ursodeoxycholic acid (UDCA) on pulmonary edema and explore the underlying molecular mechanisms. The effects of UDCA on pulmonary edema were assessed through hematoxylin and eosin (H&E) staining, lung dry/wet (W/D) ratio, TNF-α/IL-1β levels of bronchoalveolar lavage fluid (BALF), protein expression of epithelial sodium channel (ENaC), and Na + /K + -ATPase. Besides, the detailed mechanisms were explored in primary rat alveolar type (AT) II epithelial cells by determining the effects of BOC-2 (ALX [lipoxin A4 receptor] inhibitor), Rp-cAMP (cAMP inhibitor), LY294002 (PI3K inhibitor), and H89 (PKA inhibitor) on the therapeutic effects of UDCA against lipopolysaccharide (LPS)-induced changes. Histological examination suggested that LPS-induced lung injury was obviously attenuated by UDCA. BALF TNF-α/IL-1β levels and lung W/D ratios were decreased by UDCA in LPS model rats. UDCA stimulated alveolar fluid clearance (AFC) though the upregulation of ENaC and Na + /K + -ATPase. BOC-2, Rp-cAMP, and LY294002 largely suppressed the therapeutic effects of UDCA. Significant attenuation of pulmonary edema and lung inflammation was revealed in LPS-challenged rats after the UDCA treatment. The therapeutic efficacy of UDCA against LPS was mainly achieved through the ALX/cAMP/PI3K pathway. Our results suggested that UDCA might be a potential drug for the treatment of pulmonary edema induced by LPS. K E Y W O R D S alveolar fluid clearance, epithelial sodium channel, Na + /K + -ATPase, pulmonary edema, ursodeoxycholic acid