ABSTRACT
Objective To investigate the hemostatic effects of prothrombin complex concentrate carrying anionic lipid coated microbubbles (PCCMB) enhanced therapeutic ultrasound for renal trauma in rabbits models.Methods Twenty-four healthy New Zealand rabbits were randomly divided into three groups (each n=8),including simple therapeutic ultrasound group (US group),simple PCCMB injection group (SHAM group) and PCCMB injection combined with therapeutic ultrasound group (PCCMB+US group).Visual bleeding score and 10-min bleeding volume were evaluated for hemostatic efficacy.CEUS was used to assess the kidney perfusion in SHAM and PCCMB+US groups before therapeutic ultrasound,immediately and 60 min after therapeutic ultrasound.And CEUS was performed on US group 60 min after therapeutic ultrasound.The acoustic peak intensity (PI) of kidney in rabbit was measured.Results The treatment was successfully completed in all the experimental rabbits.The bleeding scores and the 10-min hemorrhagic volumes decreased significantly in PCCMB+US group compared with the other two groups (both P＜0.05).After therapeutic ultrasound,visual bleeding score of PCCMB+US group was respectively lower than that of US group and SHAM group (both P＜ 0.05).In PCCMB+ US group,PI obtained immediately and 60 min after therapeutic ultrasound were higher than that obtained before therapeutic ultrasound (both P＜0.05).There was no significant difference of PI before and after therapeutic ultrasound in US and SHAM groups (all P＞0.05).Conclusion PCCMB enhanced therapeutic ultrasound provides an effective way for renal trauma in rabbits.
ABSTRACT
Objective To explore the effects of keratinocyte growth factor receptor (KGFR) transgene on sodium channel in alveolar type Ⅱ cells with LPS-induced acute lung injury, to provide the evidence for gene treatment in acute lung injury. Method Totally 40 male Sprague-Dawtey rats were randomly divided into four groups, including normal control (n=8), injured control (n=10), normal transgene (n=10) and injured transgene (n=12). The models of acute lung injury were produced using LPS, and the successful criteria was the obvious enlargement in the lung tissue. The rats in normal transgene group and injured transgene group were injected with 1 mL of KGFR adenovirus vector through rats' tail vein. At 72 hours later, the rats in injured control group and injured transgene group were injected with LPS in dose of 5 mg/kg (BW). While rats in normal control group and normal transgene group were injected with equivalent saline simultaneously. Another 48 hours later, rats in the four groups were killed. The lung tissue were collected for analysis. The expression of sodium channel in rats' alveolar type Ⅱ cells were detected by immunohistochemistry and immunoeectron microscope. Difference among the experimental groups were estimated by ANOVA analysis (LSD-t-test). There was statistical signifi-cance when P<0.05. Results The levels of sodium channel expression in rats' alveolar type Ⅱ cells were differ-era, with normal control group (47.7±3.33), normal transgene group (46.9±5.21), injured tramgene group (29.19±4.11) and injured control group (5.1±2.3). The level of sodium channel expression in injured trans-gene group was lower than that in normal transgene group (t=9.134, P<0.001) and normal control group (t=10.601,P<0.001), but signifieantly higher than that in injured control group (t=16.466, P<0.001). Conclusions The transgene vector can effectively promote the expression of sodium channel in alveolar type Ⅱ cells in rats with LPS-indueed acute lung injury, and can alleviate sodium and water reteraion in alveolar.