Purpose Fluid therapy focused on glycocalyx (GCX) protection in hemorrhagic shock is a current focus of research. Hydroxyethyl starch (HES) solution is commonly used for fluid resuscitation; however, its effects on the GCX remain unclear. The primary aim of this study was to explore the protective effect of HES130 in maintaining GCX thickness and reducing plasma syndecan-1 expression. Methods An acute hemorrhage murine model with the dorsal skin chambers was used to measure GCX thickness and to evaluate vascular permeability. Groups of mice were treated with normal saline (NS), albumin (NS-A), HES130 (NS-V), or no exsanguination or infusion (C). We measured syndecan-1 plasma concentrations, performed blood gas analysis, and analyzed the 7-day cumulative mortality. Results GCX thickness in NS mice was significantly reduced compared to that in group C, but no other groups showed a difference compared to group C. The plasma concentration of syndecan-1 was significantly higher in NS mice than in group C. There were no significant differences in the fluorescence intensity of dextran in the interstitial space. HES70 leakage was suppressed in NS-V mice compared to those in other groups. HES70 was localized to the inner vessel wall in C, NS, and NS-A mice, but not in group NS-V. Blood gas analysis indicated that pH and lactate showed the greatest improvements in NS-V mice. The 7-day cumulative mortality rate was the highest in group NS. Conclusion Resuscitation with HES130 protected the GCX and suppressed vascular permeability of HES70 during early stages of acute massive hemorrhage.

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Introduction There is no standardized aerosol exposure apparatus to deliver heated tobacco products (HTPs) for in vivo experiments. Therefore, we developed a novel HTPs aerosol exposure apparatus for mice and demonstrated that nicotine and other chemicals in HTPs aerosol generated by the apparatus can be delivered to mice which replicate human smoke. Methods The amounts of nicotine, tar, and carbon monoxide (CO) in IQOS (Marlboro Regular HeatSticks™) aerosol generated by two types of apparatuses were determined. C57BL/6N mice were exposed to IQOS aerosol, followed by determination of the urinary nicotine metabolites. Further, the skin surface temperature of mice was monitored to confirm the vasoconstriction action of nicotine. Results The amounts of chemicals in IQOS aerosol by the novel air push-in inhalation apparatus for HTPs (APIA) was equivalent to that of the analytical vaping machine (LM4E) [1.60 ± 0.08 (APIA) vs 1.46 ± 0.07 mg/stick (LM4E) in nicotine and 0.55 ± 0.04 (APIA) vs 0.45 ± 0.01 mg/stick (LM4E) in CO]. After mice were exposed to IQOS aerosol by APIA, the urinary nicotine metabolites levels were determined; peak values in cotinine and 3-hydroxycotinine were 6.82 μg/mg creatinine at 1 h after exposure and 32.9 μg/mg creatinine at 2 h after exposure, respectively. The skin surface temperature decreased and was lower (33.5°C ± 0.5°C) at 30 min than before exposure (37.6°C ± 0.8°C). Conclusions The new apparatus for HTPs aerosol exposure to mice showed good performances in terms of both chemical analysis of collected aerosol and fluctuations in the urinary nicotine metabolites.

According to the “obesity paradox,” for severe conditions, individuals with obesity may be associated with a higher survival rate than those who are lean. However, the physiological basis underlying the mechanism of the obesity paradox remains unknown. We hypothesize that the glycocalyx in obese mice is thicker and more resistant to inflammatory stress than that in non-obese mice. In this study, we employed intravital microscopy to elucidate the differences in the vascular endothelial glycocalyx among three groups of mice fed diets with different fat concentrations. Male C57BL/6N mice were divided into three diet groups: low-fat (fat: 10% kcal), medium-fat (fat: 45% kcal), and high-fat (fat: 60% kcal) diet groups. Mice were fed the respective diet from 3 weeks of age, and a chronic cranial window was installed at 8 weeks of age. At 9 weeks of age, fluorescein isothiocyanate-labeled wheat germ agglutinin was injected to identify the glycocalyx layer, and brain pial microcirculation was observed within the cranial windows. We randomly selected arterioles of diameter 15–45 μm and captured images. The mean index of the endothelial glycocalyx was calculated using image analysis and defined as the glycocalyx index. The glycocalyx indexes of the high-fat and medium-fat diet groups were significantly higher than those of the low-fat diet group (p < 0.05). There was a stronger positive correlation between vessel diameter and glycocalyx indexes in the high-fat and medium-fat diet groups than in the low-fat diet group. The glycocalyx indexes of the non-sepsis model in the obese groups were higher than those in the control group for all vessel diameters, and the positive correlation was also stronger. These findings indicate that the index of the original glycocalyx may play an important role in the obesity paradox.

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