Objective To investigate the effects of hypertonic saline (HTS) treatment on the function and susceptibility to sepsis of reticuloendothelial system (RES) in mice with hemorrhagic shock. Methods Forty percent of total blood volume of male Balb/c mice was withdrawn by cardiac puncture. Two hours later, the mice were treated with blood infusion and normal saline (10 ml/kg) or 7.5% NaCl (10 ml/kg).The survival rate of the mice was observed after cecal ligation and puncture (CLP). The phagocytosis function of the RES was measured by carbon clearance rate(α) and carbon amount ingested by the macrophages of liver and spleen. In vitro, the peritoneal phagocyte function in solutions of different osmotic pressor was measured by assaying neutral red amount taken in. Results The survival rate after CLP in HTS treated group was 70%, whereas all the mice in the normal saline group died. At the third hour after hemorrhagic shock, the RES carbon clearance rate(α) and carbon amount ingested by the macrophages of liver in the HTS treated mice were 5.61±0.42 and 0.59±0.19 respectively, significantly higher than those in the normal saline treated mice (4.15±0.62， 0.42±0.16). In vitro, hyperosmolarity below 40 mmol/L had no significant effects on the phagocytosis activity of peritoneal macrophages in mice. Conclusion Treating hemorrhagic shock with HTS can decrease the susceptibility to sepsis and improve the RES phagocytosis function indirectly.
In this study, hypertonic saline infusion (experimental group ) and blood transfusion plus normal saline infusion (control group) were used for the treatment of uncontrolled hemorrhagic shock in dogs. The amount of blood loss from injured vessels are compared between two groups. Results: the amount of blood loss from injured vessels in shock stage were 35.2ml in the experimental group and 34.6ml in the control group, which showed no marked difference between two groups(Ｐ＞0.05).The amount of blood loss in resuscitation stage for experimental group was 15.10±1.52ml(early stage) and 14.00±1.37ml(late stage) and for control group was 14.20±1.52ml and 12.90±1.71ml respectively(Ｐ＞0.05).The amount of blood loss in resuscitation stage for both groups is much less than that in shock stage (Ｐlt;0.05).The results showed that infusion of hypertonic saline 30 min after uncontrolled shock is a safe and effective treatment which dose not cause further bleeding from the injured vessels. Clinical observation also confirmed the result.
Objective To investigate the expression of aquaporin-1( AQP1 ) in visceral and parietal pleura in SD rats and to examine the effect of AQP1 on pleural fluid turnover. Methods Five groups( n = 24 ) of SD rats were randomly assigned to received intrapleural injection of dexamethasone,lipopolysaccharide, erythromycin, hypertonic saline and normal saline, respectively. The AQP1 protein in pleural was detected with immunohistochemistry. The mRNA expression of AQP1 under stimulations at different time points was measured by real time RT-PCR. Results AQP1 was immunolocalized predominantly to the microvessels and mesothelial cells of visceral and parietal pleura. The extent of AQP1expression in parietal pleura was less than that in visceral pleura[ ( 4. 14 ±1. 12) ×104 copy /μg vs ( 7. 43 ±2. 02) ×104 copy / μg, P lt;0. 05] . AQP1 expression increased at all phases in the dexamethasone group andthe hypertonic saline group, whereas decreased in the erythromycin group and the lipopolysaccharide group.Conclusion The stimulations of dexamethasone, lipopolysaccharide, erythromycin and hypertonic saline can significantly change the AQP1 expression in pleura, which indicate that AQP1 may contribute to the accumulation and clearance of pleuritic fluids.
Objective To investigate the impact of injection of acetic acid hypertonic saline solution (AHS) in dog liver during radiofrequency ablation (RFA) on its destructive zone. Methods RFAs were performed in dog livers by using LDRF-120S mutiple probe ablation system combining 50% acetic acid 5% hypertonic saline solution injection. Thirty healthy adult hybrid dogs were randomly divided into 5 groups (n=6). Group A: RFA was performed immediately after injection of 2 ml AHS; Group B: RFA was performed 5 min after injection of 2 ml AHS; Group C: RFA was performed immediately after injection of 4 ml AHS; Group D: RFA was performed 5 min after injection of 4 ml AHS; Group E: RFA was performed immediately after injection of 6 ml AHS. Results There were no significant differences in the mean initial impedance within 5 groups. The mean ablation times were different significantly among 5 groups (F=83.831, P＜0.001). The mean ablation time was different significantly between any two groups by LSD-t analysis (P＜0.001). The mean coagulation diameters were different significantly among 5 groups （F=53.488, P＜0.001）. The mean coagulation diameter of group E was the largest among 5 groups. Besides mean coagulation diameter was no significant difference between group D and E (Pgt;0.05), the mean coagulation diameter was different significantly between any two groups by LSD-t analysis (P＜0.001). Obviously thrombus were shown in coagulation necrosis zone and nearly normal tissue with gordon amp; sweet. AHS spillage from the injection site occurred in group E. Four dogs died in group E within 14 d but no dog died in the other groups. Conclusion RFA is performed 5 min after injection of 4 ml AHS in dog liver produces the ideal ablation destructive zone.
ObjectiveTo explore the effect of hypertonic saline (HTS) pretreatment on levels of nitric oxide (NO) and endothelin-1(ET-1) and their correlation in hepatic ischemia reperfusion (HIR) injury in rats. MethodsThe HIR injury models were made by using Pringle, s maneuver in 45 healthy adult male Sprague-Dawley rats, which were randomly divided into three groups (n=15):sham operation (SO) group, HIR group, and HTS group. The animals were killed at 1, 6, and 24 h after reperfusion. The levels of serum NO and ET-1 were measured respectively, the correlation between NO level and ET-1 level at 6 h after reperfusion was analyzed. ResultsAt the time points of 1 h, 6 h, and 24 h after reperfusion, the serum NO levels in the HTS group and HIR group were all significantly lower than those in the SO group (P < 0.01), but the serum ET-1 levels were all significantly higher than those in the so group (P < 0.01). The serum NO levels at the time points of 1 h, 6 h, and 24 h in the HTS group were significantly higher than those at the same time in the HIR group (P < 0.01), but the serum ET-1 levels in the HTS group were significantly lower than those in the HIR group (P < 0.01). At all the time points, every detected goal had more marked level at the time point of 6 h after reperfusion. The NO level was negatively correlated with the ET-1 level. ConclusionsHTS could change levels of serum NO and ET-1 after HIR injury, and which has a negative correlation. Its mechanism might probably stimulate serum NO level and reduce the ET-1 level through some way so as to enable both dynamic balance to the benign development direction and achieve a protective effect.