Effects of massive blood transfusion on inflammatory factors, islet B cell function, MODS incidence and mortality in patients with severe traumatic hemorrhage / 中国输血杂志

【Objective】 To explore the effect of massive blood transfusion on inflammatory factors, islet B cell function, incidence and mortality of multiple organ dysfunction syndrome (MODS) in patients with severe traumatic hemorrhage. 【Methods】 214 traumatic hemorrhage patients who received blood transfusion and were hospitalized in the Third People′s Hospital of Xingtai from January 2015 to June 2019 were enrolled and divided into the routine blood transfusion group (n=118) and massive blood transfusion group (n=96) according to the amount and method of blood transfusion. The changes of the inflammatory factors such as TNF α and IL-6, the functional indexes of Islet B cells such as HOMA-B and Δ INS30 / Δ GLU30, and the incidence and mortality of MODS in two groups 3 d after blood transfusion were observed. 【Results】 The level of TNF α(ng/L), IL-6(ng/L), HOMA-B and Δ INS30 / Δ GLU30 were (64.21±8.41) vs (30.75±5.26), (216.52±17.99) vs (152.45±16.26) (58.55±10.23) vs (103.47±17.48) and (2.95±0.69) vs (5.87±1.30) in the massive transfusion group and routine transfusion group, respectively (P<0.01). The incidence of MODS was 63.54%(61/96) vs 40.07%(52/118)(P<0.01) while the mortality of MODS was 46.88%(40/118) vs 33.90% (P>0.05). 【Conclusion】 The massive blood transfusion could increase the incidence of MODS in patients with severe traumatic hemorrhage by promoting inflammatory reaction and dysfunction of islet B cells.

Effect of fracture of lower limbs with hemorrhage on myocardial injury and its mechanism in rats / 中国应用生理学杂志

OBJECTIVES@#To test whether myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage, in order to lay a foundation of myocardial injury after traumatic fracture for the follow-up study.@*METHODS@#Twenty SD rats were randomly divided into two groups, i. e. control group and trauma group(=10). A rat model of traumatic hemorrhage was establish, and a traumatic model of the original generation of myocardial cell culture was constructed . The level of interleukin-2(IL-2),IL-6,IL-10 and tumor necrosis factor-α(TNF-α) in rat serum was detected by ELISA at 0, 1, 2, 4, 8, 12, 16, 24 and 48 hour to find the most significant point. The pathological cardiac injury in rats was observed by HE staining under a microscope, and the apoptosis of cultured cardiomyocyte was detected by TUNEL methods. The expressions of apoptosis gene,(Bcl-2) and Bax, in myocardium of rat and cultured cardiomyocyte were detected by Western blot and RT-PCR.@*RESULTS@#At the 4 hour after trauma, IL-6 and IL-10 in the serum of rats reached its highest, IL-2 reached its lowest at the 8th hour after trauma, and TNF-αreached its highest at 1 hour after trauma, then all recovered to their normol level gradually. Myocardial HE staining indicated that cardiomyocyte was swelling, disordered derangement, inflammatory cell infiltrated; a large number of myocardial cell nuclei was dyedbrown in TUNEL test which proved that the apoptosis index increased (<0.05). Western blot and RT-PCR results showed that the expression of pro-apoptotic gene Bax was up-regulated (<0. 05), while expression of anti apoptosis gene Bcl-2 down-regulated (<0.05).@*CONCLUSIONS@#The myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage in rats, and then lead to myocardial injury.

The protective effects of hydrocortisone on glycocalyx in the intestinal capillary endothelium after trauma-hemorrhagic shock / 中华急诊医学杂志

Objective To study the protective effects of hydrocortisone on glycocalyx in the vascular endothelium after trauma-hemorrhagic shock (T/HS) because the role of glycocalyx in maintaining the permeability of vascular endothelium intact,and in turn to identify the hydrocortisone protecting intestinal microcirculation.Methods Studies were carried out,in vivo,on a model of rats with induced T/HS.Intestinal perfusion and changes in endothelial glycocalyx and the associated molecular mechanism were assessed by using laser-Doppler velocimetry and electron microscopy,and the measurements of heparan sulfate,syndacan-1,and TNF-α in the superior mesenteric vein (SMV) with ELISA and Western-blot,and the expression of NF-κB in the vascular endothelium.Protective effects of hydrocortisone on the intestinal microcirculation after T/HS were evaluated.Results Degradation of the glycocalyx in intestinal vascular endothelium occurred 1-3 hours after T/HS in rats (P ＜0.05).By 3 hours later,significant reduction in intestinal perfusion was observed (P ＜ 0.05).The level of TNF-α in the SMV and the expression of NF-κB in the vascular endothelium increased.With the use of hydrocortisone,intestinal perfusion was improved,and the degradation of glycocalyx was attenuated.Conclusions The degradation of glycocalyx is associated with the malfunction of intestinal microcirculation after T/HS.The NF-κB/TNF-α system in vascular endothelium participates in this process of glycocalyx degradation.Hydrocortisone may be a good agent to interrupt the course of glycocalx degradation.