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 effects and mechanisms of pentoxifylline ( PTX )pretreatment on acute lung injury ( ALI) induced by hemorrhagic shock in mice. Methods Ninety mice were randomly divided into three groups, ie. a control group, a hemorrhagic shock group, and a PTX group.Lung histological changes were examined by HE staining. Meanwhile, the wet-to-dry weight ratio ( W/D) and myeloperoxidase ( MPO) activity in lung were measured. The levels of TNF-αand IL-1βin lung homogenatewere measured by ELISA. The expressions of TLR4 mRNA and TLR4 protein in lung were detected by reverse transcription-polymerase chain reaction ( RT-PCR ) and Western blot, respectively. Results Hemorrhagic shock induced obvious ALI changes in lungs of the hemorrhagic shock group. W/D and MPO activity were significantly higher in the hemorrhagic shock group than the control group( P lt; 0. 01) . The expressions of TNF-α, IL-1β, TLR4 mRNA and TLR4 protein were also significantly higher than the control group( P lt;0. 01) . PTX pretreatment could relieve ALI changes induced by hemorrhagic shock, and decrease W/D and MPO activity. The expressions of TNF-α, IL-1β, TLR4 mRNA and TLR4 protein were also decreased by PTX pretreatment. Conclusions PTX pretreatment shows protective effects on ALI afterhemorrhagic shock. Its possible mechanismmay relate to down-regulation of TLR4, thus inhibit the expression of pro-inflammatory cytokins.
【摘要】 目的 观察聚明胶肽注射液和羟乙基淀粉（130/0.4）氯化钠注射液对创伤失血性休克患者的临床治疗效果。 方法 将2006年6月-2008年10月创伤失血性休克患者32例随机分为聚明胶肽组和羟乙基淀粉组，每组16例。抢救时除采用止血、扩容、纠酸等综合措施外，分别输入聚明胶肽注射液和羟乙基淀粉（130/0.4）氯化钠注射液1 500 mL。两组均监测血压、尿量和血气分析指标，比较两组指标恢复正常以及所需的时间。 结果 聚明胶肽组与羟乙基淀粉组上述指标恢复正常及所需的时间无差异，两组生存率、致残率及并发症均无差异。 结论 聚明胶肽注射液用于创伤失血性休克的疗效与羟乙基淀粉（130/0.4）氯化钠注射液相当。【Abstract】 Objective To observe the clinical effects of polygeline injection and hydroxyethyl starch(130/0.4) NaCl injection (HES)on the traumatic hemorrhagic shock. Methods A total of 32 patients with traumatic hemorrhagic shock were randomly divided into polygeline injection group and HES group,with 16 patients in each. The same measures such as hemstasis, expanding blood volume, correction of acid base disturbance and so on were adopted in the both groups. The patients in the polygeline injection group and HES group were respectively treated with polygeline injection and HES NaCl injection in a dose of 1500 mL by intravenous infusion. The time from injection to the recovery of BP, urinary output, and blood gas to normal level was recorded. Results BP, urinary output, and blood gas were all improved significantly, there was no significant difference between the two groups (Pgt;0.05). Conclusion The clinical effect of polygeline injection on stabilizing BP and improving microcirculation appears comparable to that of HES.
目的探讨胰周动脉瘤破裂出血的诊治。方法回顾3例胰周动脉瘤破裂出血患者的诊治过程，并结合相关文献进行分析。 结果3例患者胰周动脉瘤破裂出血并失血性休克，其中1例术前经CT检查获得诊断，2例术前未能诊断。2例经手术止血治愈，分别随访1年和1年2个月，未见复发及相关并发症; 1例经抢救无效死亡。结论胰周动脉瘤破裂出血病情发展迅速，术前诊断困难，尽快液体复苏及积极手术探查止血是挽救生命的关键。
ObjectiveTo determine the effects of different volume fluid resuscitation on intestinal injury and the permeability of intestine in hemorrhagic shock rats. MethodsSprague-Dawley male rats(n=72) were randomly equally divided into 4 groups after the model establishment of blood pressure-controlled hemorrhage, 45, 30, and 15 mL/(kg·h) of fluid resuscitation were performed in high dosage of resuscitation(HLR), moderate dosage of resuscitation(MLR), and low dosage of resuscitation(LLR) group respectively, but rats of Sham group didn't accept fluid resuscitation. After resuscitation, ten centimeters ileum was harvested for testing intestinal permeability. Then 6 rats of each group were sacrificed at 24, 48, and 72 hours after fluid resuscitation respectively. Over the specified time interval, blood was collected for testing levels of lactic acid and plasma tumor necrosis factor-α(TNF-α). The ileums of 3 resuscitation groups were obtained for testing the ratio of wet weight to dry weight and observing the histological changes. ResultsAfter resuscitation, the intestinal permeability was higher in HLR group(P<0.05). At 3-8 hours after resuscitation, rats of Sham group were all died, and the other rats of 3 groups were all alive. The level of plasma lactic acid was lower in LLR group than those of other 2 groups at 24 hours(P<0.05). The levels of TNF-α were higher in HLR group than those of other 2 groups at 24, 48, and 72 hours(P<0.05), and at 48 hours, level of TNF-α in LLR group was lower than MLR group(P<0.05). At 24 hours after resuscitation, ratio of intestinal wet weight to dry weight in LLR group was the lowest, and HLR group was the highest(P<0.05). According to the histopathology, intestinal injuries of the 3 groups were tend to be remission with the time, and at 48 and 72 hours after resuscitation, intestinal villus of LLR group appeared to be normal. ConclusionLimited fluid resuscitation of 15 mL/(kg·h) could not only decrease the levels of lactic acid and TNF-α, but also moderate the intestinal permeability and the intestinal injury in early stage after shock and surgery.
Objective To investigate effect of different resuscitation liquids and different resuscitation methods on contents of interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) in early resuscitation process of rats with traumatic hemorrhagic shock. Methods Sixty-four healthy SD rats (450–550 g) were chosen and divided into 4 groups randomly and averagely: crystal liquid limited resuscitation group, colloidal liquid limited resuscitation group, 7.5% NaCl limited resuscitation group, and colloidal liquid non-limited resuscitation group. There were 16 rats in each group. All the experimental rats were weighed before intraperitoneal injection of pentobarbital sodium anesthesia. Animal model was established via Chaudry’s method. The rats were killed and the abdominal aorta bloods were drew on hour 2, 6, 12, and 24 after recovering from anesthesia. The contents of IL-8 and TNF-α in plasmas were detected by enzyme linked immunosorbent assay. Results The contents of IL-8 and TNF-α among three kinds of limited resuscitation groups on hour 6 after resuscitation were significantly higher than those on hour 2 after resuscitation (P<0.05) and reached the peaks, then began to decrease. On hour 12 after resuscitation, the contents of IL-8 and TNF-α were decreased continuously among three kinds of limited resuscitation groups (P<0.05). The contents of IL-8 and TNF-α in the colloidal liquid non-limited resuscitation group at each point time were significantly higher than those among three kinds of limited resuscitation groups (P<0.05), which in the crystal liquid resuscitation group were significantly lower than those in the other limited liquid resuscitation groups (P<0.05). Conclusions In process of liquid resuscitation of rats with traumatic hemorrhagic shock, limited resuscitation method is better than that of non-limited resuscitation method. Among three kinds of limited resuscitation methods, crystal resuscitation liquid is more effective than the other two resuscitation liquids in prohibiting releases of IL-8 and TNF-α in rats with traumatic hemorrhagic shock.