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Hemorrhagic shock is a common acute and critical disease caused by trauma in clinic. In particular, local tissue hypoperfusion and cell hypoxia caused by renal ischemia and hypoxia can easily lead to acute kidney injury. In clinical practice, safer, practical, and effective resuscitation methods for patients with hemorrhagic shock are constantly explored to achieve the purpose of better protection of the kidney, such as the applications from colloidal crystal liquid to hypertonic fluid, from normal-pressure resuscitation to low-pressure resuscitation, from correcting blood pressure to restoring oxygen supply to tissue cells, from maintaining hemodynamic stability to inhibiting apoptosis, and from vasoactive drugs to Chinese traditional medicines to enzyme inhibitors. This article reviews the research progress of kidney protection for patients with hemorrhagic shock in recent years.

Massive hemorrhage is one of the main causes of death in the critically ill patient, especially in the emergency department, being the transfusion of hemocomponents a very important strategy to save the life of these patients. Massive transfusion protocols were created to ensure that these patients receive blood components efficiently. Damage control resuscitation aims to rapidly control hemorrhage and prevent or treat if applicable the lethal triad of hypothermia, acidosis and coagulopathy; for this, three strategies were established: hemodynamic resuscitation by restrictive fluid therapy, permissive hypotension and massive transfusion, metabolic resuscitation and hemostatic resuscitation protocol. The damage control protocol has demonstrated benefits and a reduction in the risk of mortality in patients with massive hemorrhage; however, it requires multidisciplinary work and adequate coordination among the services involved in the process. [ABSTRACT FROM AUTHOR]

To investigate the effect and mechanism of nucleotide binding oligomerization domain 2 (NOD2) on lung injury during hemorrhagic shock and ischemia-reperfusion. Methods Ten NOD2 knockout SD rats were set as the control group after the preparation of hemorrhagic shock model (normal saline was given at the initial stage of resuscitation).Thirty ordinary SD rats were randomly divided into three groups: the blank group (normal saline was given at the initial stage of resuscitation), the palmitoyl modification enzyme (PAT) antibody group (PAT antibody was given at the beginning of resuscitation) and the NOD2 antibody group (NOD2 antibody was given at the beginning of resuscitation), with 10 rats in each group. After 24 hours of resuscitation, blood samples were collected, and lung tissues were collected. Blood gas analysis was performed at the beginning of the experiment, at the beginning of shock and 2 hours after reperfusion. Plasma tumor necrosis factor (TNF) - α, interleukin (IL) -1β, IL-6, malondialdehyde (MDA) and myeloperoxidase (MPO) in lung tissue were detected. High mobility group B (HMGB1), palmitoylated transfer protein (ZDHHC5) and NOD2 were detected by Western blot assay. The pathological sections of lung tissue were observed under fluorescence microscope and light microscope. Results The oxygen partial pressure [p(O2)] at 240 min was significantly lower in the blank group than that in the other three groups (P＜0.05). The lactate levels at 30 min and 240 min were significantly higher in the blank group than those in the other three groups (P＜0.05). TNF- α, IL-1β, IL-6, MDA and MPO levels were the highest in the blank group (P＜ 0.05)，and which was lower in the control group than that of the anti-PAT group and the anti-NOD2 group. The expression levels of HMGB1, NOD2 and ZDHHC5 were the highest in the blank group (P＜0.05), and the expression levels of HMGB1 and NOD2 were lower in the control group than those in the anti-PAT group and anti-NOD2 group (P＜0.05). The immunofluorescence expression of palmitoylated NOD2 was significantly higher in the blank group than that in the control group, anti-PTA group and anti-NOD2 group. Compared with the control group, the alveolar endothelium and alveolar tissue were significantly damaged and the inflammatory cell infiltration was obvious in the blank group, anti-PTA group and antiNOD2 group. Conclusion In hemorrhagic shock and ischemia-reperfusion animal models, NOD2 produces palmitoylated NOD2 under the regulation of ZDHHC5, thereby promoting the release of TNF-a, IL-1b, IL-6, MDA and MPO, resulting in lung injury. [ABSTRACT FROM AUTHOR]

Competing Interests: None declared.

With the increase of caesarean section rates, and opening two -child, three -child policy, the number of pregnant women with scarred uterine is gradually increasing. The incidence of pregnancy complications, especially rupture of uterus is increasing year by year. Rupture of uterus is a serious complication of pregnancy in obstetrics, if not clearly identified, mishandled, can lead the pregnant women and fetuses to death. In this case, a pregnant woman with rupture of uterus at 14+2 w, went into hemorrhagic shock and disseminated intravascular coagulation (DIC). Exploratory laparotomy was performed while shock and DIC were corrected by transfusion and infusion, she improved and was discharged from hospital without serious complications. By reviewing the patient′ s pregnancy and the treatment process, summarizing experience, strengthening clinicians′ cognition of such diseases and familiarity with related diagnosis and treatment plans, we can early identify rupture of uterine and timely perform operation, in order to reduce the possibility of emergency and critical conditions for patients. [ABSTRACT FROM AUTHOR]