It is reported that high mobility group box 1 (HMGB1), a non-histone nuclear protein, can serve as an alarmin with damage associated molecular patterns to activate immune responses in the early stages of hemorrhagic shock (HS). However, the origin of HMGB1 and how it is released following HS is poorly understood. In this study, we teased out this mechanism. We try to record the concentration of serum HMGB1 protein following HS in clinical patients.

The study was approved by the First People's Hospital of Chenzhou, Hunan, P.R. China. Consent was obtained from patients in their hospital course. Eighteen patients were enrolled for each group. In addition, Acute Physiological and Chronic Health Evaluation II (APACHE II) score was used to evaluate the severity and morbidity of HS patients Serial blood samples were collected at indicated time points on hospital admission for HS patients (0, 2, 4, 8, 24, and 72 h following HS). Levels of HMGB1 were detected by ELISA according to the kit manufacturer's instructions.

Inclusion Criteria:

Hemorrhagic shock (HS) was defined as out-of-hospital systolic blood pressure (SBP) of 70 mmHg or less or SBP ranging 71 to 90 mmHg with a heart rate of 108 beats/min or more.

Exclusion Criteria:

pregnancy, <18 years old, more than 2,000 mL of intravenous fluids or blood before enrollment, hypothermia, drowning, asphyxia, burns, isolated penetrating head injury, time of call received by dispatch to study intervention longer than 4 h, known prisoners, and transfer from another hospital

Healthy volunteers OR Hemorrhagic shock (HS) patients enrolled in ICU

Hemorrhagic shock (HS) is a pathologic process caused by insufficient perfusion in multiple organs, and usually initiates a systemic post-traumatic inflammation response. The resulting increased inflammation response may accelerate the multiple organ dysfunctions . Extracellular high-mobility group box 1 (HMGB1) was found to mediate inflammation during sterile and infectious injury and contributes significantly to disease pathogenesis. However, the exact role of HMGB1-mediated inflammation in HS is not fully understood.

In this study, we first test the serum HMGB1 concentration in clinical HS patients and then we explored the underlying mechanism in HS animal model. An unexpected mechanism of HMGB1 released from multiple organs (especially in kidney) was found.

72 hours following hemorrhagic shock

HS was defined as out-of-hospital systolic blood pressure (SBP) of 70 mmHg or less or SBP ranging 71 to 90 mmHg with a heart rate of 108 beats/min or more. Exclusion criteria were pregnancy, <18 years old, more than 2,000 mL of intravenous fluids or blood before enrollment, hypothermia, drowning, asphyxia, burns, isolated penetrating head injury, time of call received by dispatch to study intervention longer than 4 h, known prisoners, and transfer from another hospital