Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
-
Acute traumatic coagulopathy is a complex phenomenon following injury and a main contributor to hemorrhage. It remains a leading cause of preventable death in trauma patients. This phenomenon is initiated by systemic injury to the vascular endothelium that is exacerbated by hypoperfusion, acidosis, and hypothermia and leads to systemic activation of the coagulation cascades and resultant coagulopathy. ⋯ Following localized brain injury, brain-derived extracellular vesicles are released into circulation where they induce a hypercoagulable state that rapidly turns into consumptive coagulopathy. VWF released from injured endothelial cells binds to these extracellular vesicles to enhance their activity in promoting coagulopathy and increasing endothelial permeability. However, there are numerous gaps in our knowledge of VWF following injury, providing a platform for further investigation.
-
We hypothesized that jejunal mucosal tissue blood flow would decrease following norepinephrine (NE) administration in endotoxic shock. We aimed of this study to evaluate changes in superior mesenteric venous (SMV) blood flow and jejunal mucosal tissue blood flow of the intestinal vascular system over time by administration of NE in rabbits with endotoxic shock. We created four groups (n = 8 each): control group, lipopolysaccharide (LPS; 1 mg/kg) group, NE (2 μg/kg/min) group, and LPS+NE group. ⋯ An interaction between NE and LPS was observed regarding jejunal mucosal tissue blood flow from 90 to 180 min (P = 0.033). We showed that NE maintained MAP and SMV blood flow but decreased jejunal mucosal tissue blood flow. In a rabbit model of endotoxic shock, NE had a negative effect on jejunal mucosal tissue blood flow.
-
Decompensation is a major prehospital threat to survival from trauma/hemorrhage shock (T/HS) after controlling bleeding. We recently showed higher than expected mortality from a combat-relevant rat model of T/HS (27 mL/kg hemorrhage) with tourniquet (TQ) and permissive hypotensive resuscitation (PHR) with Plasmalyte. Mortality and fluid requirements were reduced by resuscitation with 25% albumin presaturated with oleic acid (OA-sat) compared with fatty-acid -free albumin or Plasmalyte. ⋯ Decompensation was due to vascular decompensation rather than loss of cardiac performance. Albumin concentration was lower in decompensating groups, suggesting decreased stressed volume, which may explain the association of low albumin on admission with poor outcomes after trauma. Our findings suggest that acute decompensation may be common after trauma and severe hemorrhage treated with TQ and PHR and OA-sat albumin may benefit early survival and reduce transfusion volume by improving venous constriction and preventing decompensation.
-
Observational Study
Association Between the Oxygen Consumption: Lactate Ratio and Survival in Critically Ill Patients With Sepsis.
Mitochondrial dysfunction leading to impairment of oxygen extraction, referred to as cytopathic hypoxia, contributes to morbidity in sepsis. Oxygen consumption (VO2) may be a useful measure of the severity of cytopathic hypoxia. We monitored VO2 and carbon dioxide production (VCO2) in septic patients and investigated the association with hospital survival. ⋯ The VO2:lactate ratio was significantly higher in survivors, while there was no association between median VO2 alone and survival. There was a significant difference in change in VCO2 over time between survivors and non-survivors.
-
It was reported that carbon monoxide-releasing molecule-3 (CORM-3) administration immediately after hemorrhagic shock and resuscitation (HSR) ameliorates the HSR-induced acute lung injury (ALI); however, the specific mechanism of the protective effects against HSR-induced ALI remains unclear. ⋯ We identified the protective effects of CORM-3 against HSR-induced ALI. The mechanism might be related to the inhibition of p38MAPK signaling pathway in lung macrophages.