Immunopathological Alterations after Blast Injury and Hemorrhage in a Swine Model of Prolonged Damage Control Resuscitation.

Trauma-related hemorrhagic shock (HS) remains a leading cause of death among military and civilian trauma patients. We have previously shown that administration of complement and HMGB1 inhibitors attenuate morbidity and mortality 24 h after injury in a rat model of blast injury (BI) and HS. To further validate these results, this study aimed to develop a swine model and evaluate BI+HS-induced pathophysiology.

Distal organ inflammation and injury after resuscitative endovascular balloon occlusion of the aorta in a porcine model of severe hemorrhagic shock.

Background And Objective: Resuscitative Endovascular Balloon Occlusion of Aorta (REBOA) has emerged as a potential life-saving maneuver for the management of non-compressible torso hemorrhage in trauma patients. Complete REBOA (cREBOA) is inherently associated with the burden of ischemia reperfusion injury (IRI) and organ dysfunction. However, the distal organ inflammation and its association with organ injury have been little investigated.

An investigation into the relationship between small intestinal fluid secretion and systemic arterial blood pressure in the anesthetized rat.

The effects of changes in the steady level of diastolic blood pressure on fluid flux across the jejunum has been investigated in the anesthetized rat during perfusion with a nutrient-free and Na(+)-free solution. Diastolic blood pressure was manipulated by intravenous infusions, during the jejunal perfusions, of vasodilators (vasoactive intestinal polypeptide, acetyl-β-methylcholine, and phentolamine) and a vasoconstrictor (arginine vasopressin), each of which acts through a different cellular mechanism. The outcome was that fluid flux was related by a parabolic relationship with diastolic blood pressure in which net secretion occurred over the range 40-100 mmHg, whereas net absorption was recorded at diastolic pressures exceeding 100 mmHg and below 40 mmHg.

Diarrhoeal disease through enterocyte secretion: a doctrine untroubled by proof.

For almost 40 years, one of the principal causes of diarrhoeal disease has been thought to be fluid secretion emanating from the epithelial cells of the small and large intestine. Given the extremely large fluid losses seen in cholera, where secretion can be up to several litres per day, this seems a plausible hypothesis. The enterocyte (epithelial cell) secretion hypothesis rapidly displaced all other alternatives, such as vasodilatation coupled with enhanced paracellular permeability.