[Experimental models on hemorragic shock]

This review addresses the pathophysiology and treatment of hemorrhagic shock, a condition produced by rapid and significant loss of intravascular volume. Hemorrhagic shock may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion and cellular hypoxia. Multiple organ failure, a systemic inflammatory process that leads to dysfunction of different vital organs, is a frequent complication after hemorrhagic shock and accounts for a high incidence of mortality. The pathogenesis of organ injury secondary to hypovolemic insults is still not completely understood, but both experimental studies and clinical observations indicate that macrophages are activated by translocated endotoxin-bacteria and ischemia/reperfusion. Activated Kupffer cells release pathologically active substances such as inflammatory cytokines, reactive oxygen species, and nitric oxide, all of which may participate in the mechanisms of hemorrhagic shock. Moreover, increased free radical production during hemorrhagic shock and resuscitation gives place to an increase in oxidative stress that would contribute to the organ damage. In the last few years, a number of experiments have been performed in an attempt to understand the pathophysiology and treatment of hemorrhagic shock. Different studies have shown positive effects on hemorrhagic shock treatment by antioxidant, amino acid, and lipid administration.