Reperfusion injury in burned rats after delayed fluid resuscitation

Organ failure from ischemie injury is common in deaths that are due to burn when fluid resuscitation is not performed. Organ perfusion after a delay in resuscitation, however, may induce or even accelerate ischemie organ damage. To study this phenomenon, 40 rats were classified (w = 10) to serve as normal control, burn with no resuscitation, burn with early fluid resuscitation, and burn with delayed resuscitation groups. A modified Walker burn model was used to inflict 50% total body surface area scald burns on the rats. Cellular energy metabolism and tissue water content of several vital organs were measured at 8 hours after burn injury. Adenosine triphosphate, total adenine nucleotides, and energy charge in liver, heart, and kidney tissues were significantly lower (p < 0.05) with delayed fluid resuscitation compared with early resuscitation. Furthermore, in heart and kidney tissues adenosine triphosphate, total adenine nucleotides, and energy charge were significantly lower in the delayed resuscitation group compared with the group that received no fluid resuscitation. This indicates that heart and kidney tissue are more viable at 8 hours after burn injury, with no fluid resuscitation compared with delayed resuscitation. Water content of lung and muscle tissue were significandy lower (p < 0.05) in the burn group that received no fluid resuscitation compared with diat in early and delayed resuscitation groups. Water content of muscle was significandy greater with delayed resuscitation compared with the early resuscitation group. Results indicate that delayed fluid resuscitation in cases of burn shock may disrupt the cellular energy metabolism in some vital organs and cause skeletal muscle edema. When fluid resuscitation is delayed, we suggest use of pharmacologie modulators to mediate harmful substances that are released during reperfusion.