Organ damage after hemorrhagic shock: roles of anesthesia, shock duration, and assessment time

Hemorrhagic shock (HS) is a condition associated with organ failure. Animal models are widely used to study pathophysiology and potential therapies. Our aim was to clarify how anesthetic choice, shock duration, decompensation phase length, and time post-reperfusion influence plasma damage markers in HS. For this, male rats were anesthetized with either thiopental or ketamine/xylazine and subjected to HS. Blood pressure was reduced to 40 mmHg for 60 or 90 minutes, followed by reperfusion with shed blood. Blood samples were collected 4 or 24 hours after reperfusion. Liver and renal damage were observed in animals that underwent a 90-minute shock, but not a 60-minute shock. Animals anesthetized with ketamine/xylazine exhibited higher hepatic aminotransferases levels than those anesthetized with thiopental, suggesting more severe liver injury in the former group. AST levels were higher 4 hours after reperfusion. The duration of decompensation phase was positively correlated with liver injury but not with kidney dysfunction. Cardiovascular parameters and other organ damage markers were similar among the groups. Therefore, HS protocols in rats require a minimum of 90 minutes of the ischemic phase to induce consistent organ dysfunction detectable through plasma markers. The duration of the decompensation phase directly influences the outcome.