Biochemical and histopathological changes in the mortality caused by acute ischemic limb injury: a rabbits' model

Restoration of blood flow to an acute ischemic extremity may deteriorate the ischemic injury, lead to multiple organ dysfunction or even death. This paradox of continuing injury during reperfusion is not completely understood. The role of multi-organ damage in the mortality caused by ischemic limb injury is also still not clarified. The purpose of this study is to determine the biochemical and histopathological changes in the mortality caused by ischemic limb injury. After anesthesia, the hindlimbs of 14 New Zealand white rabbits were made ischemic and set into 8 hours or 12 hours of ischemia. Blood samples were obtained then the creatine kinase (CK) levels were determined and CK isoenzymes analyzed. All rabbits with 8 hours' ischemia survived well, and 5 of the 7 rabbits with 12 hours' ischemia expired within 8 hours after reperfusion. CK elevation was correlated most strongly with the time of the ischemic insults. The percentage of CK-MB isoenzyme remained unchanged after 8 hours' ischemia-reperfusion insult, while increased significantly after 12 hours' ischemia-reperfusion insult. Histologic examinations showed that the major systemic manifestation was massive destruction of the liver and kidney. The injuries are more obvious in areas with the greatest blood flow during reperfusion. We concluded that the ratio of CK-MB isoenzyme is most useful for distinguishing the risk of mortality caused by acute ischemic limb injury, and the cause of systemic complications are attributed to the multi-organ failure.