Wo. Carter et al., A MURINE SKELETAL-MUSCLE ISCHEMIA-REPERFUSION INJURY MODEL - DIFFERENTIAL PATHOLOGY IN BALB C AND DBA/2N MICE/, Journal of applied physiology (1985), 85(5), 1998, pp. 1676-1683
Ischemia-reperfusion injuries can occur with diseases such as myocardi
al infarction and stroke and during surgical procedures such as organ
transplantation and correction of aortic aneurysms. We developed a mur
ine model to mimic abdominal aortic aneurysm repair with cross-clampin
g of the aorta distal to the renal artery. After model development, we
compared the normal complement BALB/c mouse with the C5-deficient DBA
/2N mouse. To assess quantitative differences, we measured neuromuscul
ar function up to 72 h after ischemia with a subjective clinical scori
ng system, as well as plasma chemistries, hematology, and histopatholo
gy. There were significant increases in clinical scores and creatine p
hosphokinase, lactate dehydrogenase, and muscle histopathology scores
in BALB/c mice compared with those in DBA/2N mice and sham-surgery mic
e. Muscle histopathology scores of the cranial tibialis and quadriceps
correlated well with clinical signs, creatine phosphokinase, and lact
ate dehydrogenase, and indicated the greatest pathology in these muscl
e groups. We developed a murine model of skeletal muscle ischemia-repe
rfusion injury that can utilize the benefits of murine genetic and tra
nsgenic models to assess therapeutic principles of this model. Additio
nally, we have shown a significant reduction in clinical signs, plasma
muscle enzyme concentrations, and muscle pathology in the C5-deficien
t DBA/2N mouse in this model.