Background. The development of genetically engineered mice has led to incre
ased use of mouse models to study renal ischemic reperfusion injury (IRI),
We hypothesized that susceptibility to IRI could result from strain differe
nces due to genetic factors,
Methods. Our study compared recovery subsequent to renal IRI in NIH Swiss,
C57BL/6, and BALB/c mice. Serum creatinine (SCr) and blood urea nitrogen (B
UN) levels were evaluated postischemia. We also conducted reverse transcrip
tase-polymerase chain reaction (RT-PCR) analyses of renal cytokines and adh
esion molecules postischemia.
Results. At 48 hr postischemia, renal dysfunction in NIH Swiss mice was sig
nificantly reduced, compared with other groups (P<0.01), BUN measurements c
onfirmed renal protection at 48 hr in the NIH Swiss group. RT-PCR analysis
of mRNA postischemia demonstrated that, between strains, there was little d
ifference in mRNA expression for renal cytokines and adhesion molecules.
Conclusions. NIH Swiss mice appear to be resistant in susceptibility to ren
al IRI. Early expression of proinflammatory genes was nest associated with
resistance to IRI, thus genetic factors could be important in outcome after
renal IRI.