J Vet Sci.  2002 Jun;3(2):115-121.

Prior Ischemic Treatment Renders Kidney Resistant to Subsequent Ischemia

• Park KM
• Han HJ

Abstract

Prior ischemia leads to resistance against subsequent ischemic insults. The mechanisms that underlie this adaptive response remain unidentified. Thus, we studied whether the reduced susceptibility of mice previously subjected to the ischemia to ischemia/ reperfusion injury is related with altered inflammatory responses. Thirty minutes of bilateral kidney ischemia results in significantly increased plasma creatinine and blood urea nitrogen levels in BALB/c male mice. There is severe disruption of actin cytoskeleton of proximal tubular cells in the outer stripe of the outer medulla 24 hours post-ischemia. When mice are subjected to 30 minutes of bilateral ischemia 8 days later, there is no increase in plasma creatinine and blood urea nitrogen levels and the post-ischemic disruption of actin cytoskeleton of proximal tubular cells is much less. Inflammatory responses have highly implicated with ischemia/reperfusion injury. Ischemia results in the increased tissue myeloperoxidase (MPO) activity that is a marker of leukocyte infiltration. There is, however, no the post-ischemic increase of MPO activity in kidneys previously subjected to ischemia. Post-ischemic expression of tissue intercellular adhesion molecule-1 (ICAM-1) is greater in the kidney previously sham-operated than in the kidneys previously subjected to ischemia. In conclusion, prior ischemia protects kidney function and morphology against subsequent ischemia 8 days later. The resistance is associated with the reduced post-ischemic leukocyte infiltration due to the reduced post-ischemic ICAM-1 expression.

Keyword

Ischemia; Inflammation; Intercellular adhesion molecule -1; Kidney; Myeloperoxidase

MeSH Terms

*Adaptation, Physiological
Animals
Blood Urea Nitrogen
Creatinine/blood
Gene Expression Regulation
Inflammation/physiopathology
Intercellular Adhesion Molecule-1/genetics
Ischemia/*physiopathology
Kidney/*blood supply
Kidney Tubules, Proximal/physiopathology
Male
Mice
Mice, Inbred BALB C
Peroxidase/metabolism
Renal Circulation
Reperfusion Injury