Ischemic renal injury will be induced by performing transient cross-clamping of one or both renal arteries, as previously described (11). Detailed methods are outlined on the protocol page for this segment.
Renal ischaemia > Protocol Section
For induction of ischemic injury, mice will be anesthetized with an injection of 100 mg/kg ketamine, 10 mg/kg xylazine, and 1 mg/kg acepromazine i.m. The abdomen will be shaved and the animals placed on a heating table kept at 39°C to maintain constant body temperature during surgery. Depending on requiremenst of the investigator, either one or both renal pedicles will be cross-clamped, the abdominal contents replaced and the abdomen temporarily closed with several sutures. At the termination of the ischemic period, the abdomen will be reopened to remove the clamps. The kidneys will be again inspected for restoration of blood flow, and 1 ml of prewarmed (37°C) normal saline instilled into the abdominal cavity. Following abdominal suturing, the mice will be kept in a 29°C incubator overnight.
Publications for Renal ischaemia (1)
Chiao H, Kohda Y, McLeroy P, Craig L, Housini I, Star RA. Alpha-melanocyte-stimulating hormone protects against renal injury after
ischemia in mice and rats. J Clin Invest (1997) 99:1165-72
View abstract View in PubMed
Reperfusion after ischemia induces cytokines, chemoattractant chemokines,
adhesion molecules, and nitric oxide (NO). The resultant neutrophil
adherence and NO potentiates renal injury. alpha-Melanocyte-stimulating
hormone (alpha-MSH) is a potent anti-inflammatory agent that inhibits
neutrophil migration and production of neutrophil chemokines and NO. Since
neutrophils and NO promote renal ischemic injury, we sought to determine
if alpha-MSH inhibits renal injury in a model of bilateral renal ischemia.
alpha-MSH significantly reduced ischemia-induced renal damage, measured by
changes in renal histology and plasma blood urea nitrogen and creatinine
in mice. alpha-MSH significantly decreased tubule necrosis, neutrophil
plugging, and capillary congestion. Delay of alpha-MSH treatment for 6 h
after ischemia also significantly inhibited renal damage. alpha-MSH also
significantly inhibited ischemic damage in rats. To begin to determine the
mechanism of action of alpha-MSH, we measured its effects on mediators of
neutrophil trafficking and induction of the inducible isoform of NO
synthase-II. alpha-MSH inhibited ischemia-induced increases in mRNA for
the murine neutrophil chemokine KC/IL-8. alpha-MSH also inhibited
induction of mRNA for the adhesion molecule ICAM-1, which is known to be
critical in renal ischemic injury. alpha-MSH inhibited nitration of kidney
proteins and induction of NO synthase-II. We conclude: (a) alpha-MSH
protects against renal ischemia/reperfusion injury; and (b) it may act, in
part, by inhibiting the maladaptive activation of genes that cause
neutrophil activation and adhesion, and induction of NO synthase.
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