Key result
Renal ischemia increased renal tissue NO concentration by 223%, an effect demonstrated to originate from thiol-dependent tissue stores.
Why the study?
Does depletion or repletion of S-nitrosothiols alter the increase in nitric oxide levels during renal ischemia in anesthetized rats?
Population
Anesthetized rats undergoing 45 min of renal artery occlusion
Comparison
Pretreatment with buthionine sulfoximine 4… vs Ischemia alone or L-NAME 10 mg/kg alone
Design
Preclinical
Follow-up
45 min of ischemia and subsequent reperfusion
Authors
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Suggests thiol-dependent NO release in renal ischemia; hypothesis-generating for S-nitrosothiol modulation, requires human validation.
Does depletion or repletion of S-nitrosothiols alter the increase in nitric oxide levels during renal ischemia in anesthetized rats?
The increase in renal nitric oxide concentration during ischemia originates from thiol-dependent tissue stores rather than de novo synthesis.
Salom et al. (2005) studied Renal ischemia. Renal ischemia with various pretreatments (BSO, L-NAME, N-acetyl-L-cysteine, light stimulation) vs. Preischemic baseline was evaluated on Outer medullary NO concentration. Renal ischemia increased renal tissue NO concentration by 223%, an effect demonstrated to originate from thiol-dependent tissue stores.
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