[Changes in and pharmacological correction of oxidative phosphorylation in regional kidney ischemia]

Respiratory and phosphorylating capacities of kidney mitochondria were distinctly decreased within early (1.5 hr) and late (1 day) postischemic periods after long-term (2-3 hrs) ischemia of rat kidney. Preadministration of adenine (ADP, AMP) and pyridine (NAD) nucleotides into the animals prevented the decreases, while vitamin E, heparin, trifluoroperazine or aminazine proved to be ineffective. Depletion of mitochondrial nucleotide pool, which occurred during long-term ischemia of kidney and were maintained within the post-ischemic period, appears to be responsible for impairment of oxidative phosphorylation.