The effect of the activation of the mitochondrial
ATP-dependent
potassium channel (
mitoKATP) on the ultrastructure of rat lung in acute hypoxic
hypoxia (7% of
oxygen in
nitrogen, exposure 30 min) was studied. It was shown that
uridine, a precursor of the
mitoKATP activator
UDP, exerted a protective effect against hypoxic damage to the lung. The administration of
uridine to animals prior to
hypoxia decreased the number of mitochondria with altered ultrastructure and prevented the
hypoxia-induced mitochondrial swelling.
Uridine also protected the epithelial, interstitial and endothelial layers of the air-blood barrier from the
hypoxia-induced
hyperhydration. The protective action of
uridine against
hypoxia-induced
lung injury was eliminated by the selective blocker of
mitoKATP 5-hydroxydecanoate. These data suggest that one of the mechanisms of the positive effect of
uridine is related to the activation of the
mitoKATP channel, which, according to the literature and our data, is involved in the protection of tissues from
hypoxia and leads to adaptation to it. A possible role of
uridine in the maintenance of the mitochondrial structure upon
hypoxia-induced
lung injury and the optimization of
oxygen supply of the organism is discussed.