Dear Editor,
In the current issue of Renal Failure, Ilhan et al. reported that hyperbaric oxygen (HBO) therapy induced renoprotection in a rodent model of renal ischemia/reperfusion (IR) injury.Citation1 They applied HBO therapy (60 min at 2.5 ATA) for 5 days, starting 24 h after reperfusion. Animals which received HBO showed reduced tubular damage and neutrophil infiltration. Additionally, several antioxidant enzyme activities [superoxide dismutase (SOD) and glutathione peroxidase (GPx)] increased and lipid peroxidation decreased in the kidneys of HBO-treated rats. This study differs from the previous ones in that HBO therapy was administered at a delayed period of reperfusion.
The mechanisms underlying the beneficial effects of HBO therapy are still not fully understood. Ilhan et al. suggested that HBO-induced decline in neutrophil infiltration could have a key role in the protection from IR injury.Citation1 Neutrophils are, indeed, the major source of reactive oxygen species during reperfusion, and hence the inhibition of neutrophil infiltration may, in part, explain the reduced oxidative injury in HBO-treated rats. However, we think that some of the beneficial effects of HBO therapy may be mediated via the regulation of NO system. HBO is known to increase perivascular NO bioavailability in the brain.Citation2 Additionally, HBO has been shown to increase the synthesis of endothelial nitric oxide synthase (eNOS) in human umbilical vein endothelial cells.Citation3 Rubinstein et al. showed that HBO restored renal blood flow after I/R injury and suggested that this effect was related to the improvement of eNOS-mediated endothelial-dependent vasorelaxation in renal cortex.Citation4 Future studies should also address the role of NO system in HBO-mediated renoprotection after acute renal ischemia.
Musa Salmanoglu
Department of Internal Medicine,
İzmir Military Hospital, İzmir, Turkey
E-mail: [email protected]
Yalçın Önem
Department of Internal Medicine, Gülhane Military Medical Academy Haydarpaşa Teaching Hospital, Istanbul, Turkey
E-mail: [email protected]
REFERENCES
- Ilhan H, Eroglu M, Inal V, . Hyperbaric oxygen therapy alleviates oxidative stress and tissue injury in renal ischemia/reperfusion injury in rats. Ren Fail. 2012;34:1305–1308.
- Thom SR, Bhopale V, Fisher D, Manevich Y, Huang PL, Buerk DG. Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: an oxidative stress response. J Neurobiol. 2002;51:85–100.
- Buras JA, Stahl GL, Svoboda KK, Reenstra WR. Hyperbaric oxygen down-regulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. Am J Physiol Cell Physiol. 2000;278:C292–C302.
- Rubinstein I, Abassi Z, Milman F, . Hyperbaric oxygen treatment improves GFR in rats with ischaemia/reperfusion renal injury: a possible role for the antioxidant/oxidant balance in the ischemic kidney. Nephrol Dial Transplant. 2009;24: 428–436.