Hyperbaric oxygen treatment improves GFR in rats with ischaemia/reperfusion renal injury: a possible role for the antioxidant/oxidant balance in the ischaemic kidney.
BACKGROUND
Ischaemic kidney injury continues to play a dominant role in the pathogenesis of acute renal failure (ARF) in many surgical and medical settings. A major event in the induction of renal injury is related to the generation of oxygen-free radicals. Hyperbaric oxygen therapy (HBO) is indicated for treatment of many ischaemic events but not for ARF. Therefore, the present study examined the effects of HBO on kidney function and renal haemodynamics in rats with ischaemic ARF.


METHODS
Renal ischaemia was induced by unilateral renal artery clamping (45 min) in rats. Within 24 h following ischaemia, rats were treated twice with HBO of 100% O(2) at 2.5 absolute atmospheres for 90 min each (+HBO). Untreated rats (-HBO) served as a control. Forty-eight hours later, GFR, RBF and endothelial-dependent vasorelaxation were measured. In addition, the immunoreactive staining of 4-hydroxy-2-noneal (4-HNE), a major product of endogenous lipid peroxidation, and superoxide dismutase (SOD) were assessed.


RESULTS
In the -HBO group, GFR was reduced by 94% compared with the untouched normal kidney (ischaemic: 0.06 +/- 0.03 ml/min, normal: 1.02 +/- 0.13 ml). In contrast, in the +HBO group, GFR of the ischaemic kidney (0.36 +/- 0.07 ml/min) was reduced only by 68% compared with the contralateral normal kidney (1.12 +/- 0.12 ml/min). In line with these findings, HBO improved the vasodilatory response to ACh as expressed in enhancement of both total and regional renal blood flow. In addition, HBO reduced the formation of 4-HNE by 33% and 76% and increased SOD by 30% and 70% in the cortex and outer stripe region of the medulla of the ischaemic kidney, respectively.


CONCLUSIONS
HBO attenuates the decline in GFR following renal ischaemia, and improves endothelial-dependent vasorelaxation, suggesting that treatment with HBO may be beneficial in the setting of ischaemic ARF.
Rubinstein
Irit
I
Department of Physiology, the B. Rappaport Faculty of Medicine, Technion-Israel Institute of Technology and Rambam Medical Center, Haifa, 31096, Israel.
Abassi
Zaid
Z
Milman
Felix
F
Ovcharenko
Elena
E
Coleman
Rymond
R
Winaver
Joseph
J
Better
Ori S
OS
D058186:Acute Kidney Injury / Q000503:physiopathology / Q000628:therapy; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004730:Endothelium, Vascular / Q000503:physiopathology; D005919:Glomerular Filtration Rate; D006931:Hyperbaric Oxygenation; D007511:Ischemia / Q000378:metabolism / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply* / Q000293:injuries* / Q000503:physiopathology; D015227:Lipid Peroxidation; D008297:Male; D016877:Oxidants / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation; D015427:Reperfusion Injury / Q000503:physiopathology / Q000628:therapy*; D013482:Superoxide Dismutase / Q000378:metabolism; D014664:Vasodilation
D000975:Antioxidants; D016877:Oxidants; D013482:Superoxide Dismutase
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