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Reduction of hemorrhagic shock-induced acute kidney injury by lower limb ischemic preconditioning in rats.

Authors :
Ahghari, Parisa
Kadkhodaee, Mehri
Seifi, Behjat
Ranjbaran, Mina
Sedaghat, Zahra
Shams, Sedigheh
Source :
Physiology & Pharmacology. 2015, Vol. 19 Issue 1, p31-37. 7p.
Publication Year :
2015

Abstract

Introduction: During hemorrhagic shock (HS), the kidneys are one of the primary target organs involved. Oxidative stress is shown to be enhanced in different models of acute kidney injury (AKI). Remote ischemic preconditioning (RPC) by brief limb ischemia is considered to be a safe method to protect different organs from further damage. In this study, we investigated the effects of brief hind limb occlusion on protection against AKI and whether this protection is related to a reduction in oxidative stress. Materials and Methods: Twenty one rats were divided into three groups of seven rats. Shamoperated animals underwent surgical procedures, without hemorrhage. HS was induced by bleeding from a femoral arterial catheter to remove 44% of total blood volume. In RPC group, four cycles of lower limb ischemic preconditioning (5 min ischemia followed by 5 min reperfusion) were performed immediately before HS. Three hours later, plasma and renal tissue samples were collected for renal function monitoring and oxidative stress assessment. Results: Compared with the sham group, HS resulted in renal dysfunction, significantly increased blood urea nitrogen (BUN), plasma creatinine (Cr) and renal malondialdehyde (MDA) levels as well as decreased superoxide dismutase (SOD) activity in the kidneys (P0.05). In the RPC group, renal function was significantly improved. Plasma Cr and BUN and renal MDA levels were significantly lower in RPC group comparing to HS group (P0.05). Renal SOD activity was significantly higher in RPC group compared to HS group (P0.05). Conclusion: These results demonstrate that induction of brief periods of lower limb ischemic preconditioning improves kidney function, restores SOD activity and reduces oxidative stress injury caused by hemorrhagic shock. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
17350581
Volume :
19
Issue :
1
Database :
Academic Search Index
Journal :
Physiology & Pharmacology
Publication Type :
Academic Journal
Accession number :
117508055