Jacobs Journal of Nephrology and Urology

Impact of Renal Denervation and Vagal Nerve Stimulation in Ischemia-Reperfusion Injury in Rat Model

Published on: 2019-03-30

Abstract

Abstract Ischemia/reperfusion injury (IRI) is characterized by restriction of blood supply to an organ followed by restoration of blood flow and re-oxygenation. In the kidney, IRI contributes to acute kidney injury (AKI) with rapid kidney dysfunction and high mortality rates. A surgical or pharmacological blockade of renal sympathetic nerve prevents, partially, the progression of IR-induced AKI. Modulation of the cholinergic anti-inflammatory pathway (CAP) by vagus nerve stimulation (VNS) has also a delayed but effective role in renal IRI. Objectives This work aimed at investigating the combination effect of VNS and renal sympathetic denervation (RDN) in preventing deleterious effects of IRI in rats compared to the effects obtained by RDN alone and to elucidate the possible mechanisms. Methods: 32 adult male albino rats were equally allocated into 4 groups, sham group, IRI group, RDN group subjected to RDN before IRI and a group subjected to RDN and VNS before IRI. Results Compared to sham group, renal IRI led to elevation of BUN, serum creatinine and MDA levels, it also elevated TNFα and reduced GPX activity and nitrate levels in the renal tissue. In addition, IRI significantly increased BCL2 in immune-histochemical study and caused renal damage as observed by the histological light and electron microscopic examination. On the other hand, RDN demonstrated partial correction while, combination of RDN and VNS demonstrated nearly optimum recovery of renal functions, oxidant /antioxidant balance, inflammatory markers as well as marked amelioration of immunohistochemical , structural and ultra-structural studies. Conclusion VNS augmented and accelerated the reno-protective effects of RDN owing to its stimulating effect on CAP in addition to its antioxidant, anti-inflammatory as well as anti-apoptotic effects. Additionally, the delay of protective responses to VNS in the former literatures was abolished in our study when VNS was combined to RDN.

Keywords

Acute Kidney Injury; Ischemia Reperfusion Injury; Renal Denervation; Vagus Nerve Stimulation.