Intestinal Ischemic Preconditioning Modulates Oxidative Stress in Rat's Spinal Cord Ischemic Reperfusion Injury

Mohamed D Morsy^*(1)

⁽¹⁾Physiology Department, College of Medicine, King Khalid University, Saudi Arabia

⁽²⁾Public Health Department, Faculty of Medicine, Beni Suef University, Egypt

⁽³⁾Biochemistry Department, College of Medicine, Menoufiya University, Egypt

⁽⁴⁾Department of Physiology, Faculty of Medicine (Rabigh Branch), King Abdul Aziz University, Saudi Arabia

^* Corresponding author:

Mohamed Darwesh Morsy

Physiology Department

College of Medicine

King Khalid University

Saudi Arabia

Tel: +966544495223

Fax: +96672418194

E-mail: morsydarwesh@yahoo.com

Abstract

       Background: Paraplegia is a major devastating and unpredictable complication of spinal cord ischemic reperfusion injury (SC-IRI). Ischemic preconditioning (IPC) is a procedure whereby a brief episode of non-lethal ischemia to an organ produces protection against subsequent detrimental ischemic-reperfusion insult to that organ. It has been shown that IPC may not only induce a local protective effect, but also induces resistant to ischemic-reperfusion damage in remote organs what is termed remote ischemic preconditioning (rIPC).

       Aim: The aim of the present study was to investigate the potential protective effect of small intestinal ischemic preconditioning on subsequently induced SC-IRI in rats.

       Methods: Fifty male Sprague-Dawley rats were randomly divided into five groups (n=10 each): control rats (C) which underwent no surgery; Sham rats (S) were subjected to laparotomy without induction of rIPC or clamping of the aorta; remote intestinal ischemic preconditioning group (rIPC) were subjected to 3 cycles of 8-min anterior mesenteric artery occlusion followed by 5-minute reperfusion; SC-IRI rats were subjected to laparotomy with clamping of the aorta just above the bifurcation by non-traumatic vascular clamp for 45 minutes, then the clamp was released for reperfusion for 24 hours; and SC-IRI+rIPC rats underwent 3 cycles of 8-minute anterior mesenteric artery occlusion followed by 5-minute reperfusion each. Twenty four hours later, animals underwent another laparotomy and spinal cord ischemia followed by reperfusion similar to group SC-IRI. Twenty four hours after surgery; neurological assessment was done. Serum tumor necrosis factor alpha (TNF-α), spinal cord homogenate levels of prostaglandin E₂ (PGE₂), malondialdehyde (MDA) and advanced oxidative protein product (AOPP) and nitrite/nitrate (NOx) as well as superoxide dismutase (SOD) and catalase (CAT) activities were assessed. Small intestinal MDA homogenate levels and CAT activities were also measured.

       Results: Induction of intestinal rIPC 24 hours before SC-IRI produced significant reduction of the serum TNF-α, and spinal cord homogenate levels of PGE₂, MDA, AOPP and NOx as well as a significant reduction of SOD and a significant increase in CAT activity levels compared with the SC-IRI group.

       Conclusions: Remote small intestinal ischemic preconditioning ameliorated the clinical neurological dysfunction induced by ischemic reperfusion injury of spinal cord. This ameliorating effect appears to be through improvement of the oxidative stress level, lipid peroxidation and the preservation of SOD and CAT activities in the spinal cord.

Keywords: spinal cord ischemia, remote preconditioning, intestinal ischemia, oxidative stress, thoraco-abdominal aneurismal repair.

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