Application of vascular endothelial growth factor at different phases of intestinal ischemia/reperfusion: What are its effects on oxidative stress, inflammation and telomerase activity?

BACKGROUND: Intestinal ischemic reperfusion injury (IRI) represents a great challenge in clinical practice, with high morbidity and mortality. Vascular endothelial growth factor (VEGF), as a signal protein, contributes to vasculogenesis and angiogenesis. OBJECTIVES: To evaluate the local effectiveness of VEGF following intestinal IRI and its relation with application time. MATERIAL AND METHODS: Thirty Wistar albino rats were allocated to 5 groups and underwent laparotomy. The superior mesenteric arteries (SMA) were dissected in 4 groups, while the control group (Gr C) underwent a resection of small and large intestines. The VEGF group (Gr V) received VEGF following SMA dissection, with no further intervention, and the remaining 3 groups were subjected to ischemia for 90 min through occlusion of SMA and reperfusion for 4 h. Ischemic reperfusion group (Gr I/R) received no additional medication, while the remaining 2 groups received VEGF just before ischemia (Gr V+I/R) and during reperfusion (Gr I/R+V). RESULTS: Both applications of VEGF caused decreases in plasma levels of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), intestinal malondialdehyde (MDA), oxidized glutathione, protein carbonyl levels, and increases in intestinal total glutathione and superoxide dismutase (SOD) levels. Telomerase activity, which disappeared for Gr I/R, was found to be elevated following both treatment groups. Similarly, the histopathological scores were found better for both treatment groups, but Gr V-I/R represented best outcomes. CONCLUSIONS: The findings of our study revealed that VEGF, applied either before ischemia or during reperfusion, is effective on local damage following intestinal IRI. By interpreting the biochemical analysis and histopathological findings, we conclude either treatment option to be considered according to the reason of intestinal IRI.

Neuroprotective Effects of Vigabatrin on Spinal Cord Ischemia-Reperfusion Injury.

OBJECTIVE: Spinal cord ischemia is a serious and catastrophic clinicopathologic condition. Despite studies reported over the last 20 years, alternative and efficient treatment options remain unclear. We examined the neuroprotective effects of vigabatrin on a spinal ischemia-reperfusion model. METHODS: We divided 24 New Zealand rabbits into 4 groups (control, ischemia reperfusion, and low-dose and high-dose vigabatrin). The control group underwent only abdominal surgery, whereas an abdominal aortic cross-clamp model of spinal ischemia was performed in the other groups. Clips were removed after 30 minutes and 50 and 150 mg/kg vigabatrin was administered intraperitoneally to the low-dose and high-dose groups, respectively. Neurologic examination was performed for 48 hours, after which the rabbits were sacrificed and a blood sample obtained. Biochemical examination of malondialdehyde, advanced oxidation protein products, total nitric oxide, and glutathione levels and superoxide dismutase activities in plasma and tissue sample, and histopathologic examination of the spinal cord were performed and statistical results compared between the groups. RESULTS: Low-dose vigabatrin had statistically significant effects of neuroprotection on spinal ischemia. Although high-dose vigabatrin had similar effects, the results were not statistically significant for all parameters of biochemical analysis. In addition, histopathologic examination showed some toxic effects of high-dose vigabatrin. CONCLUSIONS: Neuroprotective effects of vigabatrin are shown. For clinical use, further studies are needed.