AIM Stroke, both ischemic and hemorrhagic, is a major contributor to mortality and disability worldwide. Brain arteriovenous malformations (AVMs) are intracranial vascular anomalies with direct connections between the arterial and venous systems, but not through the capillaries. Among the management techniques of AVMs, endovascular embolization may lead to ischemia that may cause the revascularization of the AVM via angiogenesis. Vascular endothelial growth factor (VEGF), an important angiogenic factor, exerts its activities through its receptors, VEGFRs. Aside from membrane-bound VEGFRs, two soluble forms, namely sVEGFR1 and sVEGFR2, are found in the plasma and act as antiangiogenic factors. The aim of the study was to investigate the levels of VEGF in the brain and sVEGFR1 and sVEGFR2 levels in the plasma of rats after cerebral ischemia. MATERIAL AND METHODS Rats were divided into three groups as follows: Group 1: Sham-operated group, Group 2: Complete occlusion of the right carotid artery, Group 3: Complete occlusion of the right carotid artery and temporary occlusion of the left carotid artery for 10 min. Blood samples were collected on days 0 and 10 prior to the sacrification to measure the sVEGFR1 and sVEGFR2 levels. On day 10, animals were sacrificed, and brain tissue was collected to analyze VEGF expression. RESULTS Postoperative sVEGFR1 levels reduced significantly in Group 3, while it remained stable in other groups. sVEGFR2 levels did not change in any group. Although VEGF staining scores in the groups that underwent ischemia procedures increased compared to group 1, no significant differences were observed. CONCLUSION Decreased levels of sVEGFR1 can be a mechanism contributing to angiogenesis in AVMs by increasing the levels of VEGF available to bind membrane-bound VEGFRs.
Birol Bayraktar, Dursun Turkoz, Aytac Turkoz