ABSTRACT
OBJECTIVE: Previous studies have shown niacin has neuroprotective effects on the central nervous system. However, its specific effect on spinal cord ischemia/reperfusion injury has not yet been explored. This study aims to evaluate whether niacin can contribute neuroprotective effects on spinal cord ischemia/reperfusion injury. METHODS: Rabbits were randomized into 4 groups of 8 animals: group I (control), group II (ischemia), group III (30 mg/kg methylprednisolone, intraperitoneal), and group IV (500 mg/kg niacin, intraperitoneal). The rabbits in group IV were premedicated with niacin for 7 days prior to inducing ischemia/reperfusion injury. The control group was subjected only to a laparotomy, while the remaining groups underwent spinal cord ischemia through a 20-minute occlusion of the aorta caudal to the left renal artery. Following the procedure, levels of catalase, malondialdehyde, xanthine oxidase, myeloperoxidase, and caspase-3 were analyzed. Ultrastructural, histopathological, and neurological evaluations were also performed. RESULTS: Spinal cord ischemia/reperfusion injury resulted in increased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3, with a concomitant decrease in catalase levels. Treatment with methylprednisolone and niacin led to decreased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3 and an increase in catalase. Both methylprednisolone and niacin treatments demonstrated improvements in histopathological, ultrastructural, and neurological assessments. CONCLUSIONS: Our findings suggest that niacin has antiapoptotic, anti-inflammatory, antioxidant, and neuroprotective effects at least equal to methylprednisolone in ischemia/reperfusion injury of the spinal cord. This study is the first to report the neuroprotective impact of niacin on spinal cord ischemia/reperfusion injury. Further research is warranted to elucidate the role of niacin in this context.
ABSTRACT
BACKGROUND: A bypass is usually required to prevent ischemia during the treatment of anterior inferior cerebellar artery (AICA) aneurysms. The intracranial (IC)-to-IC bypass provides several advantages over the extracranial-to-IC bypass in the posterior fossa. However, there are only 2 case reports about AICA revascularization with the posterior inferior cerebellar artery (PICA). We aimed to investigate the microsurgical anatomical challenges for PICA to AICA anastomosis. METHODS: Ten cadaveric heads injected with colored silicone were inspected on both sides using a lateral transcondylar approach. After the donor and recipient arteries were examined from the posterior side, neurovascular contents of the posterior fossa were excised and the origin, course, and variations of both arteries were investigated from the anterior view. The diameters of the AICA and PICA segments and the intersegment distance were measured. RESULTS: PICA variations and posteromedial origins from the vertebral artery were identified in 8 of the 20 right and 6 of the 20 left sides, and the first segment of the PICA was not present in 7 sides. Furthermore, in 18 sides, the PICA was trapped between the lower cranial nerves and dentate ligaments. Therefore the donor artery could not be brought closer than 1 cm to the recipient artery in 19 sides. Moreover, AICA variations were identified in 6 sides, and in 12 sides, the diameter of the recipient artery was <1 mm. CONCLUSIONS: The mostly PICA-related issues made PICA-to-AICA anastomosis unfeasible in all cadaveric heads included in the study.
