Effects of Phenobarbital on Rat Model of Brain Ischemia

سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 339

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شناسه ملی سند علمی:

NIMED03_059

تاریخ نمایه سازی: 7 آبان 1398

چکیده مقاله:

There are some molecular pathways in tissue damage in Ischemic Brain Insult. Attentions focused on applying for antioxidants and free radical scavengers. Oxidative stress is caused by excessive production of reactive oxygen species such as hydroxyl radical, superoxide anion radical and hydrogen peroxide. GABAergic agents are used previously for protective effects in ischemia state. In this study we aimed to testpotential protective effects of phenobarbital in tissue level in rat’s brain. Materials and Methods: Male Wistar Rats 250-350 g were kept in constant condition (12 hr. day, night and temperature) with Food and Water ad libitum. The animals were divided into 4 groups of8 including: Group 1, was negative control in which ischemia was done and 1 mg normal saline injected IP. Group 2, positive control in which ischemia induction and 100mg /kg phenytoin injected IP as a standard neuroprotective agent. Group 3, phenobarbital 20 mg/ kg was injected intraperitoneal. Brain global ischemia was done using Four Vessel occluding (4VO) method expatiated by Pulsinelli et al. with some modification. Briefly, vertebral arteries cauterized permanently via Alar foramina in first vertebra of rat under general anesthesia, after 24 hours carotid arteries occluded for duration of 20 minute before reperfusion and recovery state. 72 hours later brain removed and immediately fixed with formaldehyde 10%. After tissue processing, thin slice (2-4 Microns) prepared and stained for hematoxyline and eosin. Results: Ischemic neuronal cells was seen in control group around the brain tissues specially in hippocampus, but some degree of necrosisseen in other area of brain such as cerebellum, basal ganglia and cortex. Despite slightly ischemic cellular changes only in some area, Phenobarbital group were not have vast necrosis cell around tissues.

نویسندگان

Maryam Salari

Department of Physiology, Mashhad University of Medical Sciences, Mashhad, Iran

Hassan Abbassian

Department of Neuroscience, Mashhad University of Medical Sciences, Mashhad, Iran