Abstract

To evaluate the effects of chronic cerebral hypoxia on memory of rats submitted to bilateral common carotid artery ligation (BCCL). Every each week, for 16 weeks, 31 rats were tested for memory using a water and land mazes and compared with 30 normal rats (control group A). The variables were expressed by their mean and standard error of the mean (SEM). p<0.05 was used for rejecting the null hypothesis. The study was approved by the Ethics Committee for animal investigation. There was a significant increase in the latency time, in the survival water and land mazes, after four weeks (study group B) follow-up. However, without any medication or therapeutically induced measures, after 16 weeks (study group C) follow-up the latency mean times tend to be similar to control group (A) in the neurocognitive tests. Neurocognitive deficits after 16 weeks post-operative follow-up of rats that underwent bilateral common carotid artery ligation is a natural adaptive phenomenon. Thus, is not realistic to allow translational information from this animal model for therapeutically approaches aiming at to prevent, or to improve brain damage in human beings suffering from chronic deprivation of adequate blood supply.

Highlights

  • Since early 1960s, the mortality rate in Sprague- Dawley rats was very high when both carotid arteries were permanent occluded[1], it was realized that in Wistar rats, consistent ischemic damage of the brain was very difficult to maintain consistentely[2].Permanent occlusion of both common carotid arteries in the rat or bilateral common carotid artery ligation (BCCL) has been used as an experimental model for chronic cerebral hypoperfusion[3]

  • Each rat was placed in the entrance of the land maze and the time was recorded until the rat found the exit of the maze where its original cage with food and water were placed

  • The majority of papers dealing with chronic encephalic hypoxemia due to bilateral common carotid ligation (BCCL) indicate that it is associated with neuron apoptosis, mainly in the hippocampus, cerebral cortex, and caudate affecting the microenvironment vital for the central nervous system functions[3,5,13,14,15,16,17,18,19,20,21,22,23,24], producing cognitive changes measured by radial maze tests

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Summary

Introduction

Since early 1960s, the mortality rate in Sprague- Dawley rats was very high when both carotid arteries were permanent occluded[1], it was realized that in Wistar rats, consistent ischemic damage of the brain was very difficult to maintain consistentely[2]. Permanent occlusion of both common carotid arteries in the rat or bilateral common carotid artery ligation (BCCL) has been used as an experimental model for chronic cerebral hypoperfusion[3]. Activation of sPLA2 by calcium[8] may release ARA and to produce PGE29 to mediate compensatory vasodilatation. Auto regulation remains abnormal and the brain is more vulnerable to additional insults such as hypotension, hypoxia and further ischemia following BCCL12

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