Rodent Models of Global Cerebral Ischemia

Abstract

Brain damage after stroke and head injury remains a huge clinical problem. In stroke, the initial cause of the damage is a blockage in a blood vessel (often the middle cerebral artery) and this sets off several pathways that ultimately lead to cell death. Recent studies have demonstrated that several new mechanisms are involved in neuronal death and this has led to an increase in research into novel molecules that might prevent brain damage or improve recuperation post-stroke. There are several models of global cerebral ischemia. Two of the most widely-used models are discussed in detail in UNIT 9.5, the gerbil bilateral carotid artery occlusion (BCAO) model and rat 4-vessel occlusion (4-VO) model. Additionally, several models of focal cerebral ischemia have been developed to mimic the effects of human stroke. The rationale behind the use of animal models, the various types of models and advantage and disadvantages of each model are presented.

Protective Effects of a New C-Jun N-terminal Kinase Inhibitor in the Model of Global Cerebral Ischemia in Rats

“…During the 7-min episode of ischemia followed by reperfusion, diffuse damage to neural tissue occurs with predominant death of the neurons in the parts of the brain sensitive to ischemia, including pyramidal neurons of CA1 and CA3 areas in the hippocampus, small neurons of striatum and basal ganglia, and neurons in the layers II, III, and V of the neocortex [35,36]. Based on the analysis of neuroprotective activity of IQ-1S in rats with GCI, the CA1 hippocampal area was chosen as the neurons in this zone are most vulnerable to harmful effects of ischemia/reperfusion [41,42]. In the CA1 hippocampal region in the animals administered with IQ-1S, we observed a clear increase in numerical density of neurons, an increase in the number of unaltered neurons, and a significant decrease in the number of neurons with irreversible morphological damage such as pericellular edema suggesting a pronounced neuroprotective effect of the studied compound.…”

Indinavir inhibits the expression of cytoplasmic aromatase and nuclear SREBP in the hippocampus of reperfusion injury-induced ischemic rats

“…However, the restoration of cerebral blood flow can cause tissue injury, referred to as reperfusion injury. It is important to inhibit reperfusion injury to achieve greater brain protection [2]. Cerebral ischemia or 'ischemic stroke' is caused by advanced age, hypertension, previous stroke or transient ischemic attack, cardiac arrest, traumatic brain injury, diabetes, cigarette smoking, atrial fibrillation and high cholesterol [3] and results predominantly in neuronal death in the brain regions that are most intrinsically vulnerable, such as the CA1 region of the hippocampus [4].…”

Comparative analysis of metal-complex and aminothiol antihypoxants efficiencies in the experiment

“…Как известно, первичные изыскания новых фармакологически активных средств обычно проводятся методом скрининга на мелких грызунах -мышах, монгольских песчанках и др. [15,20]. Тем не менее литературные сведения и собственные данные, полученные ранее, говорят о том, что искомый эффект нередко выявляется на сравнительно крупных лабораторных животных заметно слабее, например на крысах, кроликах.…”