Ischemic Preconditioning May Protect Hippocampal CA1 Neurons against Lethal Ischemic Injury---Magnetic Resonance Imaging Study

Clinical studies have demonstrated that carotid artery stenosis is an important risk factor for ischemic stroke and may cause impairment of cognitive function due to hemodynamic insufficiency. Carotid recanalization including carotid endarterectomy and carotid stenting is known to reduce the risk of ischemic stroke. However, reperfusion after carotid recanalization may cause severe brain damage such as hyperperfusion syndrome and the occurrence of reperfusion injury is still unpredictable. Animal study showed that reperfusion injury after carotid artery recanalization may cause a more severe brain damage than permanent occlusion. The understanding of the mechanism of reperfusion injury is an important issue to secure the patient safety in clinical practice. Reperfusion injury following lethal cerebral ischemia can be attenuated by preconditioning of the rodent brain with sublethal cerebral ischemia which usually causes no reperfusion injury. This phenomenon is called ischemic tolerance. Ischemic tolerance can be seen in forebrain and focal cerebral ischemia and the underlying mechanism is still unknown. Diffusion/perfusion mismatch is the most widely used technique on magnetic resonance image (MRI) to identify thresholds for reversible ischemic penumbra and irreversible brain tissue damage. The salvageable ischemic penumbra area visualized by MRI may assist in individualizing therapeutic decisions and identifying effective therapies. In the present study, we wish to use ischemic preconditioning animal model to study the pathophysiological mechanism of reperfusion injury. We will study the MRI imaging change after cerebral ischemic tolerance. The degree of diffusion/perfusion mismatch will be correlated with the extent of histopathological injury and the expression of neurotrophin protein and mRNA after ischemic tolerance. The difference in MRI diffusion/perfusion and

Project ID:PC9808-0564
External Project ID:NSC98-2314-B182-054-MY2