Chronic cerebral ischemia

FurukawaM, Kashiwagi S, Matsunaga N, Suzuki M, Kishimoto K, Shirao S. Evaluation of cerebral perfusion parameters measured by perfusion CT in chronic cerebral ischemia comparison with xenon CT. J Comput Assist Tomogr 2002 26 272-278. 

Roberts, H.C., W.P. Dillon, and W.S. Smith, Dynamic CT perfusion to assess the effect of carotid revascularization in chronic cerebral ischemia. AJNR Am J Neuroradiol, 2000. 21(2) p. 421-5. 

In patients with known chronic cerebral ischemia related to underlying carotid artery stenotic lesions, CBF is usually preserved, at least initially, because of the cerebrovascular reserve. The cerebrovascular reserve represents the vasodilatation ability of cerebral arteries to compensate for a CBF tending to decrease and maintain this CBF at a normal level. In patients with chronic cerebral vascular disorders, it is necessary to quantify the residual cerebrovascular reserve and to distinguish tissue that has used only a limited fraction of its vasodilatation ability and still has cerebrovascular reserve available as a bulfer from tissue that has exhausted its vasodilatation ability and cerebrovascular reserve. The latter is at risk of ischemia, which can be triggered by any hemodynamic stress, and requires intervention to increased CBF, usually through carotid stenosis surgery or endovascular treatment, or extracranial-intracranial artery bypass (Nariai et al. 1995). 

Nariai T, Suzuki R, Hirakawa K, Maehara T, Ishii K, Senda M (1995) Vascular reserve in chronic cerebral ischemia measured by the acetazolamide challenge test comparison with positron emission tomography. AJNR Am J Neuroradiol 16 563-570... 

Kornetsky C Hyporesponsivity of chronic schizophrenic patients to dextroamphetamine. Arch Gen Psychiatry 33 1425—1428, 1976 Kosten TR Pharmacotherapy of cerebral ischemia in cocaine dependence. Drug Alcohol Depend 49 133-144, 1998... 

These compounds block N-type calcium channels in human neuroblastoma IMR-32 cells. PD-151307 (IC50 = 0.22 pM) shows about 40-fold selectivity for N- over L-type calcium channels (IC50 = 9.1 pM in GH3 cells). These compounds may also be potentially useful in the treatment of cerebral ischemia and chronic intractable pain. 

Von Lubitz DK, Lin RC, Boyd M, Bischofberger N, Jacobson KA (1999) Chronic administration of adenosine A receptor agonist and cerebral ischemia neuronal and glial effects. Eur J Pharmacol 367(2-3) 157-63... 

Sager TN, Laursen H, Hansen AJ (1995) Changes in N-acetyl-aspartate content during focal and global brain ischemia of the rat. J Cereb Blood Flow Metab 15 639-646 Sappey-Marinier D, Hubesch B, Matson GB, Weiner MW (1992) Decreased phosphorus metabolite concentrations and alkalosis in chronic cerebral infarction. Radiology 182 29-34... 

IL-6 plays a centol role in host defense and in acute and chronic inflammatory activities. It is expressed in response to various forms of cerebral injury [7,61,62]. It was found that in the rat, IL-6 mRNA is overexpressed 3 hours after permanent MCA occlusion and reaches a peak at 12 hours its expression remains high for at least 24 hours [7,63]. Higher IL-6 levels have been detected in the peripheral blood of patients with acute cerebral ischemia... 

AIF may contribute to acute neuronal injury induced by trauma, hypoglycemia or transient ischemia as well as in chronic neurodegeneradve diseases (Table 3). The translocadon of AIF has been observed in different experimental models of neurotoxicity including death of photoreceptors induced by rednal detachment, neuronal cell death induct in vivo by brain trauma and cerebral ischemia and death of cortical neurons induced in vitro by exposure to... 

Occludin =Embolic stroke in rats despite BBB breakdown lAnimal models of PD [28], cerebral ischemia [55], methamphetamine toxicity, toxic injmy [40], ethanol chronic intake, cortical cold injury, patients with MPS III [53] and cerebral malaria [65]... 

Since the early 1980s, much effort has focused on animal models of acute and chronic neurodegeneration in search of therapeutics for stroke. Neuronal cell death follows strokes, acute ischemic insults, and chronic neurodegeneration, such as Parkinson s disease, Alzheimer s disease (AD), epilepsy, and Huntington s disease. Up to 80% of all strokes result from focal infarcts and ischemia in the middle cerebral artery (MCA), so the commonly used animal models for neuroprotection are produced by temporary or permanent occlusion of the MCA.5 Lesions of the MCA include occlusion by electrocoagulation, intraluminal monofilaments, photochemical effects, thrombosis, and endothelin-1, but all of these models necessitate studying reperfusion events and validating MCA occlusion by behavioral assessments. 

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