Ischemic brain injury

Miller RJ, Banisadr G, Bhattacharyya BJ (2008) CXCR4 signaUng in the regulation of stem ceU migration and development. J Neuroimmunol 198 31-38 Minami M, Satoh M (2003) Chemokines and their receptors in the brain pathophysiological roles in ischemic brain injury. Life Sci 74 321-327... 

Liu, T.H., Beckman, J.S., Freeman, B.A., Hogan, E.L. and Hsu, C.Y. (1989). Polyethylene glycol-conjugated superoxide dismutase and catalase reduce ischemic brain injury. Am. J. Physiol. 256, H589-593. 

HYPOXIC-ISCHEMIC BRAIN INJURY AND OXIDATIVE STRESS 559... 

Hypoxic-Ischemic Brain Injury and Oxidative Stress... 

Synaptic stimulation, ischemia or seizure activates phospholipase A2 and releases arachidonic and docosahexaenoic acids. Ischemia or seizure triggers accumulation of free AA, DHA and other FFA in the brain( see also Chs 32, 37). This reflects PLA2 activation in excitable membranes [24]. While little is known about the mechanisms that control its activity, the importance of cPLA2 in ischemic brain injury is strongly supported by the recent finding that cPLA2-knockout mice have substantially reduced infarcts and neurologic deficits in a model of stroke [25],... 

Akisu M, Kultursay N, Coker I, Huseyinov A. (1998). Platelet-activating factor is an important mediator in hypoxic ischemic brain injury in the newborn rat. Flunarizine and Ginkgo biloba extract reduce PAF concentration in the brain. Biol Neonate. 74(6) 439-44. 

Guan J, WiUiams CE, Skinner SJ, Mallard EC, Gluckman PD. 1996. The effects of insulin-like growth factor (IGF)-l, IGF-2, and des-IGF-1 on neuronal loss after hypoxic-ischemic brain injury in adult rats evidence for a role for IGE binding proteins. Endocrinology 137 893-898. 

Cao G, Pei W, Ge H, et al. In vivo delivery of a Bcl-xL fusion protein containing the TAT protein transduction domain protects against ischemic brain injury and neuronal apoptosis. J Neurosci 2002 22(13) 5423-5431. 

D. Azzopardi, J. S. Wyatt, E. B. Cady, D. T. Delpy, J. Baudin, A. L. Stewart, P. L. Hope, P. A. Hamilton and E. O. Reynolds, Prognosis of newborn infants with hypoxic-ischemic brain injury assessed by phosphorus magnetic resonance spectroscopy. Pediatr. Res., 1989,25, U5-451. 

Nakatomi, H., Kuriu, T., Okabe, S., Yamamoto, S., Hatano, O., Kawahara, N., Tamura, A., Kirino, T., Nakafuku, M. (2002). Regeneration of hippocampal pyramidal neurons after ischemic brain injury by recruitment of endogenous neural progenitors. Cell, 110, 429-41. 

Sebastiao AM, de Mendonca A, Moreira T, Ribeiro JA (2001) Activation of synaptic NMDA receptors by action potential-dependent release of transmitter during hypoxia impairs recovery of synaptic transmission on reoxygenation. J Neurosci 21(21) 8564-8571 Shen H, Chen GJ, Harvey BK, Bickford PC, Wang Y (2005) Inosine reduces ischemic brain injury in rats. Stroke 36(3) 654-659... 

Chen GJ, Harvey BK, Shen H, Chou J, Victor A, Wang Y (2006) Activation of adenosine A3 receptors reduces ischemic brain injury in rodents. J Neurosci Res 84(8) 1848—1855... 

Smith ML, Auer RN, Siesjo BK (1984) The density and distribution of ischemic brain injury in the rat following 2-10 min of forebrain ischemia. Acta Neuropathol (Berl) 64 319-332 Squire LR,ZolaSM (1996) Ischemic brain damage and memory impairment a commentary. Hippocampus 6 546-552... 

Until recently, the neonate has been a black box, an eminently valued patient, yet one that is difficult to study and treat effectively. Neonatal research, in particular, is often plagued by ethical problems of invasiveness of protocols, volume of blood to be drawn, inability of the patient to speak on his/her own behalf, etc. Even simple studies that try to address neonatal outcome often pose problems in these areas, requiring volumes of blood that subsequently need to be replaced by transfusion. Because the perceived benefit to both individual patients and to society as a whole is deemed to be highly valuable, such downsides to neonatal research are often accepted as inevitable. The introduction, however, of MS analysis, utilizing low volumes of blood for multiple biomarkers, appears to be a very attractive alternative with great potential. A number of critical areas have already begun to be addressed and include such diverse entities as hypoxic-ischemic brain injury, the infant of a diabetic mother, neonatal renal function, neonatal nutrition, neonatal sepsis, and pharmaceutical development. 

Hypoxic-Ischemic Brain Injury, Perinatal Asphyxia, and Chronic Lung Disease The Potential for Proteomic Evaluation... 

Friedlander, R. M., Gagliurdini, V., Hara, H., Fink, K. B., Li, W., MacDon-old, G., Fishman, M. C., Greenberg, A. H., Moskowitz, M. A., Yuan,J., (1997). Expression of a dominant negative mutant of interleukin-1 (3 converting enzyme in transgenic mice prevents neuronal cell death induced by trophic factor withdrawal and ischemic brain injury.. Exp. Med. 185, 933—940. 

Endres M, Wang ZQ, Namura S, Waeber C, Moskowitz MA (1997) Ischemic brain injury is mediated by the activation of poly(ADP-ribose)polymerase. J Cereb Blood Flow Metab 17 1143-1151... 

Ginsberg M. D., Stemau L. L., Globus M. Y., Dietrich W. D., and Busto R. (1992) Therapeutic modulation of brain temperature relevance to ischemic brain injury. Cerebrovasc. Brain Metab. Rev. 4, 189-225. 

Oxygen free radicals are elaborated during ischemia and reperfusion and have been strongly implicated in the pathophysiology of ischemic brain injury (114). These reactions may lead to oxidative injury to cellular lipids, proteins, and nucleic acids. Evidence for free radical elaboration in ischemia is obtainable by means of a microdialysis method in which administered salicylate is converted, in the presence of hydroxyl radical, to dihydroxybenzoic acid (DHBA) species—stable adducts detectable by chromatographic methods. A study from our laboratory of... 

The aforementioned findings in rodents mirror results observed in dogs subjected to cardiac arrest with subsequent postischemic mild hypothermia of 1- to 12-h duration (38-44). For example, a 12-h period of 34°C hypothermia with hemodilution and elevated blood pressure reduced brain injury (e.g., hippocampus, neocortex, basal ganglia) and lessened functional deficits after cardiac arrest. However, in all of these studies the survival time was 4 d or less, and thus it has yet to be proven that postischemic hypothermia can permanently reduce ischemic brain injury in the dog. Based on the rodent literature, it would be useful to investigate more protracted bouts of mild hypothermia and assess longterm outcome in this intensive cardiac arrest model in the dog. 

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