Brain ischaemia

Rossi DJ, Oshima T, AttweU D (2000) Glutamate release in severe brain ischaemia is mainly by reversed uptake. Nature 403 316-321... 

Docebenone has shown anti-inflammatory effects in several animal models following local dosing phorbol ester-induced oedema and neutrophil influx in mouse skin [208,209], arachidonate-induced plasma extravasation in rabbit skin [210], the pleural reversed passive Arthus reaction in rats [211], and GPB [212], An oral dose of 80 mg/kg reduced infarct size, LTB4 levels and neutrophil infiltration in a rat myocardial infarction model [213,214], and in a rat brain ischaemia-reperfusion model oedema and LTC4 levels were reduced at 200 mg/kg [107]. Significant, but not dramatic, improvement in nasal symptoms was seen in humans following 150 mg of docebenone twice daily for 8 weeks [215], but there was no effect on bronchial hyperresponsiveness to acetylcholine in asthmatics [216]. 

The mechanism of action of this kappa mediated neuroprotective effect is under investigation. In addition to the diuretic effects mentioned above, it has been shown that CI-977 (11) is inactive in a model of focal brain ischaemia in Brattleboro rats which lack vasopressin and do not exhibit kappa-mediated water diureses [33c]. An alternative mechanism for which there is increasing evidence is an inhibition of excitatory amino-acid release. U-50488 (5) and PD 117302 (12) have been shown to block convulsions in-... 

Ketamine has been traditionally contraindicated in patients with increased ICP or reduced cerebral compliance because it increases CMR02, CBF and ICP. These deleterious effects can be antagonised by the concomitant administration of propofol, or thiopentone, and benzodiazepines. Furthermore, ketamine is an antagonist at the NMDA receptor. Nevertheless, ketamine can adversely affect neurological outcome in the presence of brain ischaemia. 

Szatkowski M. and Attwell D. (1994). Triggering and execution of neuronal death in brain ischaemia two phases of glutamate release by different mechanisms. Trends Neurosci. 17 359-365. 

Lorente de No R (1934) Studies on the structure of the cerebral cortex. II. Continuation of the study of the Ammonic system. J Psychol Neurol 46 113-177 Love S, Barber R, Wilcock GK (1998) Apoptosis and expression of DNA repair proteins in ischaemic brain injury in man. Neuroreport 9 955-959 Love S, Barber R, Wilcock GK (1999) Neuronal accumulation of poly(ADP-ribose) after brain ischaemia. Neuropathol Appl Neurobiol 25 98-103 Luskin MB (1993) Restricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zone. Neuron 11 173-189 Magavi SS, Leavitt BR, Macklis JD (2000) Induction of neurogenesis in the neocortex of adult mice. Nature 405 951-955... 

Szatkowski, M., and Attwell, D. (1994). Triggering and execution of neuronal death in brain ischaemia Two phases of glutamate release by different mechanisms. Trends Neurosci. 17, 359-365. Trotti, D., Danbolt, N. C., and Volterra, A. (1998). Glutamate transporters are oxidant-vulnerable A molecular link between oxidative and excitotoxic neurodegeneration Trends Pharmacol. Sri. 19, 328-334. 

Demougeot C, Marie C, Giroud M, Beley A. 2004. N-acetylaspartate A literature review of animal research on brain ischaemia. J Neurochem 90 776-783. 

Laham A, Claperon N, Durussel JJ, Fattal E, Delattre J, Puisieux F, Couvreur P, Rossignol P (1988) Liposomally entrapped adenosine triphosphate improved eflSciency against experimental brain ischaemia in the rat. J Chromatogr 440 455 58... 

The intimate role of perivascular astrocytes in the maintenance of the blood-brain barrier (BBB) is well established but in models of brain ischaemia it has become established18 that astrocytic swelling precedes the later breakdown of the BBB such that, although perivascular astrocytic swelling occurs within minutes of induction of ischaemia, extensive breakdown of the BBB starts at 4 to 6 h and becomes maximal only 2 to 4 days after induction of ischaemia.26... 

Okada, Y., Copeland, B. R., More, E., Tung, M.-M., Thomas, W. S., and del Zoppo, G. J., P-selectin and intercellular adhesion molecule-1 expression after focal brain ischaemia and reperfusion, Stroke, 25, 202, 1994. 

Dizdarevic K, Hamdan A, Omerhodzic 1, KominUja-Smajic E. Modified Lund concept versus cerebral perfusion pressure-targeted therapy a randomised controlled study in patients with secondary brain ischaemia. Clin Neurol Neurosurg 2012 114 142-8. 

Bhakoo, K. K., Crockard, H. A., Lascelles, P. C., Avery, S. F., 1984 Prostaglandin synthesis and oedema formation during reperfusion following experimental brain ischaemia in the gerbil. Stroke 15, 891-895. 

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