Ischemia global

Cerebrovascular Carotid spasm Compromise of ECA ostium Hyperfusion syndrome Contrast encephalopathy Transient symptomatic cerebral ischemia Global Focal Carotid dissection Carotid perforation Hyperperfusion syndrome Acute stent thrombosis Major ischemic stroke Cerebral hemorrhage... 

Sjogren s syndrome is occasionally complicated by systemic vasculitis, causing focal cerebral ischemia, global encephalopathy and aseptic meningitis (Hietaharju et al. 1993 Bragoni et al. 1994 Delalande et al 2004). 

Kawagoe, J., Abe, K., Kogure, K. (1993). Regional difference of hsp70 and hsc70 heat shock mRNA inductions in rat hippocampus after transient global ischemia. Neurosci. Lett. 153, 165-168. 

Globus MY, Busto R, Lin B, Schnippering H, Ginsberg MD. Detection of free radical activity during transient global ischemia and recirculation effects of intraischemic brain temperature modulation. J Neurochem 1995 65 1250-1256. 

Toung TJ, Hum PD, Traystman RJ, Bhardwaj A. Global brain water increases after experimental focal cerebral ischemia effect of hypertonic sahne. Crit Care Med 2002 30(3) 644-649. 

Clemens, J.A., Flo, P.P.K. and Panetta, J.A. (1991). LY178002 reduces rat brain damage after transient global forebrain ischemia. Stroke 22, 1048-1052. 

Mickel, H.S., Vaishnav, Y.N., Kempski, O., von Lubitz, D., Weiss, J.F. and Feuerstein, G. (1987). Breathing 100% oxygen after global ischemia in Mongolian gcrbils results in increased lipid peroxidation and increased mortality. Stroke 18, 426-430. 

Yu, T.L., Gu, J.L., Lysko, P.G., Cheng, H.Y., Barone, F.C. and Feuerstein, G. (1992). Neuroprotective effects of phenyl-f-butyl-nitrone in gerbil global brain ischemia and in cultured rat cerebellar neurons. Brain Res. 574, 193-197. 

Focal and global ischemia produce different distributions of injury 560 The Selective vulnerability of specific neurons or glial cells is not explained by vascular distribution 562... 

Under physiologic conditions, the balance of membrane lipid metabolism, particularly that of arachidonoyl and docosahexaenoyl chains, favors a very small and tightly controlled cellular pool of free arachidonic acid (AA, 20 4n-3) and docosahexaenoic acid (DHA, 22 6n-3), but levels increase very rapidly upon cell activation, cerebral ischemia, seizures and other types of brain trauma [1, 2], Other free fatty acids (FFAs) in addition to AA, released during cell activation and the initial stages of focal and global cerebral ischemia, are stearic acid (18 0), palmitic acid (16 0) and oleic acid (18 1). 

Jin K, Mao XO, Eshoo MW, Nagayama T, Minami M, et al. 2001. Microarray analysis of hippocampal gene expression in global cerebral ischemia. Ann Neurol 50 93. 

Kitagawa, K., Matsumoto, M., Tsujimoto, Y, Ohtsuki, T., Kuwabara, K., Matsushita, K., Yang, G., Tanabe, H., Martinou, J. C., Hori, M., and Yanagihara, T., Amelioration of hippocampal neuronal damage after global ischemia by neuronal overexpression of BCL-2 in transgenic mice. Stroke 29, 2616-2621 (1998). 

Ri-measured PO2. Global Ischemia showed complete hypoxia for both groups with or without KCI arrest. Error bars represent one standard deviation of measurements from multiple hearts (data adapted from Ph.D. thesis of HImu Shukla, UT Southwestern 1994) [405]. 

In Section 1.1.1, L-deprenyl (2) was discussed as a potent selective MAO B inhibitor. Its p-fluoro analogue, fludeprenyl (7), was shown to retain the irreversible and selective inhibitory effects of its parent compound, with similar potency in vitro in rat tissue and in vivo in mice [33]. Both compounds have also been reported to have similar protective actions against transient global cerebral ischemia in gerbils. With L-deprenyl (2), these effects occurred at doses below those which inhibit MAO B, while the effects of the p-fluoro analogue 7 occurred only at doses that also inhibit MAO B activity [33b,34]. 

An early in vivo study in the model of global forebrain ischemia in the gerbil showed that a selective agonist of A3AR, IB-MECA, acutely administered 15 min prior to ischemia, impaired post-ischemic blood flow, increased mortality and exacerbated the loss of hippocampal neurons (von Lubitz et al. 1994). IB-MECA administration 20 min prior to transient middle cerebral ischemia also resulted in a significant increase in infarct size(von Lubitz et al. 2001). 

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