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Cerebral transient

FIGURE 2.6 Dynamic susceptibility contrast imaging. Axial images of the brain are acquired repeatedly, in this case every 1.5 seconds. As a bolus of intravenously injected contrast material enters the brain, first arteries, then brain parenchyma, and finally veins demonstrate a transient loss of signal intensity. In this acute stroke patient, hypoperfusion of the left middle cerebral artery territory results in delayed arrival of the contrast bolus and prolonged stasis of contrast within the tissue. [Pg.16]

Ereret T, Valable S, Chazalviel L, Saulnier R, Mackenzie ET, Petit E, Bemaudin M, Boulouard M, Schumann-Bard P. Delayed administration of deferoxamine reduces brain damage and promotes functional recovery after transient focal cerebral iscbemia in tbe rat. Eur J Neurosci 2006 23 1757-1765. [Pg.115]

Belayev L, Pinard E, Nallet H, Seylaz J, Liu Y, Riyamongkol P, Zhao W, Busto R, Ginsberg MD. Albumin therapy of transient focal cerebral ischemia in vivo analysis of dynamic microvascular responses. Stroke 2002 33 1077-1084. [Pg.117]

Du C, Hu R, Csemansky CA, Liu XZ, Hsu CY, Choi DW. Additive neuroprotective effects of dextrorphan and cycloheximide in rats subjected to transient focal cerebral ischemia. Brain Res 1996 718 233-236. [Pg.118]

Ma J, Endres M, Moskowitz MA. Synergistic effects of caspase inhibitors and mk-801 in brain injury after transient focal cerebral ischaemia in mice. Br J Pharmacol 1998 124 756-762. [Pg.118]

Corbett D, Hamilton M, Colboume F. Persistent neuroprotection with prolonged postischemic h3fpothermia in adult rats subjected to transient middle cerebral artery occlusion. Exp Neurol 2000 163 200-206. [Pg.120]

Veltkamp R, Warner DS, Domoki F, Brinkhous AD, Toole JF, Busija DW. Hyperbaric oxygen decreases infarct size and behavioral deficit after transient focal cerebral ischemia in rats. Brain Res 2000 853 68-73. [Pg.120]

Liu S, Shi H, Liu W, Eumichi T, Timmins GS, Liu KJ. Interstitial po2 in ischemic penumbra and core are differentially affected following transient focal cerebral ischemia in rats. J Cereb Blood Flow Metab 2004 24 343-349. [Pg.121]

Morimoto T, Ginsberg MD, Deitrich WD, Zhao W. Hyperthermia enhances spectrin breakdown in transient focal cerebral ischemia. Brain Res 1997 746(l-2) 43-51. [Pg.190]

Cardioembolism Cardioembolism accounts for approximately 30% of all stroke and 25-30% of strokes in the young (age <45 years)." AF accounts for a large proportion of these strokes (15-25%). Symptoms may be suggestive, but they are not diagnostic. Repetitive, stereotyped, transient ischemic attacks (TIAs) are unusual in embolic stroke. The classic presentation for cardioembolism is the sudden onset of maximal symptoms. The size of the embolic material determines, in part, the course of the embolic material. Small emboli can cause retinal ischemic or lacunar symptoms. Posterior cerebral artery territory infarcts, in particular, are often due to cardiac embolism. This predilection is not completely consistent across the various cardiac structural abnormalities that predispose to stroke, and may be due to patterns of blood flow associated with specific cardiac pathologies. [Pg.203]

Guadet, R.J. and Levine, L. (1979). Transient cerebral ischemia and brain prostaglandins. Biochem. Biophys. Res. Commun. 86, 893-901. [Pg.81]

Understand the types of cerebrovascular disease including transient ischemic attack, cerebral infarction, and cerebral hemorrhage. [Pg.161]

There are two main classifications of cerebral ischemic events transient ischemic attacks and cerebral infarction. [Pg.161]

T. Malinski, F. Bailey, Z.G. Zhang, and M. Chopp, Nitric-oxide measured by a porphyrinic microsensor in rat-brain after transient middle cerebral-artery occlusion. J. Cereb. Blood Flow Metab. 13, 355-358 (1993). [Pg.48]

Blumberg, R. M., Cady, E. B., Wigglesworth, J. S. etal. Relation between delayed impairment of cerebral metabolism and infarction following transient focal hypoxia-ischemia in the developing brain. Exp. Brain Res. 113 130-137, 1997. [Pg.557]

Gasche, Y., Copin, J. C., Sugawara, T., Fujimura, M. and Chan, P. H. Matrix metalloproteinase inhibition prevents oxidative stress-associated blood-brain barrier disruption after transient focal cerebral ischemia. /. Cereb. Blood Plow Metab. 21 1393-1400,2001. [Pg.571]

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). [Pg.113]

Nelson I would like to return to what David Eisner mentioned about the plasma membrane determining the steady-state free Ca2+, and what Rick Paul said about sparks and long-conductance Ca2+-dependent K+ (BK) channels. We have looked at cerebral arteries from PLB knockout mice. The spark frequency and the associated transient BK current frequency are elevated by about a factor of three. SR load goes up, the membrane potential hyperpolarizes and the artery relaxes. It would be useful to measure membrane potential under all the conditions as well as determine the voltage dependence of tone, to make sure that your manipulations are not simply changing the membrane potential. [Pg.240]

In addition to coronary sclerosis, evidence is accumulating that high Lp(a) levels may be important in the development of cerebrovascular and peripheral arterial disease, as well (J6, T8, U2). Lp(a) levels not only correlated well with clinical endpoints such as transient ischemic attack and cerebral infarction, but also were associated with the extent and severity of carotid atherosclerosis, as assessed by bidirectional Doppler ultrasound (K23, M33, Z2). [Pg.94]

Benveniste H, Drejer J, Schousboe A, Diemer NH. 1984. Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis. J Neurochem 43(5) 1369-1374. [Pg.243]

Diaz-Parejo P, Stahl N, Xu W, Reinstrup P, Ungerstedt U, et al. 2003. Cerebral energy metabolism during transient hyperglycemia in patients with severe brain trauma. Intensive Care Med 29(4) 544-550. [Pg.245]

Ischaemic stroke is the third leading cause of death in industrialized countries. The debilitating or lethal consequences of transient or temporary reductions in cerebral blood flow are not only caused by necrosis in the infarct zone itself, but also by pathophysiological events in the peri-infarct zone [14]. Apparently, the release of inflammatory mediators such as cytokines and NO contributes to tissue inflammatory injury. There is also evidence for apoptosis in the peri-infarct zone. These processes offer novel targets for therapeutic strategies. In this respect, the potential of neurotrophic factor treatment is described in Section 2.4.2.6. [Pg.26]


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See also in sourсe #XX -- [ Pg.43 , Pg.50 , Pg.186 , Pg.188 ]




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