Oxygen cerebral

Among the examples of monoindole bases being discussed, vincamine (109) is the principal alkaloid of Vinca minorC. and has received some notoriety because it apparently causes some improvement in the abiUties of sufferers of cerebral arteriosclerosis (78). It is beheved that this is the result of increasing cerebral blood flow with the accompanying increase in oxygenation of tissue as a result of its action as a vasodilator. 

Kainer R. A functional model of the rat kidney. J Math Biol 1979 7 57-94. Kassissia IG, Goresky CA, Rose CP, Schwab AJ, Simard A, Huet PM, Bach GG. Tracer oxygen distribution is barrier-limited in the cerebral microcirculation. Circ Res 1995 77 1201-11. 

Perlmutter JS, Powers WJ, Herscovitch R Fox PT, Raichle ME. Regional asymmetries of cerebral blood flow, blood volume, and oxygen utilization and extraction in normal subjects. J Cereb Blood Flow Metab 1987 7 64-67. 

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... 

Burt JT, Kapp JP, Smith RR. Hyperbaric oxygen and cerebral infarction in the gerbil. Surg Neurol 1987 28 265-268. 

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. 

Schabitz WR, Schade H, Heiland S, Kollmar R, Bardutzky J, Henninger N, Muller H, Carl U, Toyokuni S, Sommer C, Schwab S. Neuroprotection by hyperbaric oxygenation after experimental focal cerebral ischemia monitored by mr-imaging. Stroke 2004 35 1175-1179. 

Roos JA, Jackson-Friedman C, Lyden P. Effects of hyperbaric oxygen on neurologic outcome for cerebral ischemia in rats. Acad Emerg Med 1998 5 18-24. 

Kawamura S, Yasui N, Shrrasawa M, Fukasawa H. Therapeutic effects of h3fperbaric oxygenation on acute focal cerebral ischemia in rats. Surg Neurol 1990 34 101-106. 

Weinstein PR, Anderson GG, Telles DA. Results of h3fperbaric oxygen therapy during temporary middle cerebral artery occlusion in unanesthetized cats. Neurosurgery 1987 20 518-524. 

Stocchetti N, Protti A, Lattuada M, Magnoni S, Longhi L, Ghisoni L, Egidi M, Zanier ER. Impact of pyrexia on neurochemistry and cerebral oxygenation after acute brain injury. J Neurol Neurosurg Psych 2005 76(8) 1135-1139. 

Nordstrom CH, Messeter K, Sundharg G, Schalen W, Werner M, Ryding E. Cerebral hlood flow, vasoreactivity, and oxygen consumption during harhiturate therapy in severe traumatic hrain lesions. J Neurosurg 1988 68(3) 424-431. 

Chan K-H, Miller JD, Dearden NM, Andrews PJ, Midgley S. The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg 1992 77(1) 55-61. 

At the present time it is difficult to single out any one factor that could be held ultimately responsible for cell death after cerebral ischaemia. Recent studies, however, have provided us with sufficient evidence to conclude that free radical damage is at least one component in a chain of events that leads to cell death in ischaemia/reperfiision injury. As noted earlier in this review, much of the evidence for free radicals in the brain and the sources of free radicals come from studies in animals subjected to cerebral ischaemia. Perhaps the best evidence for a role for free radicals or reactive oxygen species in cerebral ischaemia is derived from studies that demonstrate protective effects of antioxidants. Antioxidants and inhibitors of lipid peroxidation have been shown to have profound protective effects in models of cerebral ischaemia. Details of some of these studies will be mentioned later. Several reviews have been written on the role of oxygen radicals in cerebral ischaemia (Braughler and HaU, 1989 Hall and Btaughler, 1989 Kontos, 1989 Floyd, 1990 Nelson ef /., 1992 Panetta and Clemens, 1993). 

Kontos, H. (1989). Oxygen radicals in cerebral ischemia. In Cerebrovascular Diseases (eds. M.D. Ginsberg and W.D. Dietrich) pp. 365-371. Raven Press, New York. 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

The main mechanism of action of caffeine occurs via the blockade of adenosine receptors in the CNS. Adenosine is an autacoid, which is involved in the modulation of behavior, oxygenation of cells, and dilatation of cerebral and coronary blood vessels and indirectly inhibits the release of dopamine. The blockade of adenosine receptors by caffeine increases the activity of dopamine, which is implicated in the effects of caffeine (91). The question that arises from this observation is to know whether or not adenosine antagonists hold potential for the treatment of Parkinsonism, and further study on the adenosine receptor antagonists from medicinal plants should be encouraged. A possible source for such agents could be the medicinal flora of Asia and the Pacific, among which is the family Sapindaceae. 

Increased cerebral metabolism increased cerebral oxygen delivery. 

Improved cerebral microcirculation increased ATP synthesis increased utilisation of oxygen and glucose. 

Kety SS (1956). Human cerebral blood flow and oxygen consumption as related to aging. Journal of Chronic Disease, 3, 478-486. 

The partial oxygen pressure, p02, is particularly significant in metabolic processes of cells, and its variation from normal values often indicates pathologies (ischemic diseases, strokes, tumors). Accurate and localized measurements of the oxygen concentration are also desirable for differentiation between venous and arterial blood, or for cerebral mapping of task activation. In the past, invasive methods were used involving oxygen-sensitive electrodes which had to be placed directly in the blood or tissue and could only offer p02 from a few body points. 

Terminal activity causes an increase in local cerebral blood flow that can be quantified by measuring the accompanying increase in tissue oxygen. Alkaline pH changes... 

E.M.R. Doppenberg, A. Zauner, R. Bullock, J.D. Ward, P.P. Fatouros, and H.F. Young, Correlations between brain tissue oxygen tension, carbon dioxide tension, pH, and cerebral blood flow - a better way of monitoring the severely injured brain Surg. Neurol. 49, 650-654 (1998). 

The role of CuZnSOD on oxygen radical production in cerebral vessels has been studied. Didion et al. [28] demonstrated that endogenous CuZnSOD diminished superoxide levels in rabbit cerebral blood vessels and affected nitric oxide- and cyclooxygenase-mediated responses in cerebral microcirculation. A subsequent study by the same group [29] showed increased superoxide production and vascular dysfunction in CuZnSOD-deficient mice. Chang et al. [30] suggested that superoxide induced cytokines, which activated microglial... 

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