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Oxygen cerebral blood flow effect

Vincamine (91) is the major alkaloid of V. minor, a plant used against headache and vertigo. It exerts a sedative CNS action and produces a fall in blood pressure. The principal activity is a moderate cerebral vasodilation. Clinical studies have demonstrated that i.v. administration of 91 to humans reduces the arterial blood pressure and increases cerebral blood flow and oxygen consumption. The improved cerebral hemodynamic conditions significantly and positively affect the state of patients with advanced arteriosclerosis with beneficial effects on memory, concentration, and behavior. It has thereafter been introduced under several trade names as a pharmaceutical in many European countries (232). Vobasine (32) has been widely studied it exhibits a weak CNS depressive, analgesic, and antipyretic action (21). [Pg.134]

T.Q. Duong, C. ladecola, S.G. Kim, Effect of hyperoxia, hypercapnia, and hypoxia on cerebral interstitial oxygen tension and cerebral blood flow, Magn. Reson. Med. 45 (2001) 61-70. [Pg.265]

Sevoflurane has a dose-dependent effect on cerebral blood flow and intracranial pressure cerebral autoregulation is preserved (this is not the case with isoflurane). During hypocarbia, in the absence of nitrous oxide, 1 MAC does not increase intracranial pressure (ICP). It reduces the cerebral metabolic rate for oxygen (CMR02) by approximately 50% at concentrations approaching 2 MAC. This is similar to the reduction observed during isoflurane anaesthesia. [Pg.61]

Ketamine is generally administered to patients intravenously, but it is also effective when administered by intramuscular, oral, and rectal routes. The onset of action is generally short (10 to 15 minutes) but the duration of anesthesia of a single dose is long. Ketamine is the only intravenous anesthetic that produces an increase in heart rate and arterial blood pressure. It can also markedly increase cerebral blood flow, oxygen consumption, and intracranial pressure. [Pg.63]

Cole, D.J. Drummond, J.C. Patel, P.M. Marcantonio, S. Effects of viscosity and oxygen content on cerebral blood flow in ischemic and normal rat brain. J. Neurol. Sci. 1994, 124, 15-20. [Pg.375]

Barbiturates depress neuronal activity in the CNS. This is accompanied by decreased cerebral metabolic oxygen consumption and decreased cerebral blood flow, since the coupling of blood flow to brain metabolism is preserved with the barbiturates. It also results in a decrease in ICP. Barbiturates depress neuronal activity in the cerebral cortex, thalamus and motor centers. Barbiturates are effective anticonvulsants (see Ch. 9), reduce intraocular pressure, increase the threshold of spinal reflexes and provide excellent muscle relaxation. The barbiturates lack specific analgesic effects and are, therefore, not suitable as the sole anesthetic for invasive procedures. [Pg.286]

Jacobson, I., and Lawson, D. D., The effect of hyperbaric oxygen on experimental cerebral infarction in the dog with preliminary correlations of cerebral blood flow at 2 atmospheres of oxygen. J. Neurosurg. 20, 849-859 (1963). [Pg.130]

Several animal studies have demonstrated the beneficial effect of vasopressin on coronary and cerebral blood flow. Although vasopressin improves vital organ perfusion during VF, myocardial oxygen consumption is lower with vasopressin than with epinephrine. Vasopressin also may have a beneficial effect on renal blood flow by stimulating V2 receptors in the kidney, causing vasodilation and increased water reabsorption. With regard to splanchnic blood flow, however, most studies have shown that vasopressin has a detrimental effect compared with epinephrine. ... [Pg.176]

Leenders, K. L., Beaney, R. P., Brooks, D. J., Lammertsma, A. A., Heather, J. D., and McKenzie, C. G. (1985) Dexamethasone treatment of brain tumour patients effects on regional cerebral blood flow, blood volume, and oxygen utilisation. Neurology 35, 1610-1616. [Pg.110]

Figure I. Effect of progressively decreasing arterial oxygen tension on cerebral blood flow and cerebral oxygen uptake under conditions of respiratory acidosis. Figure I. Effect of progressively decreasing arterial oxygen tension on cerebral blood flow and cerebral oxygen uptake under conditions of respiratory acidosis.
Interruption or inclusion in cerebral blood flow leads to a decrease in supply of oxygen and nutrient to the brain, which ultimately leads to several neurodegenerative diseases. Table 122.2 showed the protective effect of EGb-761 in cerebral blood flow disorder animal models. [Pg.4699]


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