Blood flow cerebral/cerebrovascular

Detre JA, Alsop DC, Vives LR, Maccotta L, Teener JW and Raps EC (1988). Noninvasive MRI evaluation of cerebral blood flow in cerebrovascular disease. Neurology 50 633-641. 

Brain infarction was the first clinical application of SPECT. Decreases in relative cerebral perfusion were imaged by SPECT for diagnosis. Decreased rCBF is visualized in the form of decreased signal on SPECT and PET. The sensitivity and specificity of brain SPECT for infarct localization are 85.5% and 97.6%, respectively [99]. Blood-flow imaging is useful in the evaluation of response to therapy in patients with cerebrovascular diseases [100]. 

Yoshii, F., Barker, W.W., Chang, J.Y., Loewenstein, D.. Apicella, A., Smith, D.. et al. Sensitivity of cerebral glucose metabolism to age, gender, brain volume, brain atrophy, and cerebrovascular risk factors. J. Cerebr. Blood Flow Metab. 8(5), 654-661, 1988. 

Reith W, Heiland S, Erb G et al (1997) Dynamic contrast-enhanced T2>t-weighted MRI in patients with cerebrovascular disease. Neuroradiology 39 250-257 Rempp KA, Brix G, Wenz F et al (1994) Quantification of regional cerebral blood flow and volume with dynamic susceptibility contrast-enhanced MR imaging. Radiology 193 637-641... 

Go KG (1997) The normal and pathological physiology of brain water. Adv Tech Stand Neurosurg 23 47-142 Hata R, Maeda K, Hermann D, Mies G, Hossmann KA (2000) Evolution of brain infarction after transient focal cerebral ischemia in mice. J Cereb Blood Flow Metab 20 937-946 Hatashita S, Hoff JT (1990) Brain edema and cerebrovascular permeability during cerebral ischemia in rats. Stroke 21 582-588... 

Cerebral blood flow depends on cerebral perfusion pressure and cerebrovascular resistance. The perfusion pressure is the difference between systemic arterial pressure at the base of the brain when in the recumbent position and the venous pressure at exit from the subarachnoid space, the latter being approximated by the intracranial pressure. Cerebral perfusion pressure divided by cerebral blood flow gives the cerebrovascular resistance. In normal humans, cerebral blood flow remains almost constant when the mean systemic blood pressure is between approximately 50 and 170mmHg, which, under normal circumstances when the intracranial venous pressure is negligible, is the same as the cerebral perfusion pressure. This homeostatic mechanism to maintain a constant cerebral blood flow in the face of changes in cerebral perfusion pressure is known as autoregulation (Reed and Devous 1985 Powers 1993). Autoregulation is less effective in the elderly, and so postural hypotension is more likely to be symptomatic (Wollner et al. 1979 Parry et al. 2006). 

Baumgartner RW (1999). Transcranial color-coded duplex sonography. Journal of Neurology 246 637-647 Baumgartner RW, Mattie HP, Aaslid RC et al (1997). Transcranial colour-coded duplex sonography in arterial cerebrovascular disease. Cerebrovascular Diseases 7 57-63 Bishop CCR, Powell S, Insall MC et al (1986). Effect of internal carotid artery occlusion on middle cerebral artery blood flow at rest and in response to hypercapnia. Lancet i 710-712... 

Vincamine is an alkaloid extracted from the plant Vinca minor. Ethyl apovincaminate is a related synthetic ethyl ester of vincaminic acid. These drugs have spasmolytic effects similar to those of reserpine, but also have metabolic effects, including, in high doses, inhibition of phosphodiesterase. Although increased cerebral blood flow has been reported after the intravenous administration of vincamine, there have been no reliable studies of blood flow after oral medication. Improvement in scores on some psychometric tests have been obtained in some patients with cerebrovascular disease, but no clear-cut practical benefit has been demonstrated. 

Cerebral ischaemia is responsible for approximately 85% of strokes (cerebrovascular accidents) irrespective of whether they are thrombotic or embolic in nature.4 Reestablishment of blood flow (reperfusion) in the postischaemic period is often accompanied by further tissue injury that is associated with aberrant microvascular function, damage to endothelial cells, and inflammatory cell exudates.5-6 In recent years, particular attention has focused upon the contribution of neutrophils to the pathogenesis of the reperfusion injury seen in cerebral ischaemia. 

Tamaki, N., Kusunoki, T., Matsumoto, S., The effect of Vinpocetine on cerebral blood flow in patients with cerebrovascular disease. Ther Hung, 33 13-21. 1985. 

Physiological studies have shown that marked cerebrovascular and blood perfusion changes occur with CN intoxication. Slow iv infusion of KCN increased cerebral blood flow in dogs by 130 to 200%, with respective blood CN concentrations of 1.0 and 1.5 pg ml 1 (Pitt et al, 1979). Cerebral O2 consumption was unaffected at 1.0 pg CN ml 1, but decreased to 75% of control vales at 1.5 pg CN ml 1. The increased cerebral blood flow caused by CN was demonstrated in several species by Russek et al (1963). By continuous infusion of NaCN, Funata et al. (1984) found an initial increase in blood flow... 

Asenbaum S, Reinprecht A, Briicke T, Wenger S, Podreka I, Deecke L (1985) A study of acetazola-mide-induced changes in cerebral blood flow using " Tc-HM-PAO SPECT in patients with cerebrovascular disease. Neuroradiology 27 509-516 Ballinger JR, Reid RH, Gulenchyn KY (1988) Radiochemical purity of [ " Tc]HM-PAO. J Nucl Med 29 572-573 (letter)... 

Peak respiratory depression is observed within 1 hour of intramuscular administration, and there is a return toward normal starting in about 2 hours. Like other opioids, meperidine causes pupillary constriction, increases the sensitivity of the labyrinthine apparatus, and has effects on the secretion of pituitary hormones similar to those of morphine. Meperidine sometimes causes CNS excitation, characterized by tremors, muscle twitches, and seizures these effects are due largely to accumulation of a metabolite, normeperidine. As with morphine, respiratory depression is responsible for an accumulation of CO2 which, in turn, leads to cerebrovascular dilation, increased cerebral blood flow, and elevation of cerebrospinal fluid pressure. 

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