Cerebrovascular reactivity

Kleiser B, Widder B (1992). Course of carotid artery occlusions with impaired cerebrovascular reactivity. Stroke 23 171-174... 

Markus HS, Harrison MJG (1992). Estimation of cerebrovascular reactivity using transcranial Doppler, including the use of breath-holding as the vasodilatory stimulus. Stroke 23 668-673... 

Warnock NG, Gandhi MR, Bergvall UC et al (1993). Complications of intra-arterial digital subtraction angiography in patients investigated for cerebral vascular disease. British Journal of Radiology 66 855-858 Widder B, Kleiser B, Krapf H (1994). Course of cerebrovascular reactivity in patients with carotid artery occlusions. Stroke 25 1963-1967... 

Hartl WH, Janssen I, Furst H (1994). Effect of carotid endarterectomy on patterns of cerebrovascular reactivity in patients with unilateral carotid artery stenosis. Stroke 25 1952-1957... 

Markus H, Cullinane M (2001). Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion. 

The risk-benefit relationship has been evaluated in only one completed randomized trial and this failed to show any benefit from routine surgery (EC-IC Bypass Study Group 1985). However, it has been argued that patients with impaired cerebrovascular reactivity, or with maximal oxygen extraction, were not identified and perhaps it is these patients who might benefit from surgery (Warlow 1986 Derdeyn et at 2005), but proof of this hypothesis would require a further randomized trial in this specific subgroup (Karnik et at 1992). 

Totaro et al. published a detailed paper on the factors affecting measurement of cerebrovascular reactivity when measured by NIR [49]. Some of the points covered were the relative transparency of the skin, skull, and brain in the 700- to 1100-nm region and the oxygen-dependent tissue absorption changes of hemoglobin. Their study covered all relevant factors, such as age, sex, reproducibility (often neglected in many academic papers), and venous return. The test was based on a 3-min baseline, a 3-min hypercapnia (5% C02 in air), and a 2-min recovery period. 

R. Totaro, G. Barattelli, V. Quaresima, A. Carolei, and M. Ferrari, Evaluation of Potential Factors Affecting the Measurement of Cerebrovascular Reactivity by Near-Infrared Spectroscopy, Clin. Sci., 95, 497 (1998). 

Tigyi, G., Hong, L., Yakubu, M., Parfenova, H., Shibata, M. and Lefder, C. W. Lysophosphatidic acid alters cerebrovascular reactivity in piglets. Am J Physiol 268 (1995) H2048-H2055. 

Silvestrini, M., Troisi, E., Matteis, M., Cupini, L. M., and Caltagirone, C. (1996) Transcranial Doppler assessment of cerebrovascular reactivity in symptomatic and asymptomatic severe carotid stenosis. Stroke 27,970-973. 

Bodo M, Pearce FJ, Armonda RA. 2004. Cerebrovascular reactivity Rat studies in rheoencephalography. PhysiolMeas 25,137i-i384. 

Changes in NIR spectra and transcranial Doppler sonography parameters were significantly correlated with variations of end-tidal CO2 (P <. 005). Their overall conclusion was that NIR was a viable technique for evaluation of cerebrovascular reactivity for patients with cerebrovascular disease. 

Has the cerebrovascular synthesis of prostacyclin a role in the modulation of cerebrovascular reactivity or does it act solely in its capacity to repel intracerebral platelet deposition and aggregation ... 

Many other workers have now confirmed these cerebrovascular properties of indomethacin in other species, including man (Table 2). Methodological factors may explain the discrepancies in the literature. Dawson and Dalessio (1968) employed an inhalation xenon technique for the measurement of human CBF but made no correction for either arterial recirculation of %enon or for the slow extracerebral component of the washout curves. The depression of cerebrovascular reactivity by barbiturate... 

Is the acute reduction in CBF produced by indomethacin in humans, primates, rat, and gerbil a result of inhibition of prostaglandin synthesis in some compartment within the brain If endogenous arachidonic derivatives play more than a permissive role in control of cerebrovascular reactivity, then it should be possible to demonstrate that the changes in concentration of the relevant eicosanoid within the appropriate compartment within the brain should change with, for example, hypercapnia. The problem is how to estimate such eicosanoid levels in the appropriate compartment. Severe insults such as cerebral ischaemia of varying duration do result in the release... 

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