FOCAL CEREBRAL BLOOD FLOW, REACTIVITY OF CEREBRAL BLOOD VESSELS AND CEREBRAL OXYDATIVE METABOLISM IN CERTAIN GROUPS OF PATIENTS WITH ORGANIC DEMENTIA

2009 ◽  
Vol 46 (S43) ◽  
pp. 76-76
Author(s):  
Jes Olesen ◽  
Denis Simard ◽  
Olaf Paulson ◽  
Erik Skinhøj
2001 ◽  
Vol 1 ◽  
pp. 168-180 ◽  
Author(s):  
Lars Edvinsson ◽  
Peter J. Goadsby ◽  
Rolf Uddman

Amylin and adrenomedullin are two peptides structurally related to calcitonin gene-related peptide (CGRP). We studied the occurrence of amylin in trigeminal ganglia and cerebral blood vessels of the cat with immunocytochemistry and evaluated the role of amylin and adrenomedullin in the cerebral circulation by in vitro and in vivo pharmacology. Immunocytochemistry revealed that numerous nerve cell bodies in the trigeminal ganglion contained CGRP immunoreactivity (-ir); some of these also expressed amylin-ir but none adrenomedullin-ir. There were numerous nerve fibres surrounding cerebral blood vessels that contained CGRP-ir. Occasional fibres contained amylin-ir while we observed no adrenomedullin-ir in the vessel walls. With RT-PCR and Real-Time�PCR we revealed the presence of mRNA for calcitonin receptor-like receptor (CLRL) and receptor-activity-modifying proteins (RAMPs) in cat cerebral arteries. In vitro studies revealed that amylin, adrenomedullin, and CGRP relaxed ring segments of the cat middle cerebral artery. CGRP and amylin caused concentration-dependent relaxations at low concentrations of PGF2a-precontracted segment (with or without endothelium) whereas only at high concentration did adrenomedullin cause relaxation. CGRP8-37 blocked the CGRP and amylin induced relaxations in a parallel fashion. In vivo studies of amylin, adrenomedullin, and CGRP showed a brisk reproducible increase in local cerebral blood flow as examined using laser Doppler flowmetry applied to the cerebral cortex of the a-chloralose�anesthetized cat. The responses to amylin and CGRP were blocked by CGRP8-37. The studies suggest that there is a functional sub-set of amylin-containing trigeminal neurons which probably act via CGRP receptors.


1939 ◽  
Vol 85 (358) ◽  
pp. 902-902
Author(s):  
E. Arnold Carmichael

Outline of physiology of sympathetic nervous system and its effect on the cerebral blood-vessels. Other factors controlling cerebral blood-vessels, such as local intra-arterial pressure and gas tension. The action of adrenalin-like and cholin-like substances on the cerebral blood-vessels. Alteration in cerebral blood flow during a convulsion, and the accompanying changes in cerebro-spinal fluid pressure. Evidence for systemic sympathetic disturbance during a convulsion. Discussion of “vaso-vagal” attacks and “diencephalitic” epilepsy.


Cephalalgia ◽  
1985 ◽  
Vol 5 (2) ◽  
pp. 69-78 ◽  
Author(s):  
ET MacKenzie ◽  
L Edvinsson ◽  
B Scatton

The rôle of serotonin (5-HT) in the cerebrovascular bed is the subject of the following review. Cerebral blood vessels are supplied with 5-HT-containing fibres which originate in the raphé nuclei in the brainstem. The activation of this system may result in a constriction of large arteries and a dilatation of arterioles. Intra-arterial administration of 5-HT causes reduction in cerebral blood flow and metabolism provided it bypasses the blood-brain barrier. The findings, marked changes in plasma levels of 5-HT and in cerebral blood flow during a classic migraine attack, are suggestive of an involvement of the 5-HT system.


1993 ◽  
Vol 264 (5) ◽  
pp. H1740-H1743 ◽  
Author(s):  
J. L. Williams ◽  
M. Shea ◽  
S. C. Jones

Recent studies indicate that blood flow to cerebral cortex is not homogeneous but may vary both spatially and temporally. In addition, some investigators have reported that capillaries and arterioles can be recruited to increase cerebral blood flow, an issue that is extremely controversial. The goal of this study was to determine whether recruitment of cerebral blood vessels is an important mechanism in spatial and temporal heterogeneity of cerebral blood flow. In seven anesthetized ventilated rats, different fluorescent tracers were injected 45 and 10 s before decapitation. In addition, [14C]iodoantipyrine also was injected 10 s before decapitation. After the brains were sectioned, fields in the cerebral cortex were examined microscopically for fluorescence and processed for measurement of cerebral blood flow with techniques of quantitative autoradiography and image analysis. With examination of 24 +/- 2 (SE) points in cerebral cortex of each rat, similar numbers of small blood vessels (< or = 10 microns) were counted that contained fluorescent tracers injected 45 and 10 s before decapitation (346 +/- 48 and 355 +/- 42 vessels/mm2, respectively; P > 0.05). Large blood vessels (20-60 microns; 73 +/- 6 vessels in each rat) contained both fluorescent tracers. In addition, adjacent regions of high and low blood flow contained similar numbers of small and large vessels. Our findings indicate that vascular recruitment is not an important mechanism in temporal or spatial heterogeneity of cerebral blood flow.


1978 ◽  
Vol 56 (2) ◽  
pp. 115-117 ◽  
Author(s):  
Lars Gustafson ◽  
Jarl Risberg ◽  
Margareth Johanson ◽  
Margareta Fransson ◽  
V. Alexander Maximilian

1986 ◽  
Vol 65 (3) ◽  
pp. 370-375 ◽  
Author(s):  
Hideyoshi Yokote ◽  
Toru Itakura ◽  
Kunio Nakai ◽  
Ichiro Kamei ◽  
Harumichi Imai ◽  
...  

✓ The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 ± 2.8 ml/100 gm/min; control cortex 38.5 ± 3.5 ml/100 gm/min; p < 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10−5 M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% ± 0.67%/mm Hg; control cortex 3.53% ± 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.


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