| 11. |
- Suzuki, Norihiro, et al.
(författare)
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Origins and pathways of choline acetyltransferase-positive parasympathetic nerve fibers to cerebral vessels in rat
- 1990
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - 1559-7016. ; 10:3, s. 399-408
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Tidskriftsartikel (refereegranskat)abstract
- The presence of cholinergic nerve fibers in the brain vasculature has been a matter of controversy, partly due to the lack of a reliable histochemical marker. Accordingly, no distinct information about the origin and pathways for such fibers has been available. In the present study on the rat pial vasculature, utilizing a choline acetyltransferase (ChAT) antibody, which is able to demonstrate this enzyme in peripheral nervous tissue, evidence was obtained for an innervation by cholinergic fibers of large pial arteries. Vasoactive intestinal polypeptide (VIP) was present in or in close association with these fibers. By the aid of the retrograde axonal tracer True Blue (TB) applied to the middle cerebral arterial wall, such fibers were shown to originate in a subgroup of ChAT-positive cells in the sphenopalatine, otic, and internal carotid ganglia, which, in addition, contained VIP. The ChAT-positive pial nerve fibers were few in relation to the VIP-immunoreactive fibers, as was also illustrated by the few TB-positive cells in the ganglia that were ChAT positive as compared with the number of cells that were VIP positive. Only a small population of ChAT-containing neurons in these ganglia appeared to project to the pial vessels. The pathway from the sphenopalatine ganglion is via a membranous structure on the medial orbital wall, through the ethmoidal foramen, and along the internal ethmoidal artery to reach the circle of Willis. The fibers from the internal carotid and otic ganglia probably bridge to the internal carotid artery in the carotid canal, those from the otic ganglion after an initial course in the lesser superficial petrosal nerve.
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| 12. |
- Suzuki, Norihiro, et al.
(författare)
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Selective electrical stimulation of postganglionic cerebrovascular parasympathetic nerve fibers originating from the sphenopalatine ganglion enhances cortical blood flow in the rat
- 1990
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - 1559-7016. ; 10:3, s. 383-391
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Tidskriftsartikel (refereegranskat)abstract
- Recently, the origins and pathways of cerebrovascular acetylcholine- and vasoactive intestinal polypeptide-containing nerves have been elucidated in detail in the rat: The sphenopalatine ganglion is the major source for postganglionic parasympathetic fibers to the vascular beds of the cerebral hemispheres. To clarify the functional role of the nerves on cerebral blood vessels in vivo, brain cortical microvascular blood flow was measured in rats during electrical stimulation of these particular postganglionic fibers. Animals were subjected to transection of the right nasociliary nerve 2 weeks before the flow measurements to eliminate activation of peptidergic sensory fibers. Relative change in microvascular blood flow was continuously recorded by a laser-Doppler flowmeter system under alpha-chloralose anesthesia. The postganglionic fibers were electrically stimulated just proximal to the ethmoidal foramen by a bipolar platinum electrode (5 V; 0.5 ms; 3, 10, 30, 60 Hz; as a continuous stimulation for 90 s). Stimulation at 10 Hz induced a marked increase of the cortical blood flow (CoBF) on the ipsilateral side, whereas no change was observed on the contralateral side. It reached a maximum mean value of 42.5% at 46 s, and then slightly declined during the remaining stimulation period. No significant changes were observed in the mean arterial blood pressure or blood gases during or after stimulation. Both atropine and scopolamine failed to alter this flow increase. Electrical stimulation of the postganglionic fibers at different frequencies revealed a maximal increase in the CoBF at 30 Hz in the control situation (47.2%), but at 10 Hz after scopolamine administration (51.6%).
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| 13. |
- Uski, Tore, et al.
(författare)
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Actions of platelet-activating factor on isolated feline and human cerebral arteries
- 1990
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - 1559-7016. ; 10:3, s. 428-431
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Tidskriftsartikel (refereegranskat)abstract
- The effects of platelet-activating factor (PAF) were studied on isolated feline basilar arteries (BAs) and human pial arteries (PAs). PAF contracted the BAs by 67% of the contraction induced by 124 mM K+ and the PAs by 80%. The contraction in BAs was unaffected by both indomethacin and the thromboxane receptor antagonist AH23848. PAF relaxed prostaglandin F2 alpha-contracted arteries. In BAs 10(-6) M PAF reduced the contraction by 17% and in PAs by 47%. The relaxant effects in both arteries were unaffected by indomethacin. In conclusion, PAF can act both as a constrictor and as a dilator of isolated feline and human cerebral arteries. The effects are seemingly unrelated to vascular prostanoid production.
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| 14. |
- Wendt, Peter E., et al.
(författare)
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Ethanol reduces asymmetry of visual rCBF responses
- 1994
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - 0271-678X .- 1559-7016. ; 14:6, s. 963-973
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Tidskriftsartikel (refereegranskat)abstract
- Visual regional CBF (rCBF) responses were measured in 10 healthy male subjects before and after an ethanol dose of 1 g/kg body weight. This dose induces well-established cerebral vasodilatation. However, significant bilateral occipital increases were found in both conditions. Apparently, the coupling between neuronal activity and rCBF is preserved following ethanol. The occipital and posterior parietal flow increases were, however, larger on the right than the left side in the sober state. During inebriation the asymmetry disappeared, possibly representing a more undifferentiated processing of visual information. We propose that ethanol causes a reduced inhibition of the left posterior cortex and a reduction of right-hemisphere information processing.
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| 15. |
- Wendt, Peter E., et al.
(författare)
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Ethanol reduces asymmetry of visual rCBF responses
- 1994
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications Inc.. - 0271-678X .- 1559-7016. ; 14:6, s. 963-973
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Tidskriftsartikel (refereegranskat)abstract
- Visual regional CBF (rCBF) responses were measured in 10 healthy male subjects before and after an ethanol dose of 1 g/kg body weight. This dose induces well-established cerebral vasodilatation. However, significant bilateral occipital increases were found in both conditions. Apparently, the coupling between neuronal activity and rCBF is preserved following ethanol. The occipital and posterior parietal flow increases were, however, larger on the right than the left side in the sober state. During inebriation the asymmetry disappeared, possibly representing a more undifferentiated processing of visual information. We propose that ethanol causes a reduced inhibition of the left posterior cortex and a reduction of right-hemisphere information processing.
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| 16. |
- Zhang, E., et al.
(författare)
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Influence of MK-801 on brain extracellular calcium and potassium activities in severe hypoglycemia
- 1990
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 10:1, s. 136-139
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of the present study was to examine the effect of blockade of N-methyl-D-aspartate (NMDA) receptors on the depolarization associated with severe hypoglycemia, which is commonly preceded by one or a few transient depolarizations reminiscent of cortical spreading depression (CSD). In the cerebral cortices of rats [K+](e) and [Ca2+](e) were measured with ion-selective microelectrodes. NMDA blockade was achieved by injection of MK801 in doses that block CSD. In control rats, the latency from the time point when blood glucose reached minimal levels to onset of ionic shifts was 33.2 ± 3.5 min, and [K+](e) rose from 3.2 ± 0.2 to 55 ± 5 mM. All variables remained unchanged in rats treated with MK801. In another four rats treated with MK801, [Ca2+](e) declined from 1.06 ± 0.22 to 0.12 ± 0.02 mM. Plasma glucose measurements indicated that the cortex depolarized at a plasma glucose concentration between 0.7 and 0.8 mM, i.e., within a narrow range, suggesting a threshold phenomenon. In conclusion, activation of NMDA receptors seems of minor importance for hypoglycemic depolarization. The ionic transients that precede the persistent hypoglycemic depolarization are probably mediated by mechanisms distinct from those of electrically induced CSD.
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