scholarly journals Pial Vascular Behavior during Bilateral and Contralateral Cervical Sympathetic Stimulation

1986 ◽  
Vol 6 (3) ◽  
pp. 298-304 ◽  
Author(s):  
Ludwig M. Auer ◽  
Norio Ishiyama

The present study in cats investigates the effect of cervical sympathetic stimulation on changes of diameter of pial arteries and veins, CBF, and intracranial pressure (ICP) using the cranial window and hydrogen clearance techniques. During 20 min of bilateral stimulation, pial arteries maximally constricted by 12%, veins by 13–15%. While the constriction of the large arteries remained stable during the whole 20-min period of bilateral stimulation, small arteries escaped after some 2 min. A similar though weaker trend was noted for the veins. CBF was reduced at 2 min by 31%, and was not different from resting at 18 min. Contralateral stimulation for 20 min induced early constriction only in small arteries, while all other vessels remained more or less unreactive. This phenomenon is explained by interhemispheric arterial collaterals that bring sympathetic fibers mainly to small arteries contralaterally. ICP was lowered initially by 47 ± 12% during bilateral and by 23 ± 5% during contralateral stimulation. ICP escaped after 2 and 5 min during bilateral and contralateral stimulation, respectively, and even started to rise after some 10 min. From these data, it is concluded that the sympathoadrenergic system exerts a short-lasting protective effect upon cerebral vascular volume. Small arteries escape from constriction as a consequence of primarily myogenic counteraction of pial and intraparenchymal vessels, and probably additional metabolic dilatation of intraparenchymal vessels.

2009 ◽  
Vol 30 (2) ◽  
pp. 428-439 ◽  
Author(s):  
Alberto L Vazquez ◽  
Mitsuhiro Fukuda ◽  
Michelle L Tasker ◽  
Kazuto Masamoto ◽  
Seong-Gi Kim

Little is known regarding the changes in blood oxygen tension (PO2) with changes in brain function. This work aimed to measure the blood PO2 in surface arteries and veins as well as tissue with evoked somato-sensory stimulation in the anesthetized rat. Electrical stimulation of the forepaw induced average increases in blood flow of 44% as well as increases in the tissue PO2 of 28%. More importantly, increases in PO2 throughout pial arteries (resting diameters=59 to 129 μm) and pial veins (resting diameters=62 to 361 μm) were observed. The largest increases in vascular PO2 were observed in the small veins (from 33 to 40 mm Hg) and small arteries (from 78 to 88 mm Hg). The changes in oxygen saturation (SO2) were calculated and the largest increases were observed in small veins (Δ=+11%) while its increase in small arteries was small (Δ=+4%). The average diameter of arterial vessels was observed to increase by 4 to 6% while that of veins was not observed to change with evoked stimulation. These findings show that the increases in arterial PO2 contribute to the hyper-oxygenation of tissue and, mostly likely, also to the signal changes in hemoglobin-based functional imaging methods (e.g. BOLD fMRI).


1982 ◽  
Vol 2 (4) ◽  
pp. 451-456 ◽  
Author(s):  
R. Sercombe ◽  
M. Wahl

We studied the effects of microapplications of carbachol plus atropine on cat pial artery diameter in vivo during resting conditions and during stimulation of the cervical sympathetic nerve. The cats were anesthetized with α-chloralose and artificially ventilated. The pial surface was exposed by trepanation and protected by a 1–2-cm layer of oil. Calibrated applications of solutions were made by micropipette into the subarachnoid space, while the pial artery diameter was measured by the television image-splitting method. Sympathetic stimulation during 100 s induced a constrictive response of about 10%, which was constant from 60 to 100 s and which remained so during application of inert mock spinal fluid from 65 to 100 s. Application of 10−5 M carbachol plus 10−7 M atropine (solution A) or 10−4 M carbachol plus 10−6 M atropine (solution B) did not produce any significant changes in diameter during resting conditions. During sympathetic stimulation, application of solution A from 65 to 100 s induced a small nonsignificant reduction of the constriction, whereas application of solution B induced a highly significant reduction of the constriction from 9.63 ± 1.09% at 60 s to 1.20 ± 2.40% at 100 s. These results are discussed in terms of the hypothesis that carbachol may act on the sympathetic fibers on the pial arteries by a nonmuscarinic mechanism to reduce the liberation of the transmitter.


Stroke ◽  
1981 ◽  
Vol 12 (4) ◽  
pp. 528-531 ◽  
Author(s):  
L M Auer ◽  
B B Johansson ◽  
S Lund

1985 ◽  
Vol 5 (4) ◽  
pp. 517-522 ◽  
Author(s):  
Ludwig M. Auer ◽  
Klaus Leber ◽  
Ichiro Sayama

The effect of serotonin (5-HT) and its antagonist ketanserin on the cerebral circulation was investigated in two series totaling 24 cats using the cranial window technique. 5-HT elicited a marked dilatation of small pial arteries, whereas large arteries tended to constrict. Intravenous administration of ketanserin reversed the constriction of large arteries, causing dilatation, and reduced the extent of small arteries' dilatation. In a randomized study, i.v. administration of ketanserin in its solvent versus the solvent alone revealed a strong dilatatory effect of the solvent on pial arteries (17 ± 1.8%), which partly jeopardized a possible constrictory effect of ketanserin, as ketanserin plus solvent induced less dilatation of small pial arteries than the solvent alone. The present data support the view that serotonin exerts a dual effect on cerebral arteries, namely, dilatation of small and constriction of large vessels. The antagonist ketanserin reverses this effect, but the strong dilatatory effect of the solvent alone masks the antiserotoninergic effect.


1986 ◽  
Vol 250 (4) ◽  
pp. C547-C556 ◽  
Author(s):  
W. J. Stekiel ◽  
S. J. Contney ◽  
J. H. Lombard

Comparative measurements of transmembrane potential (Em) were made in situ in vascular smooth muscle cells (VSM) of mesenteric small principal arteries and veins with innervation and circulation intact. Vessels were in an externalized, topically suffused jejunal loop in 4- to 5-wk-old (initial hypertension) and 12- to 15-wk-old (established hypertension) anesthetized, spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive control rats. Comparable in vitro measurements of Em were also made in VSM of isolated intact small mesenteric vessel segments (from the 12- to 15-wk-old animals) maintained at their in situ lengths and suffused with physiological salt solution (PSS). During suffusion in situ with control PSS, VSM of both small veins and arteries in older (but not younger)SHR were less polarized than in WKY. Local chemical sympathetic denervation in situ (with 6-hydroxydopamine) hyperpolarized VSM of both vessel types in older (but not younger) SHR to the same Em levels measured in situ in respective WKY vessels. After local denervation, VSM of small arteries (but not veins) of both SHR and WKY remained less polarized in situ than in vitro, suggesting the presence of one or more circulating factors with a specific depolarizing action on the arterial side in both animal types. In vitro, VSM of both small arteries and veins from WKY but not SHR were depolarized immediately by 10(-3) M ouabain. In contrast, reduction of the PSS suffusate temperature to 16 degrees C caused a significantly greater depolarization in VSM of SHR vessels.(ABSTRACT TRUNCATED AT 250 WORDS)


2000 ◽  
Vol 279 (3) ◽  
pp. H1208-H1214 ◽  
Author(s):  
M. T. Littleton-Kearney ◽  
D. M. Agnew ◽  
R. J. Traystman ◽  
P. D. Hurn

We tested the hypothesis that intracarotid estrogen infusion increases cerebral blood flow (CBF) in a concentration-dependent manner and direct application of estrogen on pial arterioles yields estrogen receptor-mediated vasodilation. Rabbits of both genders were infused with estrogen via a branch of the carotid artery. Estrogen doses of 20 or 0.05 μg · ml−1 · min−1 were used to achieve supraphysiological or physiological plasma estrogen levels, respectively. CBF and cerebral vascular resistance were determined at baseline, during the infusion, and 60-min postinfusion, and effects on pial diameter were assessed via a cranial window. Pial arteriolar response to estrogen alone and to estrogen after administration of tamoxifen (10−7), an antiestrogen drug that binds to both known estrogen receptor subtypes, was tested. No gender differences were observed; therefore, data were combined for both males and females. Systemic estrogen infusion did not increase regional CBF. Estradiol dilated pial arteries only at concentrations ranging from 10−4–10−7 M ( P ≤ 0.05). Pretreatment with tamoxifen alone had no effect on arteriolar diameter but inhibited estrogen-induced vasodilation ( P < 0.001). Our data suggest that estrogen does not increase CBF under steady-state conditions in rabbits. In the pial circulation, topically applied estradiol at micromolar concentrations dilates vessels. The onset is rapid and dependent on estrogen receptor activation.


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