Inhibition of the Pial Artery Constriction Induced by Sympathetic Stimulation by Local Microapplication of a Cholinomimetic Agent

R. Sercombe; M. Wahl

doi:10.1038/jcbfm.1982.51

Inhibition of the Pial Artery Constriction Induced by Sympathetic Stimulation by Local Microapplication of a Cholinomimetic Agent

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1982.51 ◽

1982 ◽

Vol 2 (4) ◽

pp. 451-456 ◽

Cited By ~ 5

Author(s):

R. Sercombe ◽

M. Wahl

Keyword(s):

Splitting Method ◽

Sympathetic Stimulation ◽

Pial Surface ◽

Pial Arteries ◽

Pial Artery ◽

Cervical Sympathetic ◽

S Application ◽

Television Image ◽

Stimulation Of

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.

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The response of feline spinal pial arterioles to norepinephrine

Journal of Neurosurgery ◽

10.3171/jns.1980.52.1.0060 ◽

1980 ◽

Vol 52 (1) ◽

pp. 60-63 ◽

Cited By ~ 14

Author(s):

Robert A. Crawford ◽

Peter C. Gregory ◽

Ian R. Griffiths

Keyword(s):

Adrenergic Receptors ◽

Splitting Method ◽

Vessel Diameter ◽

Pial Arteries ◽

Content Type ◽

Sympathetic Control ◽

Adrenergic Blocker ◽

Pial Arterioles ◽

Television Image ◽

The Brain

✓ The effect of norepinephrine on the diameter of feline spinal pial arteries and arterioles was studied by microapplication of the drug to the perivascular environment. Vascular diameter was determined by the television image-splitting method. Application of norepinephrine over the range of 5 × 10−8M to 5 × 10−3M to spinal pial arterioles resulted in constriction of the vessels. The dose-response curve showed a tendency to plateau at concentrations above 5 × 10−5M, with a maximal constriction of 28.8 ± 5.1% at 5 × 10−3M. The reduction in vessel diameter to microapplication of norepinephrine was prevented with the inclusion of an equimolar concentration of the α-adrenergic blocker, phentolamine, in the injectate. The data indicate the presence of α-adrenergic receptors on the smooth muscle of spinal pial arterioles, and it is suggested that the arguments pertaining to the sympathetic control of blood flow in the brain apply also to the spinal cord.

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Role of KATP Channels in the Regulation of Rat Dura and Pia Artery Diameter

Cephalalgia ◽

10.1111/j.1468-2982.2004.00848.x ◽

2005 ◽

Vol 25 (4) ◽

pp. 249-260 ◽

Cited By ~ 16

Author(s):

A Gozalov ◽

KA Petersen ◽

C Mortensen ◽

I Jansen-Olesen ◽

D Klaerke ◽

...

Keyword(s):

Intravenous Infusion ◽

Katp Channels ◽

Organ Bath ◽

Pial Arteries ◽

Cranial Window ◽

Pial Artery ◽

Isolated Arteries

The aim of the present study was to examine the effect of KATP channel openers pinacidil and levcromakalim on rat dural and pial arteries as well as their inhibition by glibenclamide. We used an in-vivo genuine closed cranial window model and an in-vitro organ bath. Glibenclamide alone reduced the dural but not the pial artery diameter compared with controls. Intravenous pinacidil and levcro-makalim induced dural and pial artery dilation that was significantly attenuated by glibenclamide. In the organ bath pinacidil and levcromakalim induced dural and middle cerebral artery relaxation that was significantly attenuated by glibenclamide. In conclusion, KATP channel openers induce increasing diameter/relaxation of dural and pial arteries after intravenous infusion in vivo and on isolated arteries in vitro. Furthermore, dural arteries were more sensitive to KATP channel openers than pial arteries.

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Cotransmission from sympathetic vasoconstrictor neurons to small cutaneous arteries in vivo

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.277.1.h58 ◽

1999 ◽

Vol 277 (1) ◽

pp. H58-H64 ◽

Cited By ~ 14

Author(s):

Judy L. Morris

Keyword(s):

Image Analysis ◽

Electrical Stimulation ◽

Guinea Pig ◽

Neuropeptide Y ◽

Adrenoceptor Antagonist ◽

On Line ◽

Cervical Sympathetic ◽

Cervical Sympathetic Nerve ◽

Stimulation Of

This study has characterized constrictions of small cutaneous arteries in the guinea pig ear in response to electrical stimulation of the cervical sympathetic nerve (SNS) in vivo. Video microscopy and on-line image analysis were used to examine diameter changes of ear arteries (80–140 μm resting diameter) in anesthetized guinea pigs. Trains of 50–300 impulses, but not single pulses or short trains, produced frequency-dependent (2–20 Hz) constrictions. The purinoceptor antagonist suramin (30 μM) greatly reduced constrictions produced by exogenous ATP but did not affect constrictions produced by SNS at 10 Hz or exogenous norepinephrine. The α2-adrenoceptor antagonist yohimbine (1 μM) enhanced the peak amplitude of sympathetic constrictions at lower stimulation frequencies (1–5 Hz). The amplitude of constrictions to SNS at 10 Hz was reduced, and the latency of constrictions was increased by the α1-adrenoceptor antagonist prazosin (1 μM). Constrictions to SNS at 10 Hz remaining after prazosin treatment were reduced in amplitude by dihydroergotamine (2 μM) and were attenuated further by the neuropeptide Y Y1-receptor antagonist 1229U91 (0.3 μM). Thus norepinephrine and neuropeptide Y act as cotransmitters to mediate sympathetic constriction of small ear arteries at higher stimulation frequencies (10 Hz), but ATP does not seem to contribute directly to these constrictions.

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Pial Vascular Behavior during Bilateral and Contralateral Cervical Sympathetic Stimulation

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1986.52 ◽

1986 ◽

Vol 6 (3) ◽

pp. 298-304 ◽

Cited By ~ 16

Author(s):

Ludwig M. Auer ◽

Norio Ishiyama

Keyword(s):

Sympathetic Stimulation ◽

Bilateral Stimulation ◽

Pial Arteries ◽

Vascular Volume ◽

Small Arteries ◽

Contralateral Stimulation ◽

Cranial Window ◽

Cervical Sympathetic ◽

Arteries And Veins ◽

Hydrogen Clearance

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.

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Failure of sympathetic stimulation to affect responsiveness of rabbit polymodal nociceptors

Journal of Neurophysiology ◽

10.1152/jn.1985.54.3.513 ◽

1985 ◽

Vol 54 (3) ◽

pp. 513-519 ◽

Cited By ~ 54

Author(s):

V. K. Shea ◽

E. R. Perl

Keyword(s):

Impulse Activity ◽

Receptive Fields ◽

Testing Temperature ◽

Maximum Temperature ◽

Sympathetic Stimulation ◽

Great Auricular Nerve ◽

C Fibers ◽

Cervical Sympathetic ◽

Polymodal Nociceptor ◽

Stimulation Of

The responses of polymodal nociceptors with unmyelinated (C) fibers of the rabbit's great auricular nerve were examined with and without intermittent stimulation of the ipsilateral cervical sympathetic trunk. The receptive field of each polymodal nociceptor was heated twice in a stepwise manner from 30 to 50 or 55 degrees C in 5 degree C steps. For each unit, one heating trial was a control trial and the other was accompanied by sympathetic stimulation. The order of the control and sympathetic stimulation trials and the maximum testing temperature were varied systematically among the units examined. The initial responses of polymodal nociceptors in the first heating trial in the presence of sympathetic stimulation were similar to the responses of units whose first heating was a control trial. Units whose receptive fields were tested to a maximum temperature of 50 degrees C in the first trial displayed enhanced responses to heat in their second trial (sensitization), while units tested initially to 55 degrees C responded less briskly during their second heating trial (depression). However, the occurrence of sympathetic stimulation in the second heating trials had no apparent effect on the responses to heat of sensitized or depressed elements. Alterations in the numbers of impulses, instantaneous frequency, or pattern of impulse activity of individual units could not be attributed to sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of sympathetically induced vasomotion on tissue-capillary fluid exchange

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00280.2006 ◽

2006 ◽

Vol 291 (4) ◽

pp. H1761-H1767 ◽

Cited By ~ 25

Author(s):

Terumi Sakurai ◽

Naohito Terui

Keyword(s):

Physiological Role ◽

Tissue Perfusion ◽

Fluid Exchange ◽

In Vivo Experiments ◽

Rabbit Ear ◽

Cervical Sympathetic ◽

Capillary Fluid ◽

Stimulation Of

The spontaneous and rhythmic constriction of peripheral arterioles, which is not associated with the cardiac or respiratory cycles, is called vasomotion. Vasomotion is observed in various tissues of various species, but the physiological role of vasomotion has not been clarified because of the difficulty in controlling the appearance of vasomotion in in vivo preparations. We developed a method of controlling vasomotion in in vivo experiments. The electrical stimulation of the cervical sympathetic nerve could reproducibly evoke vasomotion in rabbit ear skin. The frequencies of the evoked vasomotion were 0.04–0.07 Hz, which corresponded to spontaneously occurring vasomotion that has been reported before. Vasomotion was always evoked between 25 and 35°C. At lower than 17°C or higher than 37°C, vasomotion was not evoked. With the use of this method of evoking vasomotion in vivo, the role of vasomotion in tissue perfusion was examined. A tracer (Cr-EDTA) was injected into the ear tissue, and tracer fading was then measured by using a camera. The rates of fading (clearance) of the tracer with vasomotion were significantly greater (1.7 to 8.1 times) than those without vasomotion. These results provided evidence that vasomotion enhanced tissue perfusion.

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Changes in the Permeability of the Salivary Gland Caused by Sympathetic Stimulation and by Catecholamines

The Journal of General Physiology ◽

10.1085/jgp.46.2.225 ◽

1962 ◽

Vol 46 (2) ◽

pp. 225-243 ◽

Cited By ~ 36

Author(s):

K. Martin ◽

A. S. V. Burgen

Keyword(s):

Ultrastructural Change ◽

Submaxillary Gland ◽

Sympathetic Stimulation ◽

Duct System ◽

Free Diffusion ◽

Transfer Rates ◽

Cervical Sympathetic ◽

Molecular Radius ◽

Intercellular Gaps ◽

Stimulation Of

The permeability of the submaxillary gland of cats and dogs has been tested by determining the rates at which non-electrolytes penetrate from the plasma into the saliva. Electrical stimulation of the cervical sympathetic trunk or administration of epinephrine or norepinephrine increases the permeability of the gland enabling glucose (molecular radius, MR = 3.5 Å), sucrose (MR = 4.4 Å), raffinose (MR = 5.6 Å), polyglycol 1000 (MR = 7.2 Å), and polyglycol 1540 (MR = 8.1 Å) to penetrate into the saliva from which they are otherwise excluded. Inulin (MR = 14.7 Å) does not enter the saliva under these circumstances. Analysis of the transfer rates suggests that the molecules diffuse through a pore structure permitting free diffusion for molecules with a radius less than 5.7 Å. Close intraarterial injection of C14-glucose demonstrates that at least part of this permeability is located in the duct system of the gland. Since epinephrine does not enable sucrose to enter the cells of the gland, it appears that penetration from the extracellular space into the saliva occurs by diffusion through intercellular gaps. The characteristics of the permeability allow conclusions as to the localisation and geometry of the ultrastructural change produced.

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Microvascular features that suggest effectors of blood-flow regulation in the brain: Evidence by SEM of corrosion casts of intracerebral vessels

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100158923 ◽

1990 ◽

Vol 48 (3) ◽

pp. 274-275

Author(s):

Enrico D.F. Motti ◽

Hans-Georg Imhof ◽

Gazi M. Yasargil

Keyword(s):

Blood Flow ◽

Perfusion Pressure ◽

Corrosion Casts ◽

Cerebral Microcirculation ◽

Pial Arteries ◽

Random Occurrence ◽

Brain Arteries ◽

Homogeneous Network ◽

The Brain

Physiologists have devoted most attention in the cerebrovascular tree to the arterial side of the circulation which has been subdivided in three levels: 1) major brain arteries which keep microcirculation constant despite changes in perfusion pressure; 2) pial arteries supposed to be effectors regulating microcirculation; 3) intracerebral arteries supposed to be deprived of active cerebral blood flow regulating devices.The morphological search for microvascular effectors in the cerebrovascular bed has been elusive. The opaque substance of the brain confines in vivo investigation to the superficial pial arteries. Most morphologists had to limit their observation to the random occurrence of a favorable site in the practically two-dimensional thickness of diaphanized histological sections. It is then not surprising most investigators of the cerebral microcirculation refer to an homogeneous network of microvessels interposed between arterioles and venules.We have taken advantage of the excellent depth of focus afforded by the scanning electron microscope (SEM) to investigate corrosion casts obtained injecting a range of experimental animals with a modified Batson's acrylic mixture.

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