scholarly journals Reaction of pial arteries and veins to hypercapnia in hypertensive and normotensive rats.

Stroke ◽  
1985 ◽  
Vol 16 (2) ◽  
pp. 320-323 ◽  
Author(s):  
B B Johansson ◽  
L M Auer ◽  
I Sayama
Keyword(s):  
Pial Arteries ◽  
Arteries And Veins

scholarly journals Changes in Cerebral Arterial, Tissue and Venous Oxygenation with Evoked Neural Stimulation: Implications for Hemoglobin-Based Functional Neuroimaging

2009 ◽  
Vol 30 (2) ◽  
pp. 428-439 ◽  
Author(s):  
Alberto L Vazquez ◽  
Mitsuhiro Fukuda ◽  
Michelle L Tasker ◽  
Kazuto Masamoto ◽  
Seong-Gi Kim
Keyword(s):  
Brain Function ◽  
Functional Neuroimaging ◽  
Sensory Stimulation ◽  
Average Diameter ◽  
Neural Stimulation ◽  
Blood Oxygen ◽  
Pial Arteries ◽  
Small Arteries ◽  
Arteries And Veins ◽  
Stimulation Of

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).

scholarly journals Dynamics of pial vessels reactivity after brief cerebral ischemia

2015 ◽  
Vol 14 (1) ◽  
pp. 74-78 ◽  
Author(s):  
O. P. Gorshkova ◽  
M. V. Lensman ◽  
A. I. Artem'eva ◽  
D. P. Dvoretsky
Keyword(s):  
Cerebral Ischemia ◽  
Brain Perfusion ◽  
Artery Occlusion ◽  
Global Cerebral Ischemia ◽  
Pial Arteries ◽  
Pial Vessels ◽  
Transient Global Cerebral Ischemia ◽  
Pial Vessel ◽  
Arteries And Veins

Cerebral blood vessel reactivity is one of the main determinants of final outcome of brain ischemia. Most of studies on the vascular mechanisms of ischemic brain injury, however, focus on the acute changes within ischemic period or several hours after it. Dilatatory capacity of cerebral arterioles (perfusion reservoir) is considered as an important factor of brain perfusion elevation in critical situations.The aim of the present study was to examine the pial vessel reactivity in response to hypercapnia in rats, subjected to transient global cerebral ischemia, at 7, 14 and 21 days after ischemia. Materials and methods. Transient global cerebral ischemia was induced in anesthetized Wistar rats by bilateral common carotid artery occlusion for 12 min with simultaneous controlled hypotension to 45±3 mm Hg, followed by blood reinfusion and recovery from anesthesia. Three different groups of rats were re-anesthetized at 7, 14 or 21 days after ischemia and subjected to microvascular reactivity studies using in vivo video microscopy. Hypercapnia was caused by i.v. injection of acetazolamide. The changes in diameter of pial arteries and veins in response to hypercapnia were measured. Results and discussion. Global cerebral ischemia led to marked decrease in pial vessels (both arteries and veins) reactivity in response to hypercapnia, caused by i.v. injection of acetazolamide. In intact rats, i.v. injection of acetazolamide led to pial arteries dilation and pial veins constriction; in animals subjected to ischemia-reperfuion. the numbers of dilated large arteries and constricted small veins were much less, as well as the extent of arterial dilation. Reactivity changes were observed in all time points studied. Conclusions. Thus, transient global cerebral ischemia cause marked and long lasting (3 weeks) decrease in pial vessel reactivity in response to hypercapnia.

Neuropeptide Y: Immunocytochemical localization to and effect upon feline pial arteries and veins in vitro and in situ

1984 ◽  
Vol 122 (2) ◽  
pp. 155-163 ◽  
Author(s):  
LARS EDVINSSON ◽  
PIERS EMSON ◽  
JAMES McCULLOCH ◽  
KAZUHIKO TATEMOTO ◽  
ROLF UDDMAN
Keyword(s):  
Neuropeptide Y ◽  
Immunocytochemical Localization ◽  
Pial Arteries ◽  
Arteries And Veins

scholarly journals Vasomotor Effects of Neurotransmitters and Modulators on Isolated Human Pial Veins

1987 ◽  
Vol 7 (5) ◽  
pp. 612-618 ◽  
Author(s):  
Jan Erik Hardebo ◽  
Jan Kåhrström ◽  
Christer Owman ◽  
Leif G. Salford
Keyword(s):  
Substance P ◽  
Vasoactive Intestinal Polypeptide ◽  
Adrenergic Receptors ◽  
Calcium Influx ◽  
Free Solution ◽  
Pial Arteries ◽  
Calcitonin Gene ◽  
Lower Maximum ◽  
Arteries And Veins

Vasomotor reactivity of human pial veins, obtained in conjunction with neurosurgical operations, was studied in vitro. The effect of transmitters in nerves previously recognized in these vessels, as well as that of neuromodulators, was characterized. A comparison of these effects with their effects in the nearby pial arteries of the same patients was made. It was found that the veins were equipped with more sensitive α-adrenergic receptors (lower EC50 values) than the arteries. The reverse was found for 5-hydroxytryptamine. Acetylcholine, which causes an endothelium-dependent dilation of pial arteries, contracted the veins despite an apparently intact endothelium. Considering the lower maximum values in veins, responses to histamine, the neuropeptides calcitonin gene-related peptide, bradykinin, and neuropeptide Y; and prostaglandins (PGE1 and PGF2α) were principally the same in the arteries and veins. The dilatory responses to vasoactive intestinal polypeptide and substance P were less pronounced in veins than in arteries. The veins only transiently contracted to a depolarizing potassium solution; calcium influx promotors and inhibitors, as well as calcium-free solution, did not affect the contractile ability of the vein, contrasting to the reactivity of the artery. This clearly indicates that the veins are not substantially dependent upon calcium influx for their acute contractile ability.

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
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.

scholarly journals Reaction of pial arteries and veins to sympathetic stimulation in the cat.

Stroke ◽  
1981 ◽  
Vol 12 (4) ◽  
pp. 528-531 ◽  
Author(s):  
L M Auer ◽  
B B Johansson ◽  
S Lund
Keyword(s):  
Sympathetic Stimulation ◽  
Pial Arteries ◽  
Arteries And Veins

Interaction of histamine with noradrenergic constrictory mechanisms in cat cerebral arteries and veins

1983 ◽  
Vol 61 (7) ◽  
pp. 756-763 ◽  
Author(s):  
Paul M. Gross ◽  
A. Murray Harper ◽  
Graham M. Teasdale
Keyword(s):  
Cerebral Arteries ◽  
Sympathetic Nerves ◽  
Histamine Receptor ◽  
Inhibitory Influence ◽  
Sympathetic Nerve Stimulation ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Arteries And Veins ◽  
Stimulation Of

We examined responses of pial arteries and veins in situ to noradrenergic stimuli in the presence of histamine. Electrical stimulation of sympathetic nerves and perivascular microapplication of norepinephrine in mock cerebrospinal fluid produced constriction of arteries and veins in anesthetized cats. During simultaneous perivascular injection of histamine, these noradrenergic responses were attenuated or reversed. In both arteries and veins, constriction from sympathetic nerve stimulation was prevented by simultaneous application of the histamine receptor agonists, pyridylethylamine (H1) or impromidine (H2), results that suggest interference involving both types of histamine receptors. In arteries, impromidine, but not pyridylethylamine, inhibited constriction resulting from exogenous norepinephrine. Our findings indicate that histamine may have an inhibitory influence, exerted through both receptor types, on noradrenergic mechanisms in cerebral vessels.

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