scholarly journals Hyperperfusion Counteracted by Transient Rapid Vasoconstriction Followed by Long-Lasting Oligemia Induced by Cortical Spreading Depression in Anesthetized Mice

2015 ◽  
Vol 35 (4) ◽  
pp. 689-698 ◽  
Author(s):  
Miyuki Unekawa ◽  
Yutaka Tomita ◽  
Haruki Toriumi ◽  
Takashi Osada ◽  
Kazuto Masamoto ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Regional Cerebral Blood Flow ◽  
Considerable Increase ◽  
Spreading Depression ◽  
Mean Transit Time ◽  
Regional Cerebral Blood ◽  
Pial Arteries ◽  
Cortical Capillaries ◽  
Arterial Constriction ◽  
Doppler Flowmeter

Cortical spreading depression (CSD) involves mass depolarization of neurons and glial cells accompanied with changes in regional cerebral blood flow (rCBF) and energy metabolism. To further understand the mechanisms of CBF response, we examined the temporal diametric changes in pial arteries, pial veins, and cortical capillaries. In urethane-anesthetized mice, the diameters of these vessels were measured while simultaneously recording rCBF with a laser Doppler flowmeter. We observed a considerable increase in rCBF during depolarization in CSD induced by application of KCl, accompanied by a transient dip of rCBF with marked vasoconstriction of pial arteries, which resembled the response to pin-prick-induced CSD. Arterial constriction diminished or disappeared during the second and third passages of CSD, whereas the rCBF increase was maintained without a transient dip. Long-lasting oligemia with a decrease in the reciprocal of mean transit time of injected dye and mild constriction of pial arteries was observed after several passages of the CSD wave. These results indicate that CSD-induced rCBF changes consist of initial hyperemia with a transient dip and followed by a long-lasting oligemia, partially corresponding to the diametric changes of pial arteries, and further suggest that vessels other than pial arteries, such as intracortical vessels, are involved.

scholarly journals Dynamic diameter response of intraparenchymal penetrating arteries during cortical spreading depression and elimination of vasoreactivity to hypercapnia in anesthetized mice

2016 ◽  
Vol 37 (2) ◽  
pp. 657-670 ◽  
Author(s):  
Miyuki Unekawa ◽  
Yutaka Tomita ◽  
Kazuto Masamoto ◽  
Haruki Toriumi ◽  
Takashi Osada ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cortical Spreading Depression ◽  
Regional Cerebral Blood Flow ◽  
Spreading Depression ◽  
Regional Cerebral Blood ◽  
Basal Diameter ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Dynamic Diameter ◽  
Current Potential

Cortical spreading depression (CSD) induces marked hyperemia with a transient decrease of regional cerebral blood flow (rCBF), followed by sustained oligemia. To further understand the microcirculatory mechanisms associated with CSD, we examined the temporal changes of diameter of intraparenchymal penetrating arteries during CSD. In urethane-anesthetized mice, the diameter of single penetrating arteries at three depths was measured using two-photon microscopy during passage of repeated CSD, with continuous recordings of direct current potential and rCBF. The first CSD elicited marked constriction superimposed on the upstrokes of profound dilation throughout each depth of the penetrating artery, and the vasoreaction temporally corresponded to the change of rCBF. Second or later CSD elicited marked dilation with little or no constriction phase throughout each depth, and the vasodilation also temporally corresponded to the increase of rCBF. Furthermore, the peak dilation showed good negative correlations with basal diameter and increase of rCBF. Vasodilation induced by 5% CO2 inhalation was significantly suppressed after CSD passage at any depth as well as hyperperfusion. These results may indicate that CSD-induced rCBF changes mainly reflect the diametric changes of the intraparenchymal arteries, despite the elimination of responsiveness to hypercapnia.

scholarly journals Noradrenergic Agonists and Antagonists Influence Migration of Cortical Spreading Depression in Rat—a Possible Mechanism of Migraine Prophylaxis and Prevention of Postischemic Neuronal Damage

2005 ◽  
Vol 25 (9) ◽  
pp. 1225-1235 ◽  
Author(s):  
Frank Richter ◽  
Oskar Mikulik ◽  
Andrea Ebersberger ◽  
Hans-Georg Schaible
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Neuronal Damage ◽  
Regional Cerebral Blood ◽  
Adrenergic Agonist ◽  
Adult Rats ◽  
Arterial Blood ◽  
Β Blocker ◽  
Β Receptor ◽  
Focal Brain Ischemia

Cortical spreading depression (CSD) is thought to be a neuronal mechanism that expands the penumbra zone after focal brain ischemia and that causes migraine aura. Both adrenergic agonists and antagonists significantly influence the size of the penumbra zone and decline the frequency of migraine. To study whether these compounds act by influencing CSD, we applied different drugs topically to an area of the exposed cortex of anesthetized adult rats and observed the migration of CSD-related DC potential deflections across the treated area. The adrenergic agonist norepinephrine (1 mmol/L) and the α2-agonist clonidine (0.56 mmol/L) blocked reversibly the migration of CSD. The β-blocker propranolol (250 μmol/L to 1 mmol/L) dose-dependently diminished migration velocity or even blocked migration of CSD. The CSD blockade by the α2-antagonist yohimbine (1.75 mmol/L) was because of its action on inhibitory 5-HT1A receptors. None of the substances in the concentrations used had influence on regional cerebral blood flow or on systemic arterial blood pressure. The data suggest that the interference of these compounds with CSD may contribute to their beneficial therapeutic effect. The effect of β-receptor antagonists in human migraine needs further exploration, since these drugs also work in migraine without aura.

scholarly journals Interrelationships Among Regional Cerebral Blood Flow, Mean Transit Time, Vascular Volume and Cerebral Vascular Resistance

Stroke ◽  
1974 ◽  
Vol 5 (6) ◽  
pp. 719-724 ◽  
Author(s):  
YOSHIHIRO KURIYAMA ◽  
TAKASHI AOYAMA ◽  
KUNIHIKO TADA ◽  
SHOTARO YONEDA ◽  
TADAATSU NUKADA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Transit Time ◽  
Regional Cerebral Blood Flow ◽  
Mean Transit Time ◽  
Regional Cerebral Blood ◽  
Vascular Volume ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Effects of Repeated Temporary Clipping of the Middle Cerebral Artery on Pial Arterial Diameter, Regional Cerebral Blood Flow, and Brain Structure in Cats

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 914-920 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Shigeru Tsunoda ◽  
Tetsuya Morimoto ◽  
Taiji Ishida ◽  
Yasunori Sasaoka
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Edema ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Arterial Diameter ◽  
Pial Arteries ◽  
Temporary Clipping

Abstract Temporary clipping of the major arterial trunk is an important maneuver to control excessive unexpected bleeding in neurosurgical operations; however, repeated temporary clipping can give rise to severe neurological deficits after surgery. The present study was performed to confirm and explain these clinical findings. Initially, a single 20-minute or 1-hour occlusion of the middle cerebral artery was performed in each of 5 cats. Pial arterial diameter was determined by video imaging, regional cerebral blood flow was measured by autoradiography, and cerebral edema and infarction were observed. In the 20-minute occlusion group, no abnormal changes were found 5 hours after recirculation. In the 1-hour occlusion group, pial arteries were dilated by 45%, and regional cerebral blood flow increased to more than twice the resting cortical values. The extent of cerebral edema was 41.2 ± 7.5% (SE) and infarction was 34.5 ± 9.5% (SE) of the hemisphere. In the second experiment, three 20-minute occlusions of the middle cerebral artery in a 1-hour interval were performed in 20 cats. In 10 of them, thiopental (40 mg/kg) was used to protect the brain. In the group without barbiturate treatment, pial arteries were dilated by 40% at the end of experiment, regional cerebral blood flow decreased to about 70% compared with single 20-minute occlusion, cerebral edema was 19.5 ± 8.1% (SE), and infarction was 8.1 ± 3.7% (SE) of the hemisphere. In the treated group, these were only trivial changes. The effect of repeated clipping may cumulatively cause brain damage, and barbiturates should be used whenever repeated clipping is necessary.

Effects of Nitrous Oxide on Human Regional Cerebral Blood Flow and Isolated Pial Arteries

1994 ◽  
Vol 81 (2) ◽  
pp. 396-402 ◽  
Author(s):  
Peter Reinstrup ◽  
Erik Ryding ◽  
Lars Algotsson ◽  
Leif Berntman ◽  
Tore Uski
Keyword(s):  
Blood Flow ◽  
Nitrous Oxide ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Pial Arteries

rCBF After Tia and during Migraine Attacks

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 43-46 ◽  
Author(s):  
Jes Olesen ◽  
Sissel Vorstrup ◽  
Martin Lauritzen
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Cerebral Blood Flow ◽  
Carotid Stenosis ◽  
Regional Cerebral Blood Flow ◽  
Spreading Depression ◽  
Cerebral Damage ◽  
Regional Cerebral Blood ◽  
Flow Changes ◽  
Ct Studies

TIA is usually caused by embolism from a carotid stenosis. The stenosis has no hemodynamic significance, but recent studies of regional cerebral blood flow have indicated that this occurs in a few cases. Traditionally, TIA are not considered to cause cerebral damage, but CT-studies have revealed a number of silent infarcts and rCBF measurements have shown even more persistent abnormalities of blood flow. In classic migraine, alterations of rCBF are completely different, indicating a mechanism progressing in the cerebral cortex, probably the spreading depression of Leao. Similar blood flow changes are not seen in common migraine, where tomographic rCBF determinations have been normal.

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