P2 purinoceptor-mediated dilations in the rat middle cerebral artery after ischemia-reperfusion

1999 ◽  
Vol 276 (1) ◽  
pp. H33-H41 ◽  
Author(s):  
Sean P. Marrelli ◽  
Andrei Khorovets ◽  
T. David Johnson ◽  
William F. Childres ◽  
Robert M. Bryan
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Potassium Channels ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Ischemia Reperfusion ◽  
Cerebral Arteries ◽  
Receptor System ◽  
Middle Cerebral Arteries ◽  
Calcium Activated Potassium Channels

Endothelial-mediated dilations to selective P2Y1 and P2Y2 purinoceptor agonists [2-methylthioadenosine triphosphate (2MeS-ATP) and uridine 5′-triphosphate (UTP), respectively] were evaluated in middle cerebral arteries (MCAs) of rats after 2 h of ischemia followed by 24 h of reperfusion (I/R). MCAs were harvested, pressurized to 85 mmHg, and luminally perfused. 2MeS-ATP, which dilates by the synthesis and release of nitric oxide (NO), had significantly reduced maximum dilations following I/R. Reduced smooth muscle sensitivity to NO may explain the reduced dilation to 2MeS-ATP. In contrast, the dilations elicited by UTP were potentiated in that the concentration of agonist necessary to produce one-half of the maximum dilation was reduced by 75%. The potentiated dilation to UTP was the result of an endothelial factor having all the characteristics of the endothelium-derived hyperpolarizing factor (EDHF). That is, it was neither NO nor a cyclooxygenase metabolite, and its actions involved calcium-activated potassium channels and smooth muscle hyperpolarization. We conclude that the effect of I/R on endothelial-mediated dilations depends on the receptor system and the mechanism of dilation. Dilations elicited by 2MeS-ATP were attenuated, while dilations UTP were potentiated due to the upregulation of the EDHF mechanism.

Stimulation of α2Adrenoceptors Dilates the Rat Middle Cerebral Artery

1996 ◽  
Vol 85 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Robert M. Bryan ◽  
M. Y. Eichler ◽  
M. W. G. Swafford ◽  
T. D. Johnson ◽  
M. S. Suresh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Pertussis Toxin ◽  
Saline Solution ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries ◽  
Physiologic Saline ◽  
Stimulation Of

Background Because alpha 2 adrenoceptor agonists are used as adjuncts to anesthetics, their effects on the cerebrovascular circulation are of prime importance. We studied changes in the diameter of rat middle cerebral arteries after stimulation of alpha 2 adrenoceptors with UK14,304. Methods Rat middle cerebral arteries were isolated, cannulated at each end with a glass micropipette, and pressurized to 85 mmHg. The middle cerebral arteries were immersed in a bath (37 degrees C) containing physiologic saline solution, and luminally perfused with physiologic saline solution (100 microliters/ min). Changes in vessel diameter were measured after magnification with a microscope. Results Resting diameter of the middle cerebral arteries was 239 +/- 13 microns (n = 8) for the first study. A dose-dependent dilation was produced by addition of UK14,304 to the extraluminal bath; a 10-15% increase in diameter occurred at a concentration of 10(-4)M. The dilations produced by UK14,304 were blocked with selective alpha 2-antagonists, idazoxan and rauwolscine, but not by the selective alpha 1-antagonist, prazosin. The dilations could be blocked by removal of the endothelium, or the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (10(-5) M). The inhibitory effects of N-nitro-L-arginine methyl ester were reversed with the addition of 10(-3) M L-arginine, but not 10(-3) M D-arginine. Furthermore the dilation produced by UK14,304 was completely abolished with pertussis toxin (100 ng/ml). Conclusions It was concluded that the stimulation of alpha 2 adrenoceptors with UK14,304 produced a dilation in the rat middle cerebral artery that (1) was dependent on intact endothelium, (2) involved nitric oxide, and (3) acted via a pertussis toxin-sensitive G protein.

Veränderungen zerebrovaskulärer Perfusionsindices nach Karotis-Thrombendarterektomie

VASA ◽  
1999 ◽  
Vol 28 (4) ◽  
pp. 279-282 ◽  
Author(s):  
Müller ◽  
Behnke ◽  
Walter
Keyword(s):  
Middle Cerebral Artery ◽  
Carotid Endarterectomy ◽  
Cerebral Artery ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Transcranial Doppler Ultrasound ◽  
Blood Velocity ◽  
Hyperperfusion Syndrome ◽  
Middle Cerebral Arteries ◽  
Patients At Risk

Background: To study the pattern of cerebral blood flow velocity and cerebral resistance changes after carotid endarterectomy. Patients and methods: In 81 patients (mean age ± SD, 64 ± 8 years) with unilateral carotid endarterectomy (CEA) the systolic, diastolic and mean blood velocities, and the pulsatility index (PI) were recorded in both middle cerebral arteries preoperatively and repetitively postoperatively with the use of transcranial Doppler ultrasound (TCD). Results: In the middle cerebral artery ipsilateral to CEA mean blood velocity was increased 6 hours (64 ± 25 cm/sec; p < 0.005) and 7 days (54 ± 15 cm/sec; p < 0.05) after CEA and had returned to the preoperative level (49 ± 11 cm/sec) after 3 months. Compared to preoperatively (0.86 ±. 22), the PI was significantly increased at 6 hours examination (1.03 ±. 23, p < 0.005), and remained increased thereafter. A pathologically increased mean blood velocity (> 83 cm/sec) 6 hours after CEA occurred in 11 patients, two of them developed a slight hyperperfusion syndrome. In the contralateral middle cerebral artery, only the diastolic blood velocity showed significant changes (preoperatively, 35 ± 12 cm/sec; 3 months after CEA, 33 ± 8 cm/sec; p < 0.05). Conclusions: Using TCD, hemodynamic changes occur predominantly in the middle cerebral arteries ipsilateral to CEA. Early postoperative TCD studies may be of help to identify patients at risk to develop a hyperperfusion syndrome.

scholarly journals Investigation of Postmortem Functional Changes in Human Cerebral Arteries

1993 ◽  
Vol 13 (2) ◽  
pp. 346-349 ◽  
Author(s):  
Hisashi Onoue ◽  
Nobuyoshi Kaito ◽  
Shogo Tokudome ◽  
Toshiaki Abe ◽  
Koichi Tashibu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Vascular Endothelium ◽  
Cerebral Arteries ◽  
Time Dependent ◽  
Functional Changes ◽  
Human Cadavers

This study demonstrated the time-dependent changes in postmortem responses of isolated human middle cerebral artery strips to vasodilators. The relaxation induced by prostaglandin (PG) I2 or nitroglycerin remained stable for 24 h postmortem. In arterial strips precontracted with PGF2α, substance P and bradykinin both elicited relaxation that was almost completely abolished by removal of the endothelium. The endothelium-dependent response to both peptides was significantly degraded in strips obtained >12 h postmortem. These results indicate a selective functional or anatomical vulnerability of the vascular endothelium compared with that of the vasodilator mechanisms of the smooth muscle in the postmortem period. However, cerebral arteries isolated from human cadavers within 12 h postmortem should be adequate for studies of both smooth muscle and endothelial reactivity to vasodilators.

scholarly journals Cerebral haemodynamics in early puerperium: A prospective study

Ultrasound ◽  
2017 ◽  
Vol 25 (2) ◽  
pp. 107-114 ◽  
Author(s):  
GP Anzola ◽  
R Brighenti ◽  
M Cobelli ◽  
A Giossi ◽  
S Mazzucco ◽  
...  
Keyword(s):  
Prospective Study ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Velocity Ratio ◽  
Mean Flow ◽  
Middle Cerebral Arteries ◽  
A Prospective Study ◽  
Mean Flow Velocity

Aim Prospective study on 900 consecutive puerperae to assess normal values and range of the blood flow velocity in the middle cerebral artery in both hemispheres. Material and method M1 and M2 segments of both middle cerebral arteries were assessed in all subjects within 96 hours of delivery. Mean flow velocity was recorded after adjusting for insonation angle. Lindegaard index (LI = middle cerebral artery–Internal Carotid Artery mean flow velocity ratio) was calculated whenever the mean flow velocity exceeded 100 cm/second. Asymmetry indexes were calculated inter hemispherically for M1 and M2 segments separately. Results Mean flow velocities were 74 ± 17 and 72 ± 17 in right and 73 ± 17 and 72 ± 17 cm/second in the left M1 and M2, respectively. A total of 136 subjects (12.1%) exceeded the threshold of 100 cm/second, but LI was consistently <3 in all of them. Mean flow velocity was inversely and independently correlated to haemoglobin levels and to parity. Mean asymmetry indexes were 0.25 ± 23 in M1 and 0.45 ± 25 in M2. Conclusion Mean flow velocity in the middle cerebral artery of healthy subjects in early puerperium is higher than in age-matched non-puerperal women and may exceed the threshold of 100 cm/second with no evidence of intracranial spasm, because of blood loss during delivery. Mean flow velocity is independently correlated with parity. Right-to-left mean flow velocity asymmetry may reach 50% as a consequence of a transient imbalance in vascular tone regulation.

Mechanisms underlying epithelium-dependent relaxation in rat bronchioles: analogy to EDHF-type relaxation in rat pulmonary arteries

2010 ◽  
Vol 298 (4) ◽  
pp. L531-L542 ◽  
Author(s):  
Christel Kroigaard ◽  
Thomas Dalsgaard ◽  
Ulf Simonsen
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Potassium Channels ◽  
Pulmonary Arteries ◽  
Muscle Layer ◽  
Functional Studies ◽  
Adrenoceptor Agonist ◽  
Calcium Activated Potassium Channels ◽  
Oxide Synthase

This study investigated the mechanisms underlying epithelium-derived hyperpolarizing factor (EpDHF)-type relaxation in rat bronchioles. Immunohistochemistry was performed, and rat bronchioles and pulmonary arteries were mounted in microvascular myographs for functional studies. An opener of small (SKCa) and intermediate (IKCa)-conductance calcium-activated potassium channels, NS309 (6,7-dichloro-1H-indole-2,3-dione 3-oxime) was used to induce EpDHF-type relaxation. IKCa and SKCa3 positive immunoreactions were observed mainly in the epithelium and endothelium of bronchioles and arteries, respectively. In 5-hydroxytryptamine (1 μM)-contracted bronchioles (828 ± 20 μm, n = 84) and U46619 (0.03 μM)-contracted arteries (720 ± 24 μm, n = 68), NS309 (0.001–10 μM) induced concentration-dependent relaxations that were reduced by epithelium/endothelium removal and by blocking IKCa channels with charybdotoxin and in bronchioles also by blocking SKCa channels with apamin. Inhibition of cyclooxygenase, nitric oxide synthase, and cytochrome 2C isoenzymes, or blockade of large (BKCa)-conductance calcium-activated potassium channels with iberiotoxin, failed to reduce NS309 relaxation. In contrast to the pulmonary arteries, relaxations to a β2-adrenoceptor agonist, salbutamol, were reduced in bronchioles by removing the epithelium or blocking IKCa and/or SKCa channels. Extracellular K+ (2–20 mM) induced relaxation in both bronchioles and arteries. An inhibitor of Na+-K+-ATPase, ouabain, abolished relaxations to NS309, salbutamol, and K+. These results suggest that IKCa and SKCa3 channels are located in the epithelium of bronchioles and endothelium of pulmonary arteries. Analog to the endothelium-derived hyperpolarizing factor (EDHF)-type relaxation in pulmonary arteries, these channels may be involved in EpDHF-type relaxation of bronchioles caused by epithelial K+ efflux followed by activation of Na+-K+-ATPase in the underlying smooth muscle layer.

Clinical and Radiological Features of Patients With Aplastic or Twiglike Middle Cerebral Arteries

Neurosurgery ◽  
2011 ◽  
Vol 70 (6) ◽  
pp. 1472-1480 ◽  
Author(s):  
Byung-Sun Seo ◽  
Yoon-Soo Lee ◽  
Hyuk-Gee Lee ◽  
Jeong-Ho Lee ◽  
Kee-Young Ryu ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Clinical Manifestations ◽  
Radiological Features ◽  
Middle Cerebral Arteries ◽  
Indirect Revascularization ◽  
Surgical Treatments ◽  
Normal Embryonic Development ◽  
Arterial Anomalies

Abstract BACKGROUND: An aplastic or twiglike middle cerebral artery (Ap/T-MCA) is an extremely rare congenital anomaly related to interference in the normal embryonic development of the MCA. OBJECTIVE: To evaluate the clinical and radiological features of patients with an Ap/T-MCA. METHODS: A total of 1749 conventional cerebral angiography procedures were performed in 1282 patients from January 2005 to July 2011 at Daegu Fatima Hospital. The images were evaluated for cerebral arterial anomalies. The radiological features of an Ap/T-MCA, coexisting anomalies, and clinical manifestations were recorded. These prospectively maintained databases were analyzed retrospectively. RESULTS: Ap/T-MCAs were found in 15 patients (1.17% angiographic incidence). The anomalies were confined to unilateral M1 segment, and no stenoses were seen in the adjacent major arteries. Of 15 patients, 6 (40%) had hemorrhagic strokes, 5 (33.3%) had ischemic strokes, and 4 (26.7%) had no symptoms. Aneurysms were found in 5 patients (33.3%). Coexisting cerebral arterial anomalies were seen in 12 patients (80%). Ten patients underwent conservative treatments, and the remaining 5 underwent surgical treatments, such as hematoma aspiration, indirect revascularization, and clipping or coiling of aneurysms. CONCLUSION: An Ap/T-MCA is a rare anomaly and should be differentiated from moyamoya conditions and degenerative steno-occlusive diseases of the middle cerebral artery. Coexisting anomalies of the anterior or middle cerebral arteries are frequent. This anomaly is vulnerable to both hemorrhagic and ischemic strokes.

scholarly journals Impaired Vascular Reactivity of Isolated Rat Middle Cerebral Artery after Cortical Spreading Depression in Vivo

2004 ◽  
Vol 24 (5) ◽  
pp. 526-530 ◽  
Author(s):  
Iris Seitz ◽  
Ulrich Dirnagl ◽  
Ute Lindauer
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cortical Spreading Depression ◽  
Vascular Reactivity ◽  
Spreading Depression ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Middle Cerebral Arteries ◽  
Isolated Rat

Cortical spreading depression (CSD) is accompanied by hyperemia followed by long-lasting hypoperfusion and impaired cerebrovascular reactivity. The authors show that vasodilation to extraluminal acidosis (pH 7.0) and increased concentrations of extraluminal potassium (12, 20, 40 mmol/L) was significantly reduced in isolated rat middle cerebral arteries after CSD in vivo before the artery was isolated, compared with sham-operated controls. Application of 80-mmol/L potassium induced vasoconstriction after CSD. Therefore, the impairment of vascular reactivity after CSD in vivo occurs, at least in part, at the vascular level itself.

scholarly journals Responses of Isolated Feline and Human Cerebral Arteries to Prostacyclin and Some of its Metabolites

1983 ◽  
Vol 3 (2) ◽  
pp. 238-245 ◽  
Author(s):  
Tore Uski ◽  
Karl-Erik Andersson ◽  
Lennart Brandt ◽  
Lars Edvinsson ◽  
Bengt Ljunggren
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Species Differences ◽  
Cerebral Arteries ◽  
Pial Arteries ◽  
Contractile Effect ◽  
Resting Tension ◽  
As Species ◽  
Middle Cerebral Arteries

The effects of prostacyclin (PGI2) were studied in isolated cat basilar and middle cerebral arteries and in human pial arteries. In feline vessels with low resting tension, PGI2 had a contractile effect that reached a maximum of 132% (basilar artery) and 23% (middle cerebral artery) of the potassium-induced (127 m M) contraction. In potassium-contracted feline vessels, PGI2 caused a further contraction. When these vessels were contracted by PGF2α, PGI2 induced relaxation, which was most marked in the middle cerebral artery. PGI2 consistently relaxed the middle cerebral artery contracted by the prostaglandin endoperoxide analogue U-44069, whereas the basilar artery was almost unaffected. In human pial arteries with low resting tension, PGI2 had no effects in concentrations below 10−6 M, whereas higher concentrations induced contractions. In potassium-contracted (35 or 127 m M) preparations, PGI2 in concentrations below 10−6 M produced relaxation; in higher concentrations further contraction was induced. Human pial arteries contracted by PGF2α, U-44069, noradrenaline, or 5-hydroxytryptamine consistently relaxed in response to PGI2 (< 10−6 M). The PGI2 metabolite 6-keto-PGE1 had effects similar to those of PGI2, but proved to be less potent on human pial vessels. 6-Keto-PGF1α was ineffective, whereas 6, 15-diketo-PGF1α had minor relaxant effects. The results suggest that consideration must be given to regional as well as species differences concerning the cerebrovascular effects of PGI2.

scholarly journals Neuropeptide Y—Mediated Constriction and Dilation in Rat Middle Cerebral Arteries

2001 ◽  
Vol 21 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Junping You ◽  
Lars Edvinsson ◽  
Robert M. Bryan
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Neuropeptide Y ◽  
Cerebral Arteries ◽  
Npy Receptor ◽  
Middle Cerebral Arteries ◽  
Oxide Synthase ◽  
Npy Receptors ◽  
Stimulation Of

Neuropeptide Y (NPY) is an important vasoconstrictor in the cerebral circulation. Its constrictor response is because of activation of NPY receptors on the vascular smooth muscle (VSM). Little is known regarding the effects of NPY on the endothelium. In the current study, the authors tested the hypothesis that NPY can either constrict or dilate rat middle cerebral arteries (MCAs). Constriction is elicited by stimulating receptors on the VSM; dilation is elicited by stimulating receptors on the endothelium. Middle cerebral arteries were isolated, cannulated with micropipettes, pressurized to 85 mm Hg, and luminally perfused. The extraluminal application of NPY (mixed agonist), [Leu31, Pro34]-NPY (Y1 agonist), or NPY-[13–36] (Y2 agonist) produced concentration-dependent constrictions. BIBP 3226 (Y1 selective antagonist) significantly attenuated the NPY-and [Leu31, Pro34]-NPY–induced constrictions. The luminal application of NPY, [Leu31, Pro34]-NPY, and NPY-[13–36] produced concentration-dependent dilations of MCAs. The maximum dilation produced by the NPY receptor agonists was approximately 40% of the dilation elicited by the luminal administration of 10−5 mol/L ATP. Dilations elicited by luminal NPY, [Leu31, Pro34]-NPY, or NPY-[13–36] were abolished by inhibition of nitric oxide synthase with 10−5 mol/L Nω-nitro-L-arginine methyl ester (L-NAME) or removal of the endothelium. Dilations produced by luminal NPY or luminal [Leu31, Pro34]-NPY were not affected by BIBP 3226. Stimulation of NPY receptors on vascular smooth muscle constricted MCAs. Stimulation of an NPY receptor other than the Y1 subtype on endothelium dilated the MCAs by releasing nitric oxide.

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