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.

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.

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.

Nitric oxide-synthesizing perivascular nerves in the rat middle cerebral artery

1997 ◽  
Vol 273 (2) ◽  
pp. R661-R668 ◽  
Author(s):  
C. S. Ignacio ◽  
P. E. Curling ◽  
W. F. Childres ◽  
R. M. Bryan
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries ◽  
Nerve Bundles ◽  
Perivascular Nerves ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Ethmoidal Foramen ◽  
Active Precursor

Although perivascular nerves containing nitric oxide synthase (NOS) have been anatomically described for rat cerebral arteries, a dilator function for these nerves has eluded investigators when using isolated vessels. Rat middle cerebral arteries (MCAs) were isolated, pressurized, and electrically stimulated. The resting diameter of the MCAs after pressurization was 233 +/- 4 microns (n = 17) in one study. The MCAs showed a frequency-dependent dilation when stimulated. Maximum dilation (25-30% increase in diameter) occurred at a frequency of 8-16 Hz. Removal of endothelium or glibenclamide (10(-5) M), a blocker of ATP-sensitive potassium channels, had no effect on the dilations. The dilations were completely blocked with NG-nitro-L-arginine methyl ester (L-NAME) (10(-5) M), a general NOS inhibitor, and cold storage (24 h). The inhibition by L-NAME could be reversed by the addition of 10(-8) M L-arginine, the active precursor of NOS. Furthermore, 7-nitroindazole (10(-4) M), an inhibitor specific for the neuronal isoform of NOS, reduced the dilations by 43% (P < 0.05). Transections of nerve bundles originating from the sphenopalatine ganglia at the ethmoidal foramen blocked the dilations produced by electrical stimulations. We conclude that rat cerebral arteries have functionally intact perivascular nerves that dilate by releasing nitric oxide.

Endothelial-mediated dilations of rat middle cerebral arteries by ATP and ADP

1997 ◽  
Vol 273 (3) ◽  
pp. H1472-H1477 ◽  
Author(s):  
J. You ◽  
T. D. Johnson ◽  
W. F. Childres ◽  
R. M. Bryan
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Cerebral Arteries ◽  
Nitric Oxide Synthase Inhibitor ◽  
Middle Cerebral Arteries ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Maximum Removal

The hypothesis that ATP and ADP produce dilations of rat middle cerebral arteries (MCAs) by different mechanisms was tested. Vessel diameters were measured from pressurized, perfused MCAs after application of different agonists. The luminal administration of ATP and ADP elicited concentration-dependent dilations (35% maximum). Removal of endothelium abolished the dilation to intraluminal ATP and attenuated the dilation to intraluminal ADP. The dilations to ATP were abolished with N omega-nitro-L-arginine methyl ester (L-NAME; 10 microM), a nitric oxide synthase inhibitor, at ATP concentrations of 1 microM and below. However, at concentrations of 10 microM ATP and above, L-NAME had no effect on the response. The dilations to ADP were attenuated by L-NAME to the same degree as removal of endothelium. The mechanism for dilation by ATP was identical to that of UTP, a selective P2u purinoceptor agonist. The mechanism of dilation by ADP was similar to that of 2-methylthioadenosine 5'-triphosphate, a selective P2y purinoceptor agonist. We conclude that ATP and ADP elicit dilations of rat MCA by different mechanisms. ATP and ADP likely stimulate P2u and P2y purinoceptors, respectively.

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 of endothelial P2Y1- and P2Y2-mediated vasodilatation involve differential [Ca2+]i responses

2001 ◽  
Vol 281 (4) ◽  
pp. H1759-H1766 ◽  
Author(s):  
Sean P. Marrelli
Keyword(s):  
Nitric Oxide ◽  
Simultaneous Measurement ◽  
Cerebral Arteries ◽  
No Synthase ◽  
Fura 2 ◽  
Middle Cerebral Arteries ◽  
Intracellular Ca ◽  
The Difference ◽  
Stimulation Of

The present study was designed to evaluate the role of endothelial intracellular Ca2+ concentration ([Ca2+]i) in the difference between P2Y1- and P2Y2-mediated vasodilatations in cerebral arteries. Rat middle cerebral arteries were cannulated, pressurized, and luminally perfused. The endothelium was selectively loaded with fura 2, a fluorescent Ca2+indicator, for simultaneous measurement of endothelial [Ca2+]i and diameter. Luminal administration of 2-methylthioadenosine 5′-triphosphate (2-MeS-ATP), an endothelial P2Y1 agonist, resulted in purely nitric oxide (NO)-dependent dilation and [Ca2+]i increases up to ∼300 nM (resting [Ca2+]i = 145 nM). UTP, an endothelial P2Y2 agonist, resulted in dilations that were both endothelium-derived hyperpolarizing factor (EDHF)- and NO-dependent with [Ca2+]iincreases to >400 nM. In the presence of N G-nitro-l-arginine-indomethacin to inhibit NO synthase and cyclooxygenase, UTP resulted in an EDHF-dependent dilation alone. The [Ca2+]ithreshold for NO-dependent dilation was 220 vs. 340 nM for EDHF. In summary, the differences in the mechanism of vasodilatation resulting from stimulation of endothelial P2Y1 and P2Y2purinoceptors result in part from differential [Ca2+]i responses. Consistent with this finding, these studies also demonstrate a higher [Ca2+]i threshold for EDHF-dependent responses compared with NO.

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 Estrogen reduces mouse cerebral artery tone through endothelial NOS- and cyclooxygenase-dependent mechanisms

2000 ◽  
Vol 279 (2) ◽  
pp. H511-H519 ◽  
Author(s):  
Greg G. Geary ◽  
Diana N. Krause ◽  
Sue P. Duckles
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Nitric Oxide Synthase ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Estrogen Replacement ◽  
Luminal Diameter ◽  
Small Resistance ◽  
Oxide Synthase

Gender and estrogen status are known to influence the incidence and severity of cerebrovascular disease. The vasoprotective effects of estrogen are thought to include both nitric oxide-dependent and independent mechanisms. Therefore, using small, resistance-sized arteries pressurized in vitro, the present study determined the effect of gender and estrogen status on myogenic reactivity of mouse cerebral arteries. Luminal diameter was measured in middle cerebral artery segments from males and from females that were either untreated, ovariectomized (OVX), or OVX with estrogen replacement (OVX + EST). The maximal passive diameters of arteries from all four groups were similar. In response to increases in transmural pressure, diameters of arteries from males and OVX females were smaller compared with diameters of arteries from either untreated or OVX + EST females. In the presence of N G-nitro-l-arginine methyl ester, artery diameters decreased in all groups, but diameters remained significantly smaller in arteries from males and OVX females compared with untreated and OVX + EST females. After endothelium removal or when inhibition of nitric oxide synthase and cyclooxygenase were combined, differences in diameters of arteries from OVX and OVX + EST were abolished. These data suggest that chronic estrogen treatment modulates myogenic reactivity of mouse cerebral arteries through both endothelium-derived cyclooxygenase- and nitric oxide synthase-dependent mechanisms.

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.

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