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At least 19 recordsLinked to original sources
PubMed2006

Reduced pretreatment ipsilateral middle cerebral artery cerebral blood flow is predictive of symptomatic hemorrhage post-intra-arterial thrombolysis in patients with middle cerebral artery occlusion.

BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) can be a devastating complication associated with thrombolytic therapy for acute ischemic stroke. We hypothesized that patients with lower prethrombolysis cerebral blood flow (CBF) were at a higher risk of symptomatic ICH (sICH). METHODS: Twenty-three patients who underwent quantitative CBF assessment with Xenon CT studies for acute stroke before intra-arterial (IA) thrombolysis for a middle cerebral artery (MCA) or internal carotid artery terminus occlusion within 6 hours of symptom onset were studied. Univariate and multivariate analysis were carried out to determine predictors of sICH post-IA thrombolysis. Receiver operating characteristic curves were generated to determine the association between mean ipsilateral CBF and the occurrence of sICH. RESULTS: The mean age of our cohort was 68+/-12 years and a mean National Institutes of Health Stroke Scale (NIHSS) score of 18+/-3. In univariate analysis, patients with higher percent of core infarct, hyperglycemia, and reduced mean ipsilateral CBF were at risk of sICH. In multivariate analysis only mean ipsilateral CBF was associated with higher rates of sICH (odds ratio 1.58; 95% CI, 1.01 to 2.51; P<0.04). The area under the receiver operating characteristic curve was 0.87 (95% CI, 0.76 to 0.97; P<0.005). CONCLUSIONS: Patients with lower pre-IA thrombolysis mean ipsilateral MCA CBF are at significantly higher risk for sICH in the setting of a MCA or carotid terminus occlusion. The threshold identified in this study may be useful for selection of patients with acute MCA occlusions for acute stroke thrombolysis.

Aged↗
PubMed1989

Comparison of the muscarinic receptors in the coronary artery, cerebral artery and atrium of the pig.

The affinity of various muscarinic antagonists for the muscarinic receptors mediating contraction (induced by acetyl-beta-methylcholine) of the isolated pig coronary and basilar artery was determined in order to compare the muscarinic receptor subtype involved in the contractile response of these arteries. In order to identify the muscarinic receptor subtype(s) involved, the affinity of the antagonists for the M2 receptor present in the pig atria was also investigated. The following muscarinic antagonists were used: atropine, pirenzepine, AF-DX 116 (11-2[[2-[(diethylamino)methyl]-1- piperidinyl]acetyl]-5,11-dihydro-6H- pyrido[2,3-b][1,4]benzodiazepin-6-one),4-DAMP(4-diphenylacetoxy-N- methylpiperidine methiodide), HHSiD (hexahydrosiladifenidol), methoctramine (N,N'-bis[6-[(2- methoxybenzyl)amino]hexyl]-1,8-octane-diamine tetrahydrochloride) and ipratropium. The order of affinity of the antagonists with respect to the muscarinic receptor in the coronary artery was clearly different from that for the muscarinic receptor in the basilar artery. The order of affinity established on the basilar artery closely resembled that for the M2 receptor in the atria. It is concluded that the muscarinic receptors on smooth muscle of the coronary and basilar arteries are not identical. The muscarinic receptor involved in the contraction of the basilar artery adheres to the M2 receptor subtype. A comparison of the selectivity of the antagonists suggests that the muscarinic receptor involved in the contraction of the coronary artery belongs to the M3 (like in exocrine glands) or M4 (as found in ileal smooth muscle) receptor subtype.

Animals↗
PubMed2002

Patch angioplasty to repair the arteriotomy defect in the wall of the middle cerebral artery after failure of superficial temporal artery-middle cerebral artery anastomosis in moyamoya disease--case report.

A 65-year-old woman presented with moyamoya disease associated with a saccular aneurysm of the posterior cerebral artery. The surgical plan required superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis to be conducted before neck clipping of the aneurysm to provide collateral flow via the STA to prevent ischemia if temporary occlusion of the parent artery of the aneurysm was needed. However, the anastomotic procedure failed because the STA was occluded at the site of temporary clip application. End-to-end anastomosis of the STA was planned after excising the occluded site of the STA, but end-to-end anastomosis could not be performed because the donor artery was too short for anastomosis to the branch of the MCA. Therefore, patch grafting using a piece of wall of the STA was performed to repair the arteriotomy defect in the wall of the MCA, followed by neck clipping of the saccular aneurysm in the posterior circulation via the subtemporal approach. Vascular reconstruction can be recommended if arterial anastomosis between a superficial skin artery and a branch of the MCA is impossible due to an intraoperative accident or technical difficulty and reperfusion is necessary.

Aged↗
PubMed1996

Developmental changes in alpha 1-adrenergic receptors, IP3 responses, and NE-induced contraction in cerebral arteries.

Cerebral arteries show significant developmental and artery-specific changes in noradrenergic-mediated contraction. To test the hypothesis that these changes result from differences in the density of alpha 1-adrenergic receptors (alpha 1-ARs) and/or norepinephrine (NE)-induced inositol 1,4,5-trisphosphate [Ins(1,4,5)P3,IP3] synthesis, we quantified these variables and the NE-induced contraction in the common carotid artery (Com) and main branch cerebral arteries (MBC) from term fetal (approximately 140 gestational day) and newborn (2- to 5-day) sheep and compared them with adult values. In fetal and newborn Com, maximal contractions to NE (percent K+ maximum response) were 132 +/- 14 and 118 +/- 9%, respectively (adult = 92 +/- 7%). For fetal and newborn middle cerebral artery, these values were 34 +/- 10 and 43 +/- 7%, respectively (adult = 24 +/- 7%). alpha 1-AR density values in Com of fetal and newborn sheep were 113 +/- 18 and 106 +/- 4 fmol/mg protein, respectively (adult = 54 +/- 3 fmol/mg protein). For the MBC, density values were 47 +/- 2 and 24 +/- 3 fmol/mg protein, respectively (adult = 23 +/- 3 fmol/protein). In term fetal and newborn MBC, NE produced dose-dependent increases in Ins(1,4,5)P3, the maximal increases above basal values being 245 +/- 40 and 189 +/- 16%, respectively (adult = 254 +/- 35%). Neither fetus nor newborn Com showed significant Ins(1,4,5)P3 responses to NE. We concluded that in fetal and newborn Com and MBC, alpha 1-AR density and NE-induced Ins(1,4,5)P3 response varied as a function of developmental age and specific vessel. However, these variations did not correlate with NE-induced maximum contraction. Thus we reject the hypothesis that age-dependent and vessel-specific differences of cerebral artery adrenergic-mediated contraction are a function of alpha 1-AR density or Ins(1,4,5)P3 response. Rather, the differences would appear to result from other factors such as non-Ins(1,4,5)P3-mediated calcium activation and/or sensitivity to Ins(1,4,5)P3. The studies also suggest considerable potential for maturational modulation of pharmacomechanical coupling and homeostatic regulation of cerebrovascular tone.

Aging↗
PubMed2000

Nitric-oxide synthase-containing nerves facilitate adrenergic transmitter release in sheep middle cerebral arteries.

Cerebral blood vessels contain both sympathetic and nitric oxide (NO) synthase (NOS)-containing nerves. NO has been proposed to modulate smooth muscle function and adrenergic nerve activity, and the nature of this modulation is controversial: some data show NO inhibits norepinephrine (NE) release, whereas others suggest that NO augments release. To test the hypothesis that in cerebral arteries NO released by NOS-containing nerves augments stimulation-evoked NE release, we used direct measurement of NE and NO release in isolated sheep middle cerebral arteries. The facial artery, which has not been reported to be innervated with NOS-containing nerves, was used as an artery comparison model. HPLC and redox electrochemical detection was used to measure NE, and NO was measured by chemiluminescence. Stimulation-evoked NE release from the middle cerebral artery significantly declined in the presence of the NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME). The effect of L-NAME was reversed by the addition of the NO donor S-nitroso-N-acetyl-DL-penicillamine. In contrast, in facial arteries, L-NAME had no effect on stimulation-evoked NE release, whereas S-nitroso-N-acetyl-DL-penicillamine still significantly elevated NE release. Activation of perivascular nerves significantly increased NE release in both the middle cerebral and facial arteries. However, when NO was measured in the same samples, stimulation-evoked release of NO was significantly increased compared with basal release only in middle cerebral arteries. These data support the concept that cerebral arteries in the sheep contain both adrenergic and NOS-containing nerves. Furthermore, this study provides succinct evidence that NO released from NOS nerves augments stimulation-evoked NE release.

Animals↗
PubMed1990

Mechanism underlying responses to histamine of isolated monkey and human cerebral arteries.

Cerebral artery strips obtained from Japanese monkeys partially contracted with prostaglandin F2 alpha responded to histamine with a relaxation that was attenuated by treatment with cimetidine or chlorpheniramine and was abolished by their combined treatment. Endothelium denudation suppressed the relaxation; the remaining relaxation was not influenced by the H1 antagonism but was abolished by the H2 antagonism. Treatment with methylene blue slowed the development of relaxation and, in the presence of cimetidine, depressed the magnitude of relaxation. Indomethacin did not alter the response. In the main trunk of human middle cerebral arteries obtained during autopsy, histamine predominantly caused contractions, whereas third and fifth branches responded exclusively with a dose-dependent relaxation. The contraction was abolished by chlorpheniramine, and the relaxation was attenuated by either chlorpheniramine or cimetidine. Removal of endothelium suppressed or reversed the relaxation to a contraction. It appears that the histamine-induced relaxation is mediated by endothelial H1 receptors responsible for the release of endothelium-derived relaxing factor and also by H2 receptors in smooth muscle, whereas the contraction is associated with activation of smooth muscle H1 receptors. Involvement of the receptor subtypes in the observed response of monkey and human cerebral arteries quantitatively differs. Physiological and pathophysiological roles of endogenous histamine acting on the large cerebral arteries may be postulated.

Animals↗
PubMedDate not supplied

Influence of superficial temporal artery to middle cerebral artery bypass on cerebral blood flow in dogs with middle cerebral artery occlusion.

Eight dogs had a superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis, followed immediately by ligation of the ipsilateral middle cerebral artery. Subsequently, utilizing the radioactive microsphere technique, regional cerebral blood flow determinations were made both before and after ligation of the superficial temporal artery. A significant reduction in blood flow of 20-35% was noted in both cerebral hemispheres, caudate and thalamic nuclei, brain stem and cerebellum following occlusion of the bypass. It is our impression that this generalized reduction in flow is due to a redistribution of blood from normal areas previously supplied by the bypass. This implies that the newly created extracranial to intracranial arterial anastomosis reduces the shunting of blood from zones of higher to zones of lower flow through the circle of Willis and leptomeningeal collaterals. It also suggests a mechanism for the development in neurological function referable to areas of the brain remote from the bypass which is detected in some patients after STA-MCA anastomosis.

Animals↗
PubMed1997

Changes in umbilical artery, middle cerebral artery, and aorta blood flow Doppler waveform pulsatility indices after funisocentesis.

This study evaluates the effect of funisocentesis on umbilical artery, fetal cerebral artery, and aortic circulation. The pulsatility index in the umbilical artery, fetal middle cerebral artery, and descending aorta was measured by pulsed Doppler ultrasonography before and after 41 diagnostic funisocenteses. Percutaneous umbilical artery blood sampling was associated with a significant decrease in umbilical artery pulsatility index (mean -0.132, standard deviation 0.259, P = 0.002) and in middle cerebral artery pulsatility index (mean -0.143, standard deviation 0.260, P = 0.001). The decline in resistance to flow of the umbilical artery (r = 0.340, P = 0.029) and middle cerebral artery (r = 0.457, P = 0.002) was correlated with gestational age at sampling. These findings suggest that alterations in the waveforms from both the umbilical and the fetal cerebral circulations can be induced by fetal blood sampling.

Aorta, Thoracic↗
PubMed1985

"Reverse" superficial temporal artery-middle cerebral artery bypass.

A new technical variant on the superficial temporal artery-middle cerebral artery anastomosis was performed in a patient with occlusions of both the left internal and external carotid arteries and persistent ischemic symptomatology. Instead of anastomosing the proximal segment of the superficial temporal artery to the middle cerebral artery as is conventionally done, the distal segment of the superficial temporal artery was anastomosed to a cortical branch of the left middle cerebral artery. Reconstituted flow of the left superficial temporal artery via right superficial temporal artery collateral branches proved adequate to relieve the patient's ischemic episodes. "Reverse" superficial temporal artery-middle cerebral artery anastomosis should be considered in those cases where occlusive disease of the external carotid circulation renders conventional bypass procedures ineffective in the treatment of ischemic symptomatology.

Arterial Occlusive Diseases↗
PubMed1979

Release of endogenous norepinephrine from a rabbit cerebral artery.

Cerebral arteries are relatively unresponsive to sympathetic nerve stimulation, in spite of extensive adrenergic innervation. To determine whether these nerves are functional, release of endogenous norepinephrine (NE) was measured using a radioenzymatic assay. Fractional release of NE per stimulation pulse was more than 5 times greater from the rabbit basilar artery than from the ear artery. Thus, while the NE content of the two vessels is quite similar, transmitter release is considerably greater in the basilar artery. Since NE accumulation is also much greater in the basilar artery, it seems possible that an active parameter such as NE release or accumulation may be a better index of functional nerve capacity than NE content. Previous studies have shown that alpha adrenergic blocking agents do not block the contractile response to nerve stimulation of the basilar artery, but actually increase it. Thus, the possibility that blockade of presynaptic adrenergic receptors leads to increased transmitter release was tested. Indeed, both phenoxybenzamine and phentolamine significantly increased stimulation-evoked NE release. It appears that postsynaptic events in cerebral arteries are atypical, while release of transmitter, including modulation by presynaptic alpha adrenergic receptors is similar to other blood vessels.

Animals↗
PubMed1991

[Neonatal focal seizures and transitory inappropriate ADH secretion syndrome due to an infarction in the region of the middle cerebral artery].

Cerebral arterial infarction is a very rare condition during the neonatal period. In recent times, cerebral infarctions with an atypical bland course are reported in healthy, unsuspected newborns. For the first time, we saw focal seizures and a transient syndrome of inappropriate ADH secretion in a full-term, male newborn with an infarction of the middle cerebral artery as the first sign of this disorder. On the basis of these rare clinical manifestations, the literature about neonatal cerebral infarction is reviewed. The diagnostic possibilities and prognostic expectations are discussed. It is the aim of this case report to call attention to this rare disease in order to avoid a delay in diagnosis and therapy, even if the initial manifestations are atypical.

Cerebral Arteries↗
PubMed1998

Surgical treatment of aneurysms of the anterior cerebral artery.

Cerebral aneurysms occur on the anterior cerebral artery in three locations: the anterior communicating artery, the pericallosal artery, and the A1 segment. Anterior communicating artery aneurysms show great morphologic variability and are the most frequent aneurysms seen in modern series. The anatomy, management, neuroradiology, surgical technique, and clinical outcome referable to each location on the anterior cerebral artery are discussed in this article.

Cerebral Angiography↗
PubMed2001

Hypothermia on NO-mediated neurogenic relaxation and on hypoxic inhibition in the response of canine cerebral arteries.

Cerebral arteries are innervated by nitric oxide (NO)-mediated vasodilator nerves, and hypoxia has been shown to attenuate neurogenic vasorelaxation. The present study examines the effects of hypothermia on neurogenic vasorelaxation and on the hypoxia-induced inhibition of the neurogenic vasorelaxation response. In isolated canine cerebral arteries, relaxant responses to transmural electrical stimulation (5 Hz for 40 s), mediated via NO synthesized from L-arginine, were not influenced by lowering the bathing media temperature from 37 degrees C to 30 degrees C but were attenuated at 25 degrees C. On the other hand, relaxations caused by nicotine and exogenous NO were not significantly attenuated but were prolonged by cooling to 25 degrees C. The responses associated with nerve stimulation by electrical pulses or nicotine were depressed by hypoxia (from about 500 mmHg of partial O2 pressure to about 45 mmHg) under normothermia. However, hypothermia at 25 degrees C prevented the inhibition by hypoxia of the neurogenic relaxation. It is concluded that the hypothermia-induced inhibition in the response to electrical nerve stimulation is not associated with a decreased synthesis and release of NO in vasodilator nerves nor with a reduced ability of smooth muscle to relax in response to NO. Interference with the propagation of action potentials might be involved in the inhibition via a fall of temperature. The fact that the hypoxia-induced impairment of vasodilator nerve function was prevented by cooling may partially explain the efficacy of hypothermia in protecting against ischemic neuronal injury in the brain.

Animals↗
PubMed2004

Distinguishing between anterior cerebral artery and middle cerebral artery perfusion by color-coded perfusion direction mapping with arterial spin labeling.

The purpose of this study was to evaluate collateral circulation by describing anterior cerebral artery and middle cerebral artery perfusion areas. Pairs of image sets spin labeled on the medial and lateral side were used. A pixel-by-pixel t test was performed, with blue gradation used to display lateral perfusion (ie, middle cerebral artery) and orange gradation for anterior cerebral artery perfusion. Extensions of anterior cerebral artery perfusion areas in cases of middle cerebral artery stenosis were described. This method may aid in estimation of collateral circulation for stroke treatment.

Cerebral Angiography↗
PubMed1982

Effect of superior cervical ganglionectomy on the sensitivity of rabbit ear artery and cerebral arteries of rabbit and cat to vasoactive agents.

The effect of sympathetic denervation on the sensitivity of the rabbit ear and basilar arteries and the cat middle cerebral artery to vasoactive agents was examined in relation to the functional significance of the innervation. Fourteen days after superior cervical ganglionectomy, the catecholamine fluorescence disappeared and the norepinephrine content drastically decreased and transmural nerve stimulation ceased to elicit any response in all these arteries. In the rabbit ear artery, denervation resulted in a significant leftward shift of dose-response curves for norepinephrine (8.2-fold), serotonin (7.7-fold), histamine (2.9-fold) and potassium (1.2-fold). In contrast, there was no significant shift of dose-response curves to these drugs in the rabbit basilar and cat middle cerebral arteries. These results indicate that after chronic superior cervical ganglionectomy, postjunctional supersensitivity developed in the rabbit ear artery, but no pre- or postjunctional supersensitivity occurred in the rabbit basilar and cat middle cerebral arteries. The difference may be in part attributable to the reported closer synaptic cleft distance of the sympathetic nerve terminals in the ear than in the cerebral arteries examined. These results further suggest that the sympathetic adrenergic nerve exerts a tonic influence over the rabbit ear artery, but little or none in normal cerebral blood vessels.

Animals↗
PubMed2004

Effect of magnesium, high altitude and acute mountain sickness on blood flow velocity in the middle cerebral artery.

Cerebral blood flow is thought to increase at high altitude and in subjects suffering from acute mountain sickness (AMS); however, data from the literature are contentious. Blood flow velocity in the middle cerebral artery (MCAv) may be used as a proxy measure of cerebral blood flow. Using transcranial Doppler sonography, MCAv was measured during normo- and hyper-ventilation in subjects who participated in a trial that tested the effect of magnesium supplementation on the prevention of AMS. First, MCAv was recorded at 353 m (baseline). Subjects were then randomized to receive oral magnesium citrate and matching placebo. A second measurement was taken after a 24 +/- 2 h ascent from 1130 m to 4559 m (altitude I), and a third after a 20-24 h stay at 4559 m (altitude II). Using multivariate linear regression, an association was sought between MCAv and magnesium supplementation, subjects' age and gender, altitude itself, a temporary stay at altitude, and the presence of AMS (Lake Louise Score >6 with ataxia, nausea and/or headache). Subjects with AMS had additional Doppler recordings immediately before and after rescue medication (oxygen, dexamethasone and acetazolamide). Forty-seven subjects had measurements at baseline, 39 (21 receiving magnesium and 18 placebo) at altitude I and 26 (13 receiving magnesium and 13 placebo) at altitude II. During hyperventilation, MCAv decreased consistently (for each measurement, P<0.001). Magnesium significantly increased MCAv by 8.4 cm.s(-1) (95% confidence interval, 1.8-15), but did not prevent AMS. No other factors were associated with MCAv. Eleven subjects had severe AMS [median score (range), 11 (8-16)] and, after rescue medication, the median score decreased to 3 (range, 0-5; P=0.001), but MCAv remained unchanged (65 +/- 18 cm.s(-1) before compared with 67 +/- 16 cm.s(-1) after rescue medication; P=0.79). MCAv was increased in subjects who received magnesium, but was not affected by exposure to high altitude or by severe AMS.

Administration, Oral↗
PubMed1993

Nitric oxide synthase-containing neural processes on large cerebral arteries and cerebral microvessels.

We studied whether neural processes containing nitric oxide synthase (NOS) are associated with large cerebral arteries and/or intraparenchymal microvessels. The presence of NOS-positive nerves on large cerebral arteries was examined in whole-mount preparations processed for NADPH diaphorase histochemistry, a procedure that stains NOS-containing neurons. The association between NOS-containing neural processes and intracerebral microvessels was studied by electron microscopy in ultrathin brain sections reacted with antibodies against NOS. A dense perivascular plexus of NADPH diaphorase positive axons was observed in the anterior portion of the circle of Willis and its branches while in the basilar artery the innervation was less dense. Lesions of the major sources of perivascular innervation of the cerebral arteries indicated that these nerve fibers arise from the sphenopalatine ganglia. Within the brain parenchyma, NOS immunoreactivity was observed in dendrites and axonal terminals closely associated with the basal lamina of arterioles and capillaries. We conclude that NOS-containing nerves of peripheral origin innervate large cerebral arteries while NOS-containing neural processes of central origin, especially dendrites, are closely associated with cerebral arterioles and capillaries. The presence of NOS in perivascular dendrites raises the possibility that these structures are a major source of NO during neural activity. These findings, collectively, provide morphological evidence supporting the hypothesis that NOS neurons participate in the mechanisms that match neural activity to cerebral blood flow.

Amino Acid Oxidoreductases↗