Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BASILAR ARTERY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1997

Transiently increased basilar artery flow velocity following severe head injury: a time course transcranial Doppler study.

BACKGROUND AND PURPOSE: Transcranial Doppler ultrasonography has been used to study changes in cerebral hemodynamics following head injury. However, most studies evaluated the anterior circulation and little information exists on transcranial Doppler of the vertebrobasilar arteries after head injury. METHODS: Thirty-two patients with a Glasgow Coma Scale (GCS) score between 4-8 and 11 patients with a GCS score between 9-14 were studied using transcranial Doppler ultrasonography for the first 10 days after injury. Daily variations in the mean blood flow velocities of all major cerebral arteries were recorded. RESULTS: In patients with GCS score between 4-8, the mean blood flow velocities in the middle cerebral and basilar arteries gradually increased beginning on day 2 postinjury and peaked on the 4th-5th day after injury. Those changes were more prominent, and appeared earlier, in the basilar artery. The ratio between the mean flow velocities of the middle cerebral artery and the basilar artery during the first 4 days was significantly lower than in normal controls, indicating a particular increase of flow velocity in the basilar artery. Nineteen out of 32 patients (60%) with severe head injury showed mean blood flow velocity increased over 75 cm/sec in the basilar artery. Mean blood flow velocity >90 cm/sec in the basilar artery, compatible with vasospasm, was observed in 12 of 32 patients (37%). Spasm in the middle cerebral artery was observed in 12 (37%) of patients; 10 of them also had evidence of basilar artery spasm. On the whole, 14 of 32 (43%) patients had evidence of spasm either in the middle cerebral or basilar arteries or in both. In 5 of 11 patients (50%) with moderate head injury (GCS score 9-14), blood flow velocity in the basilar artery greater than 75 cm/sec was observed, but in only two of them it reached the values over 90 cm/sec. Vasospasm in the middle cerebral artery was noted in one patient. CONCLUSIONS: A significant number of patients develop increased flow velocities compatible with vasospasm in the basilar artery after severe head injury. This phenomenon may represent an additional factor that contributes to the poor outcome of severely head-injured patients.

Adolescent↗
PubMed1984

Lack of a causal relationship between the vasodilator effect of papaverine and cyclic AMP production in the dog basilar artery.

The effects of papaverine and isoprenaline on smooth muscle cells of the dog basilar artery were investigated using radioimmunoassay, electrophysiological and isometric tension recording methods. For comparative purposes, the actions of these drugs on the guinea-pig basilar artery were also examined. Papaverine and isoprenaline (1 microM and 10 microM) increased the amount of cyclic AMP in both dog and guinea-pig basilar arteries. Papaverine (up to 100 microM) and isoprenaline (up to 1 microM) had no effect on the membrane potential and membrane resistance measured by recording the amplitudes of the electrotonic potentials in smooth muscle cells of the dog and guinea-pig basilar arteries. The action potential evoked by outward current pulses after pretreatment with tetraethylammonium chloride (5-10 mM) was inhibited by papaverine (greater than 1 microM) but not by isoprenaline (up to 10 microM) in smooth muscle cells of the dog and guinea-pig basilar arteries. In the dog basilar artery, papaverine (greater than 1 microM) consistently inhibited the contractions evoked by excess concentrations of [K]o (greater than 20.2 mM) or 5-hydroxytryptamine (10 nM-10 microM), dose-dependently. Isoprenaline (1 microM) had only slight effects on the contraction evoked by low concentrations of 5-hydroxytryptamine (10 nM). In the Ca2+-free solution containing EGTA (2 mM), the contraction evoked by 5-hydroxytryptamine (10 microM) or caffeine (10 mM) was dose-dependently inhibited by papaverine (greater than 1 microM). However, isoprenaline (1 microM) had no effect on these contractions. These results indicate that the vasodilator actions of papaverine on the dog basilar artery are mainly due to inhibition of the voltage-dependent influx of Ca2+ and also to inhibition of the receptor-activated release of Ca2+ stored in the cell. Since isoprenaline increased the cyclic AMP to the same extent as papaverine but had no effect on the electrical and mechanical responses, the inhibitory actions of papaverine on this tissue may not be causally related to the increased levels of cyclic AMP induced by inhibition of phosphodiesterase.

Animals↗
PubMed1997

Role of Ca(2+)-activated K+ channels in acetylcholine-induced dilatation of the basilar artery in vivo.

1. We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine. 2. Topical application of acetylcholine (10(-6) and 10(-5) M) increased diameter of the basilar artery from 238 +/- 7 microns to 268 +/- 7 and 288 +/- 7 microns, respectively (P < 0.05 vs. baseline diameter). Iberiotoxin (10(-8) M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10(-8) M iberiotoxin, 10(-6) and 10(-5) M acetylcholine increased diameter of the basilar artery from 239 +/- 7 microns to 246 +/- 7 and 261 +/- 7 microns, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P < 0.05). 3. Sodium nitroprusside (10(-7) and 10(-6) M) increased diameter of the basilar artery from 242 +/- 9 microns to 310 +/- 12 and 374 +/- 13 microns, respectively (P < 0.05 vs. baseline diameter). In the presence of iberiotoxin (10(-8) M), sodium nitroprusside (10(-7) and 10(-6) M) increased diameter of the basilar artery from 243 +/- 6 microns to 259 +/- 9 and 311 +/- 12 microns, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P < 0.05). 4. Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener. 5. These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which cyclic GMP causes dilatation of the basilar artery in vivo.

Acetylcholine↗
PubMed1998

Impairment in biochemical level of arterial dilative capability of a cyclic nucleotides-dependent pathway by induced vasospasm in the canine basilar artery.

The authors investigated the changes and the potential of cyclic nucleotide-dependent signal transduction, which induces smooth muscle relaxation, in the basilar artery with severe vasospasm in dogs with double experimental subarachnoid hemorrhage (SAH) to explore at which biochemical level the arterial dilative capability was impaired. The amount of cyclic adenosine and guanosine monophosphates (cAMP and cGMP) decreased significantly in the basilar artery after SAH. The activities of adenylate and guanylate cyclases also were decreased significantly in the smooth muscle cells of the basilar artery 4 days after SAH. In addition to the failure of the pathways to produce cyclic nucleotides, the activities of cAMP- and cGMP-dependent protein kinases, which are representative actual enzymes that amplify the signal for vascular dilation, also significantly decreased together with the almost total loss of activation by cyclic nucleotides in the same basilar artery after SAH. It was revealed that the system for smooth muscle relaxation was impaired severely in the cerebral arteries with severe vasospasm after SAH, on the biochemical basis of significantly less vasodilative capability and in several of the steps to produce the cyclic nucleotides of intracellular signal transduction.

Adenylyl Cyclases↗
PubMed1993

Calpain-calpastatin system of canine basilar artery in vasospasm.

Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, while contraction was induced in the normal canine basilar artery by a local application of KCl or serotonin after transclival exposure. The control animals were injected with saline instead of fresh blood. The activation of mu-calpain, a Ca(++)-dependent neutral protease, in the basilar artery was studied by evaluating the conversion from its inactivated into its activated form on immunoblots. In addition, the activity of calpastatin, an intrinsic inhibitor of calpain, in the basilar artery was determined by assay. The majority of the mu-calpain was inactivated in the control group. In the spastic group, mu-calpain was generally activated markedly in the early stage of vasospasm and moderately thereafter. The contraction induced by KCl or serotonin application was classified into the early phasic and the later tonic stages; mu-calpain was usually activated in the phasic stage and inactivated in the tonic stage. Calpastatin activity was significantly decreased during vasospasm, whereas it was not significantly changed in KCl- or serotonin-induced contraction. The final activity of mu-calpain results from the balance of mu-calpain and calpastatin. This suggests that mu-calpain activity was enhanced continuously in the spastic group and transiently in the KCl or serotonin group, and that the continuous activation of mu-calpain during vasospasm probably induced more proteolytic changes compared to those in the KCl or serotonin group.

Animals↗
PubMed1985

Detection of basilar artery thrombosis by CT.

A case is presented with distal basilar artery occlusion diagnosed by computed tomography (CT). The normal basilar artery imaged on plain CT scans has an attenuation value not higher than that of whole blood. If the CT attenuation value of the vessel is higher than that of blood, basilar artery occlusion is probably present. In the case presented the cause was traumatic thrombo-embolic occlusion of the basilar artery.

Adult↗
PubMed1994

Vasomotor effects of histamine on bovine and equine basilar arteries in vitro.

The vasomotor effects of histamine on isolated bovine and equine basilar arteries were examined. Histamine induced contractions in both these preparations. The maximal response to and pEC50 value for histamine of the equine artery were larger than those of bovine tissue. Similar results were obtained with endothelium-denuded basilar arteries. Diphenhydramine (H1-receptor antagonist) inhibited histamine-induced contractions of the basilar arteries from both species in a concentration-dependent manner and its pA2 values (with 95% confidence limits) were 7.61 (7.39-7.83) and 8.15 (8.01-8.29) for the bovine and equine preparations, respectively. Cimetidine (H2-receptor antagonist) slightly potentiated histamine-induced contractions of bovine, but not equine, basilar arteries. 2-Thiazolylethylamine (H1-receptor agonist) induced contractions in both preparations, whereas impromidine (H2-receptor agonist) induced weak relaxation of the bovine, but not the equine, tissue. These findings indicate that bovine basilar arterial smooth muscle cells possess H1- and H2-receptors. Stimulation of the former results in contraction, whereas stimulation of the latter results in weak relaxation. Equine basilar arterial smooth muscle cells possess H1-receptors, stimulation of which results in contraction.

Animals↗
PubMedDate not supplied

MR imaging of basilar artery occlusion.

We studied six patients with basilar artery occlusion using magnetic resonance imaging. Two patients also had arteriography. All had signs consistent with pontine infarction; three had a "locked in" syndrome. Magnetic resonance imaging (five done within 24 h of onset of progression of neurologic symptoms) revealed a linear structure of increased signal intensity in the pontine cistern on T1-weighted parasagittal images and absence of flow void phenomena. Hyperintense signals at various brain stem levels corresponding to the course of the basilar artery were noted on T2-weighted images. Multiple parenchymal abnormalities were noted in the brain stem (six), cerebellum (four), occipital lobes (two), and thalamus (two). Magnetic resonance performed early in the course of basilar artery occlusion is a high-yield, safe procedure and might eliminate the need for arteriography.

Adult↗
PubMed1990

Clinical features of proven basilar artery occlusion.

Our study describes the early symptoms and signs of 85 patients with either basilar artery occlusion or bilateral distal vertebral artery occlusion documented by selective angiography. The most common prodromal symptoms were vertigo, nausea, and headache, which occurred during the 2 weeks before the stroke. Angiographic findings of 49 patients were classified into proximal, middle, and distal basilar artery occlusions. Twenty-two of these patients had additional vertebral artery lesions. A fourth group was composed of 36 patients with bilateral distal vertebral artery occlusion without opacification of the basilar artery through a vertebral artery injection. Onset was sudden in 20 patients; sudden, but preceded by prodromal symptoms in 11 patients; and progressive in 54 patients. Patients with progressive strokes often had bilateral vertebral artery occlusions. Most patients with acute onset had occlusion of the middle and distal basilar artery. An embolic origin of basilar artery occlusion from an arteriosclerotic vertebral artery lesion was assumed to be an important mechanism. An embolus reaching the basilar artery may not necessarily reach the top of the artery, but may also become lodged more proximally.

Adult↗
PubMed1977

Basilar artery ectasia demonstrated by computed tomography.

Basilar artery eclasia was demonstrated by computed tomography (CT) in 4 cases. The course and diameter of the basilar artery as seen by CT closely approximated those aspects of the artery visualized by angiography. The clinical manifestations of basilar ectasia correlated with what brain stem structures were impinged upon by the ectatic artery.

Aged↗
PubMed1993

Immunoblotting of contractile and cytoskeletal proteins of canine basilar artery in vasospasm.

Vasospasm was produced in the canine basilar arteries by a two-hemorrhage method, and voltage- and receptor-dependent contractions of the normal canine basilar arteries were induced by local applications of potassium chloride (KCI) and serotonin, respectively, after transclival exposure. Actin, myosin, desmin, filamin, talin, vinculin, and alpha-actinin in the basilar artery were studied by immunoblotting. The immunoblots showed a decrease or loss in immunoreactivity of some native proteins and generation of protein fragments, smaller in size than native proteins, in spastic, KCI, and serotonin groups, indicating a proteolytic degradation. In the spastic group on Day 2, actin, desmin, and filamin were usually degraded slightly; myosin moderately; and talin and alpha-actinin substantially. Vinculin and metavinculin remained intact. In the spastic group on Day 7, actin and desmin were usually decomposed slightly; myosin, filamin, and vinculin substantially; and talin, metavinculin, and alpha-actinin markedly. In the KCI and serotonin groups, slight degradation was usually observed in filamin, often in alpha-actinin, and occasionally in actin, whereas desmin, vinculin, and metavinculin were not degraded. In addition, myosin was usually degraded moderately in the KCI group and slightly in the serotonin group, and talin was generally decomposed slightly in the KCI group and moderately in the serotonin group. The degraded fragments, although variable in number and immunoreactivity, were similar in size in the three groups. We suggest that the intracellular devices responsible for contraction of the basilar arteries are degraded more severely in the spastic group than in the KCI or serotonin group, probably by similar proteolytic mechanism and progressively with the passage of time after subarachnoid hemorrhage in vasospasm.

Animals↗
PubMed1990

Impairment of endothelium-dependent dilatation of basilar artery during chronic hypertension.

The goal of this study was to determine whether responses of the basilar artery are altered during chronic hypertension. We measured the diameter of the basilar artery using intravital microscopy in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine (10 microM) dilated the basilar artery by 25 +/- 4% (means +/- SE) in WKY but by only 2 +/- 2% in SHR. Bradykinin (1.0 microM) dilated the basilar artery by 12 +/- 1% in WKY, but did not alter diameter in SHR (-0.1 +/- 2%). In contrast, nitroglycerin produced similar vasodilatation in WKY and SHR. Next, we examined the possibility that impaired vasodilatation in SHR may be related to the production of a cyclooxygenase constrictor substance. Indomethacin (10 mg/kg iv) did not restore vasodilatation in response to acetylcholine and bradykinin in SHR. Finally, we examined the role of nitric oxide in dilatation of the basilar artery in response to acetylcholine and bradykinin in WKY. NG-Monomethyl-L-arginine (L-NMMA; 1.0 microM) had little effect on baseline diameter but inhibited vasodilation in response to acetylcholine and bradykinin. Vasodilatation in response to nitroglycerin was not altered by L-NMMA. These findings suggest a profound impairment of endothelium-dependent dilatation of the basilar artery during chronic hypertension. In addition, impaired vasodilatation is not related to the production of a cyclooxygenase constrictor substance. Furthermore, dilatation of the basilar artery in WKY in response to acetylcholine and bradykinin appears to be related to the production of nitric oxide or a substance capable of liberating nitric oxide.

Acetylcholine↗
PubMed1980

Localization of atherosclerotic lesions in the human basilar artery.

The topography of atherosclerotic lesions in the human basilar arteries has been studied quantitatively by digitizing images of the excised vessels and producing contour probability maps. Fifteen basilar arteries were obtained at autopsy (age--61 +/- 2; males--6, females--9; black--6, white--9), fixed in formalin, opened along the ventral aspect and stained grossly with Sudan IV to delineate fat-containing lesions. Photographs of the flattened arteries were analyzed and the presence or absence of sudanophilic lesions was determined at approximately 1000 identical sites on all vessels. The probability of finding a lesion at each site was determined and a contour probability map was constructed. Fifty-two percent of the area of the mean contour map was involved with lesions. The extent of the sudanophilic lesions decreased as one proceeded distally from the origin of the basilar artery at the confluence of the vertebral branches (i.e. proximal 1/3--56%; middle 1/3--49%; distal 1/3--43%; P less than 0.04). Significantly more sudanophilic material was observed on the ventral (outer curvature) as opposed to the dorsal (inner curvature) surfaces (55%, 43% respectively; P less than 0.03). These data suggest that hemodynamic forces associated with confluent flow and curvature may be important in the localization of sudanophilic lesions in the proximal and ventral aspects of the human basilar artery.

Adolescent↗
PubMed2003

Heralding manifestations of basilar artery occlusion with lethal or severe stroke.

BACKGROUND: Basilar artery occlusion usually causes severe disability or death. Until the recent developments in local intra-arterial or systemic intravenous fibrinolysis, interest in early diagnosis was low because there was no satisfactory treatment. Thus there is little information about the initial phase of the disease. OBJECTIVE: To report on the early clinical features and patterns of evolution of severe symptomatic basilar artery occlusion. METHODS: 24 patients with established basilar artery occlusion (confirmed by angiography or at necropsy) were reviewed retrospectively, focusing on the early clinical aspects and time course of the disease. RESULTS: The most common initial symptoms were motor deficits (16/24, including facial palsies), articulatory speech difficulties (15/24), vertigo, nausea or vomiting (13/24), and headaches (10/24). The most frequent objective initial findings were motor deficits (22/24), facial palsies (19/24), eye movement abnormalities (15/24), lower cranial nerve deficits (15/24), altered level of consciousness (12/24), and bilateral extensor plantar responses (9/24). Onset of the disease was gradual in nearly all patients and in half the warning signs were present for up to two months before the final stage. Headaches and visual disturbances were early signs, while speech difficulties and motor deficits were late signs. Once permanent neurological deficits were present, the final illness was reached within six hours in 41%, between six and 24 hours in 32%, and in two to three days in 27%. CONCLUSIONS: All the patients reviewed presented some symptoms and signs pointing to brain stem involvement. Only 8% (2/24) had an acute course with no adequate warning signs.

Adult↗
PubMed1993

Neural mechanism underlying basilar arterial constriction by intracisternal L-NNA in anesthetized dogs.

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.

Anesthesia↗
PubMed1991

Changes in responsiveness of the canine basilar artery to endothelin-1 after subarachnoid hemorrhage.

The effect of endothelin-1 (ET-1) on the basilar arteries from control and subarachnoid hemorrhage (SAH) dogs were examined. The maximal contraction of the basilar artery in response to ET-1 was markedly decreased in the SAH group. Treatment with 10(-8)M phorbol 12-myristate 13-acetate (PMA) reduced the contractile responses to ET-1 in the basilar arteries from control dogs. ET-1-induced contractions of the basilar arteries from control dogs were similar to those in strips from SAH dogs by the treatment with 10(-8) M PMA. Ca(2+)-induced contraction of the basilar arteries which were depolarized with isotonic K+ (64 mM) were significantly attenuated in SAH dogs. Treatment with PMA also reduced the contractile responses to Ca2+ in the basilar arteries from control dogs. These results indicate that decreased contractile responses of the basilar arteries to ET-1 and Ca2+ in the SAH group may be related to changes in the activity of the protein kinase C in vascular smooth muscle.

Animals↗
PubMed1995

Vertebrobasilar infarcts in patients with dolichoectatic basilar artery.

We reported 18 patients who had stroke in the posterior circulation with dolichoectatic basilar artery. TIAs preceded posterior circulation infarct in 5 patients. Strokes involved medulla oblongata (3), pons (4), cerebellum (4), mesencephalon (4), thalamus or occipital lobe (3). Dolichoectatic basilar artery also produced hydrocephalus in one patient. The mechanism of stroke may be due to penetrating artery occlusion, basilar artery thrombosis or an embolism from the abnormal basilar artery. Short-term prognosis was poor seeing that 4 patients died within 12 days of stroke.

Adult↗
PubMed2004

Influence of exercise on dilatation of the basilar artery during diabetes mellitus.

Our goal was to examine whether exercise training alleviates impaired nitric oxide synthase (NOS)-dependent dilatation of the basilar artery in Type 1 diabetic rats. To test this hypothesis, we measured in vivo diameter of the basilar artery in sedentary and exercised nondiabetic and diabetic rats in response to NOS-dependent (acetylcholine) and -independent (nitroglycerin) agonists. To determine the potential role for nitric oxide in vasodilatation in sedentary and exercised nondiabetic and diabetic rats, we examined responses after NG-monomethyl-l-arginine (l-NMMA). We found that acetylcholine produced dilatation of the basilar artery that was similar in sedentary and exercised nondiabetic rats. Acetylcholine produced only minimal vasodilatation in sedentary diabetic rats. However, exercise alleviated impaired acetylcholine-induced vasodilatation in diabetic rats. Nitroglycerin produced dilatation of the basilar artery that was similar in sedentary and exercised nondiabetic and diabetic rats. l-NMMA produced similar inhibition of acetylcholine-induced dilatation of the basilar artery in sedentary and exercised nondiabetic and diabetic rats. Finally, we found that endothelial NOS (eNOS) protein in the basilar artery was higher in diabetic compared with nondiabetic rats and that exercise increased eNOS protein in the basilar artery of nondiabetic and diabetic rats. We conclude that 1) exercise can alleviate impaired NOS-dependent dilatation of the basilar artery during diabetes mellitus, 2) the synthesis and release of nitric oxide accounts for dilatation of the basilar artery to acetylcholine in sedentary and exercised nondiabetic and diabetic rats, and 3) exercise may exert its affect on cerebrovascular reactivity during diabetes by altering levels of eNOS protein in the basilar artery.

Acetylcholine↗