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At least 163 records · Page 9Linked to original sources
PubMed1993

[A pathological study of basilar artery sclerosis resulting from vertebral artery asymmetry].

We conducted a pathological study of the arteries of Willis ring in 130 autopsied specimens to evaluate the influence of vertebral artery (VA) asymmetry on basilar artery (BA) sclerosis. The cases studied comprised 109 of non-brainstem infarction (control) and 21 of thrombotic basilar artery occlusion (BAO). The frequency of VA asymmetry was significantly higher (p < 0.01) in BAO cases (13 out of 21 cases; 61.9%) than in the controls (35 out of 109; 32.1%). In the controls, the mean scores for stenosis of the caudal (p < 0.01) BA were significantly higher in VA asymmetry pattern than in VA normal pattern, but the mean score of the rostral BA was nearly equal in both patterns. In BAO cases with VA asymmetry, the score for stenosis was higher in the caudal portion than in the rostral portion, and occlusion was frequently found in the lower BA and continuing from the thicker VA to the BA. These findings suggest that atherosclerotic changes may occur more preferentially in the lower BA in cases of VA asymmetry, and that VA asymmetry is considered to be one of the risk factors for BA occlusion.

Adult↗
PubMed1987

Alpha-glucosidase deficiency and basilar artery aneurysm: report of a sibship.

Glycogen deposition in vascular smooth muscle has been demonstrated previously in alpha-glucosidase deficiency but has not been clinically significant. Three sons of healthy, nonconsanguineous parents developed progressive proximal muscular weakness secondary to alpha-glucosidase deficiency. Each patient developed a fusiform basilar artery aneurysm, which was complicated by fatal rupture in two patients and a cerebellar infarction in the third. Postmortem examination demonstrated severe vacuolation of skeletal muscle, liver, and vascular smooth muscle with accumulation of periodic acid-Schiff-positive, diastase-sensitive material. In the surviving brother, similar glycogen deposition was demonstrated in the smooth muscle of the superficial temporal artery. Basilar artery aneurysm formation in this sibship may be a consequence of alpha-glucosidase deficiency.

Adolescent↗
PubMed1993

ATP-sensitive potassium channels in the basilar artery during chronic hypertension.

We examined the hypothesis that dilatation of the basilar artery in response to activation of ATP-sensitive potassium channels is impaired in stroke-prone spontaneously hypertensive rats (SHRSP). Changes in basilar artery diameter in response to aprikalim, a direct activator of ATP-sensitive potassium channels, were measured in anesthetized SHRSP and normotensive Wistar-Kyoto (WKY) rats through a cranial window. Topical application of aprikalim increased basilar artery diameter in WKY rats. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, abolished aprikalim-induced vasodilatation. Thus, ATP-sensitive potassium channels are functional in the basilar artery of WKY rats in vivo. Aprikalim (10(-6) mol/L) dilated the basilar artery by 31 +/- 5% (mean +/- SEM) in WKY rats but only 5 +/- 1% in SHRSP. The concentration-response curve to aprikalim in SHRSP was significantly shifted to the right, but the response to the highest concentration of aprikalim (10(-5.5) mol/L) was similar in SHRSP and WKY rats. Vasodilatation in response to norepinephrine was also impaired in SHRSP. Dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, and nitroprusside, a direct activator of guanylate cyclase, were normal in SHRSP. The findings suggest that dilatation of the basilar artery in response to direct activation of ATP-sensitive potassium channels is impaired in SHRSP compared with WKY rats in vivo.

Adenosine Triphosphate↗
PubMed2004

Randomized comparison of intra-arterial and intravenous thrombolysis in a canine model of acute basilar artery thrombosis.

We compared the rates of recanalization cerebral infarct and hemorrhage between intra-arterial (i.a.) reteplase and intravenous (i.v.) alteplase thrombolysis in a canine model of basilar artery thrombosis. Thrombosis was induced by injecting a clot in the basilar artery of 13 anesthetized dogs via superselective catheterization. The animals were randomized in a blinded fashion, 2 h after clot injection and verification of arterial occlusion, to receive i.v. alteplase 0.9 mg/kg over 60 min and i.a. placebo, or i.a. reteplase 0.09 units/kg over 20 min, equivalent to one-half the alteplase dose, and i.v. placebo. Recanalization was studied for 6 h after treatment with serial angiography; the images were later graded in a blinded fashion. Blinded interpretation of postmortem MRI was performed to assess the presence of brain infarcts and/or hemorrhage. At 3 h after initiation of treatment, partial or complete recanalization was observed in one of six dogs in the i.v. alteplase group and in five of seven in the i.a. reteplase group (P = 0.08). At 6 h, no significant difference in partial or complete recanalization was observed between the groups (two of six vs. five of seven; P = 0.20). Postmortem MRI revealed infarcts in four of six animals treated with i.v. alteplase and three of seven treated with i.a. reteplase (P = 0.4). Intracerebral hemorrhage was more common in the i.v. alteplase group (four of six vs. none of seven; P = 0.02). This study thus suggests that i.a. thrombolysis affords a recanalization rate similar to that of i.v. thrombolysis, but with a lower rate of intracerebral hemorrhage.

Animals↗
PubMed1994

Endothelial modulation of vascular tone in isolated porcine and bovine basilar arteries.

Endothelium-dependent modulation of vascular tone was investigated in isolated porcine and bovine basilar arteries. L-Nitro-arginine (NO synthase inhibitor) and methylene blue (soluble guanylate cyclase inhibitor) increased, but indomethacin (cyclooxygenase inhibitor) decreased the vascular tone in the basilar arteries from both species. Bradykinin evoked relaxation of precontracted porcine basilar artery, but not bovine basilar artery. Sodium fluoride (endothelial G-protein activator) produced relaxation of precontracted basilar arteries from both species. The effects of bradykinin and sodium fluoride were completely abolished by endothelial denudation and markedly inhibited by L-nitro-arginine and methylene blue, but not by indomethacin. Sodium nitroprusside (guanylate cyclase activator) evoked relaxation of precontracted endothelium-denuded basilar arteries from both species. These results suggest that there is species variation in endothelium-dependent modulation of vascular tone in the basilar artery.

Amino Acid Oxidoreductases↗
PubMed2006

Basilar artery diameter and 5-year mortality in patients with stroke.

BACKGROUND AND PURPOSE: Few and conflicting data exist on the case fatality rate in stroke patients with basilar artery dolichoectasia. We analyzed basilar artery characteristics (diameter, height of bifurcation, transverse position) and 5-year mortality (all-cause, nonstroke vascular, and stroke) in patients with brain infarction. METHODS: The basilar artery diameter was measured with a 16-diopter lens in 466 consecutively recruited patients with brain infarction confirmed by magnetic resonance imaging. The height of the bifurcation and the transverse position of the basilar artery were assessed on semiquantitative scales. Patients were followed up for a median of 5.3 years (range, 1.5 to 6.6) and were classified as having had stroke, nonstroke vascular, and nonvascular death according to the French national registry of death certificates. RESULTS: Of the 157 deaths, 88 were vascular (including 54 stroke deaths). Basilar artery diameter was associated with an increased 5-year stroke mortality rate but not with all-cause or nonstroke vascular mortality. The adjusted hazard ratio (HR) of stroke mortality per 1-mm increase in basilar artery diameter was 1.23 (95% confidence interval [CI], 1.07 to 1.41). A higher risk of stroke death was associated with basilar artery diameter at the 95th percentile (diameter >4.3 mm; adjusted HR 3.69; 95% CI, 1.63 to 8.38) and the height of bifurcation (adjusted HR for score >1, 2.08; 95% CI, 0.93 to 4.68) but not with transverse position. CONCLUSIONS: Basilar artery diameter was independently associated with cerebrovascular mortality. A diameter >4.3 mm may be a marker for a high risk of fatal stroke.

Aged↗
PubMed1990

[Fenestrated basilar artery with ruptured cerebral aneurysms: case report].

Two cases of aneurysms with basilar artery fenestration are presented. A 45 year-old lady had a saccular aneurysm associated with a fenestrated basilar artery. The fenestration was located in the proximal third of the basilar artery. The aneurysm arose from the proximal end of the fenestration, projecting antero-inferiorly. Via a left retromastoid craniectomy, the aneurysm was successfully obliterated through the space between the eighth cranial nerve and the lower cranial nerve complexes. Postoperative deficit in the lower cranial nerves was minimal and transient. The other patient, a 63 year-old lady, had multiple aneurysms arising from the anterior circulation associated with a basilar artery fenestration. These aneurysms were clipped uneventfully. Surgical approach to an aneurysm arising from the basilar artery fenestration is discussed with other related literature. Full study of posterior circulation with multiple projection is mandatory to detect basilar artery fenestration, and the possible presence of saccular aneurysm at the site of the anomaly.

Basilar Artery↗
PubMed1990

[Basilar artery occlusion after STA-SCA anastomosis; case report].

A case of basilar artery occlusion after STA-SCA bypass surgery is reported. The patient was a 56 year old male and presented a TIA of vertigo and speech disturbance. The preoperative angiogram revealed severe stenosis of the basilar artery in its midportion between the bifurcation of AICA and that of SCA. After surgery, the patient's clinical course was uneventful, but the angiogram showed that the previous stenotic segment of the basilar artery had been occluded and the distal portion of the basilar artery and its branches were perfused through the widely-patent STA-SCA bypass. About 6 months after the operation, the patient developed a pontine infarction in the right paramedian region, which was confirmed on MRI. The angiogram revealed that the occlusion of the basilar artery extended further proximally to a point just distal to the bifurcation of AICA. So it was suspected that the perforating branches of the basilar artery to the pons were occluded with the extension of the thrombosis of the basilar artery. The hemodynamic changes associated with the EC-IC bypass was thought to be responsible for the occlusion of the previous stenotic lesion.

Arteries↗
PubMed1992

Impairment of endothelium-dependent dilatation of the basilar artery during diabetes mellitus.

The goal of this study was to determine whether responses of the basilar artery are altered during diabetes mellitus. We measured the diameter of the basilar artery in vivo in non-diabetic and diabetic rats (streptozotocin; 50-60 mg/kg i.p.). Responses of the basilar artery to agonists, which presumably produce dilatation by releasing endothelium-derived relaxing factor (EDRF), were impaired in diabetic rats compared to non-diabetic rats. Acetylcholine (1.0 and 10 microM) dilated the basilar artery by 13 +/- 2 and 26 +/- 4% (means +/- S.E.M.), respectively, in non-diabetic rats, but by only 4 +/- 1 and 9 +/- 2%, respectively, in diabetic rats (P less than 0.05). Bradykinin (1.0 and 10 microM) dilated the basilar artery by 14 +/- 2 and 35 +/- 6% (means +/- S.E.M.), respectively, in non-diabetic rats, but by only 5 +/- 1 and 6 +/- 2%, respectively, in diabetic rats (P less than 0.05). The response to nitroglycerin was similar in non-diabetic and diabetic rats. Thus, impairment of vasodilatation in diabetic rats in response to acetylcholine and bradykinin is not related to non-specific impaired of vasodilatation. Next, we examined the possibility that impaired dilator responses of the basilar artery in response to acetylcholine and bradykinin in diabetic rats may be related to the activation of the thromboxane A2-prostaglandin H2 receptor. SQ 29548 (a specific thromboxane A2-prostaglandin H2 receptor antagonist) did not alter responses of the basilar artery to acetylcholine and bradykinin. These findings suggest that diabetes mellitus impairs endothelium-dependent dilatation of the basilar artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1976

Experimental evaluation of the spasmogenicity of dopamine on the basilar artery.

Arteriograms of the basilar artery reveal that dopamine given intracisternally to dogs can generate cerebral vasospasm. This finding supports a recent hypothesis of others that dopamine may play a role in the pathogenesis of vasospasm, especially since many substances are known which fail to produce such spasm. Compared to blood or prostaglandin E2, however, the spasm induced by dopamine was delayed in onset, less in incidence, and usually less intense. Possible explanations for such experimental differences are discussed.

Animals↗
PubMed1989

Vasorelaxing action of melatonin in rabbit basilar artery.

1. In rabbit basilar arteries, melatonin (10(-5)-10(-3) M) and nifedipine (10(-10)-10(-8) M) inhibited the responses to KCl and 5-hydroxytryptamine. 2. Melatonin or nifedipine inhibited the Ca2+-responses in a Ca2+-free medium containing KCl (40 mM) or 5-HT (10(-5) M). 3. A combined treatment with nifedipine and melatonin caused no further inhibition of the Ca2+ response in the presence of K+ as compared to a single treatment with melatonin. 4. However, the combined treatment caused a greater inhibition of the Ca2+-response in the presence of 5-HT than the single treatment with either agent. 5. These results suggest that melatonin and nifedipine inhibit the same Ca2+ channels activated by KCl. Further, 5-HT-activated Ca2+ channels which are inhibited by melatonin may be different from nifedipine-sensitive Ca2+ channels activated by 5-HT.

Animals↗
PubMed2002

Endovascular treatment of kissing aneurysms at the fenestrated basilar artery. Case report with literature review.

BACKGROUND: Basilar artery fenestrations are most commonly located in the proximal basilar trunk close to the vertebrobasilar junction and may harbor saccular aneurysms. Surgical treatment of such aneurysms has been reported in several cases previously, despite the difficulty of the surgical approach. Endovascular treatment may provide a more convenient treatment alternative in such cases. This case is also interesting in that two discrete aneurysms arise from each limb of the fenestration. CASE REPORT: A 20-year-old man presented with acute subarachnoid hemorrhage. He had two kissing aneurysms at the fenestrated proximal basilar artery as demonstrated by MRA and selective angiography. The two aneurysms were successfully treated with GDCs via the contralateral vertebral arteries. One-year control angiogram showed stable occlusion. CONCLUSION: Aneurysms at the fenestrated basilar artery may be effectively treated with endovascular coil occlusion. The occurrence of multiplicity and the treatment alternatives are discussed, with relevant literature review.

Adult↗
PubMed1997

Functional activity of Ca2+-dependent K+ channels is increased in basilar artery during chronic hypertension.

We examined the hypothesis that activity of Ca2+-dependent K+ channels is increased in the basilar artery during chronic hypertension. Diameter of the basilar artery was measured using a cranial window in anesthetized normotensive Wistar-Kyoto rats (WKY, arterial pressure = 109 +/- 3 mmHg, mean +/- SE) and stroke-prone spontaneously hypertensive rats (SHRSP, arterial pressure = 179 +/- 4 mmHg). Responses of the basilar artery to topical application of tetraethylammonium ion (TEA), an inhibitor of Ca2+-dependent K+ channels, were examined in WKY and SHRSP. Vessel diameter decreased by 2 +/- 1 and 4 +/- 0.1% in WKY and by 7 +/- 2 and 18 +/- 1% in SHRSP (P < 0.05 vs. WKY) in response to 10(-4) and 10(-3) M TEA, respectively. Similar results were obtained using iberiotoxin (10(-8) and 10(-7) M), a highly selective inhibitor of Ca2+-dependent K+ channels. In contrast to constrictor responses to TEA and iberiotoxin, constrictor responses of the basilar artery in response to serotonin and U-46619 were similar in WKY and SHRSP. In WKY rats that were made chronically hypertensive (arterial pressure = 172 +/- 6 mmHg) after treatment for 4 wk with N(G)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, constriction of the basilar artery in response to TEA was also enhanced. These findings suggest that activity of Ca2+-dependent K+ channels is enhanced in the basilar artery in vivo in two models of chronic hypertension. Thus Ca2+-dependent K+ channels in the basilar artery may be activated during chronic hypertension, perhaps as a response to elevation of intracellular concentration of Ca2+.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2002

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

The first goal of the present study was to examine the influence of gender on reactivity of the basilar artery. The second goal of this study was to examine the effect of diabetes mellitus on reactivity of the basilar artery in male and female rats. We examined in vivo responses of the basilar artery in male and female nondiabetic and diabetic rats in response to a nitric oxide synthase (NOS)-dependent (acetylcholine) and -independent (nitroglycerin) agonist. In nondiabetic male and female rats, acetylcholine and nitroglycerin produced dose-related dilatation of the basilar artery. However, the magnitude of vasodilatation in response to acetylcholine and a high concentration of nitroglycerin was significantly greater in female than in male rats. Acetylcholine (1.0 microM) dilated the basilar artery by 11 +/- 2% in nondiabetic males versus 25 +/- 4% in nondiabetic females (P<0.05). Nitroglycerin (1.0 microM) dilated the basilar artery by 37 +/- 8% in nondiabetic males versus 62 +/- 5% in nondiabetic females (P<0.05). Thus, there is a significant effect of gender on reactivity of the basilar artery during physiologic conditions. Dilatation of the basilar artery in response to acetylcholine, but not nitroglycerin, was impaired in diabetic male and female rats compared to their nondiabetic counterparts. Acetylcholine (1.0 microM) dilated the basilar artery by only 5 +/- 1% in diabetic males and by only 4 +/- 1% in diabetic females. In summary, dilatation of the basilar artery in response to NOS-dependent agonist was significantly greater in nondiabetic female than in nondiabetic male rats. In addition, diabetes mellitus impaired NOS-dependent dilatation of the basilar artery not only in male rats, but also in female rats. We suggest that the results of these studies provide insight into the pathogenesis of cerebrovascular abnormalities observed in postmenopausal women.

Acetylcholine↗
PubMed1984

[Regional lysis of acute basilar artery occlusion--case report].

Thrombosis of the basilar artery is not a rare disease, and the mortality is reported to be 60 to 80%. Present standard therapy with heparin infusions yields poor results. The high risk of intracerebral haemorrhage prohibits systemic fibrinolytic therapy. Due to these facts and good experience in our department with the use of local intracoronary lysis in acute myocardial infarction, the method of local thrombolysis was applied in a case of acute basilar artery thrombosis. Fibrinolytic therapy was started via an angiography catheter placed in the vertebral artery in a 28 year-old woman with hemiplegia and severe brain stem symptoms. The patient received 200,000 IU streptokinase within 2 hours and subsequently 300,000 IU urokinase within 10 hours. The vessel re-opened completely. The neurological symptoms decreased during the following weeks. Based on this experience and according to rare reports in the literature we believe local low-dose thrombolysis to be a causal therapy promising success for acute thrombosis of the basilar artery. This therapy can be carried out in every medical centre able to perform selective angiography and experienced in the administration of fibrinolytic drugs.

Adult↗
PubMed1993

Endothelial thromboxane production plays a role in the contraction caused by 5-hydroxytryptamine in rat basilar arteries.

The goal of the present study was to characterize the role of the endothelium in the 5-hydroxytryptamine (5-HT)-induced contraction of the rat basilar artery. Rat basilar artery segments were mounted in myographs to study their isometric tension development. 5-HT caused dose-dependent contractions that were minimally affected by endothelium removal. The dose-response curve obtained with the 5-HT1 receptor agonist, 5-carboxamidotryptamine (5-CT), was biphasic in arteries with endothelium; removal of the endothelium eliminated the first phase of the contraction. The 5-HT2 receptor antagonist, ketanserin (30 nM), shifted the dose-response curve to 5-HT to the right; in arteries with endothelium, the curve became biphasic. Ketanserin inhibited the second phase of the dose-response curve to 5-CT. The mixed 5-HT1/5-HT2 receptor antagonist, metergoline (30 nM), shifted the dose-response curve to 5-HT non-competitively to the right and depressed both phases of the dose-response curve to 5-CT. In basilar arteries with endothelium and treated with ketanserin, the thromboxane A2 receptor antagonist, ICI 192605 (1 microM), significantly decreased the responsiveness to 5-HT and the dose-response curve for 5-HT became monophasic. ICI 192605 and the thromboxane A2 synthase inhibitor, ridogrel (10 microM), both suppressed the first phase of the dose-response curve to 5-CT. These data indicate that both endothelial 5-HT1 and smooth muscle 5-HT2 receptors participate in the contractions caused by 5-HT in the rat basilar artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Hyperdense basilar artery. An early computed tomography sign of thrombosis.

Noncontrast computed tomographic scans (CT scans) may show a hyperdense basilar artery before a brainstem infarct is visualized. This early sign should assist clinicians in confirming the diagnosis of basilar artery thrombosis. In a review of admission records of 750 patients with acute cerebrovascular disease from July 1991 to June 1993, at Saint Louis University Hospital, 20 patients were identified with clinical signs of nonlacunar, vertebrobasilar distribution infarction. Eight of these had pontomesencephalic ischemia. Their neuroimaging studies and medical records were evaluated. Four patients with acute clinical signs of pontomesencephalic infarction were found to have a hyperdense basilar artery on CT scans. The scans of 2 patients were excluded because of dolichoectasia; in the other 2 patients, the basilar artery appeared normal on the CT scan. The hyperdense basilar artery was detected within the early hours of neurological symptoms and often was the only detectable abnormality on the scan. In 3 patients extensive brainstem infarcts subsequently developed and they died. Basilar artery thrombosis was confirmed by pathological study in all these patients. In the fourth patient basilar artery occlusion and a large pontine infarct were evident by magnetic resonance imaging and angiography. A hyperdense basilar artery is a common feature on CT scans of patients presenting with an early clinical diagnosis of thrombosis. Untreated, the hyperintense basilar artery often portends a poor prognosis. Its ready recognition should guide further interventional studies and treatment.

Adult↗