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At least 235 records · Page 13Linked to original sources
PubMed1997

[Basilar artery aneurysm associated with agenesis of unilateral internal carotid artery: two case reports].

Two patients presented with a basilar artery aneurysm associated with agenesis of the right internal carotid artery. In both cases, the right middle cerebral artery was supplied by the basilar artery via the enlarged right posterior communicating artery, and the right anterior cerebral artery was supplied by the left internal carotid artery via the anterior communicating artery. The first patient was a 65-year-old woman who suffered from a subarachnoid hemorrhage due to rupture of a basilar bifurcation aneurysm, which was demonstrated as a "de novo" aneurysm 13 years after successful clipping of the anterior communicating artery aneurysm. Delayed surgery was planned, but she died due to recurrent hemorrhage. The second patient was a 67-year-old woman who had had a history of progressive left sided weakness over the previous few years. Conventional angiography and 3 dimensional CT angiography showed a large aneurysm of the basilar artery trunk with a wide neck. Endovascular embolization was performed with mechanically detachable coils, and the aneurysm was incompletely occluded. The patient regained complete strength in the left arm after the treatment, but the follow-up angiography at 5 months disclosed recanalization of the treated aneurysm, associated with shift of the packed coils. Hemodynamic stress resulting from unique collateral circulation with agenesis of the internal carotid artery may cause a predisposition to "de novo" aneurysm formation or recanalization of an occluded aneurysm with coils.

Aged↗
PubMed1989

Role of endothelium in hypoxic contraction of canine basilar artery.

1. Reversible contraction of canine basilar artery, produced by hypoxia, persisted after mechanical and chemical removal of the endothelium. The removal of endothelium was confirmed by scanning electron microscopy as well as by the abolition or reversal of the relaxant response to acetylcholine or arginine8-vasopressin. 2. Hydroquinone, believed to block selectively endothelium-mediated relaxation, also preferentially attenuated hypoxic contractions even in the absence of endothelium but did not reduce responses to 5-hydroxytryptamine (5-HT) or high external potassium. 3. Contractions induced by red blood cell haemolysate, which occur independently of the endothelium, were also selectively attenuated by hydroquinone. 4. Contractions caused by hypoxia were inhibited by pretreatment with adenosine or by its application after contraction had developed. 5. Hypoxic contraction in canine basilar artery may result partly from a direct effect on smooth muscle as well as through the endothelium. 6. Hydroquinone may have an additional locus of action in smooth muscle cells besides its well known effect on the endothelium.

Adenosine↗
PubMed1994

Effect of diabetes mellitus on responses of the rat basilar artery to activation of beta-adrenergic receptors.

The goal of this study was to determine whether diabetes mellitus alters reactivity of the basilar artery in vivo to activation of beta-adrenergic receptors. We measured diameter of the basilar artery in non-diabetic and diabetic (streptozotocin 50-60 mg/kg i.p.) rats during superfusion with isoproterenol and norepinephrine, which dilate cerebral blood vessels via activation of beta-adrenergic receptors. Dilatation of the basilar artery in response to isoproterenol and norepinephrine was significantly less in diabetic compared to non-diabetic rats. To determine whether impaired dilatation of the basilar artery in diabetic rats in response to isoproterenol and norepinephrine was related to an alteration in catalytic activity of adenylate cyclase, we examined dilatation of the basilar artery in response to forskolin, a direct activator of adenylate cyclase. In contrast to that observed for isoproterenol and norepinephrine, forskolin produced similar dilatation of the basilar artery in non-diabetic and diabetic rats. Thus, the findings of the present study suggest that diabetes mellitus impairs dilatation of the basilar artery in vivo in response to activation of beta-adrenergic receptors. In addition, impairment of beta-adrenergic mediated dilatation of the basilar artery during diabetes mellitus does not appear to be related to an alteration in catalytic activity of adenylate cyclase.

Adrenergic beta-Agonists↗
PubMed1995

Dilatation of the basilar artery in response to selective activation of endothelin B receptors in vivo.

The objective of this study was to examine effects of activation of endothelin (ET) B receptors on tone of the basilar artery in vivo. By using a cranial window in anesthetized rats, we examined the effects of IRL 1620, a selective ETB receptor agonist, on diameter of the basilar artery. Under control conditions, diameter of the basilar artery was 214 +/- 6 microns (mean +/- S.E.). Topical application of IRL 1620 (10(-8) mol/l) for 4 min dilated the basilar artery by 30 +/- 4%. Marked desensitization of vasodilator responses was observed in response to a second application of IRL 1620, but not acetylcholine, which indicates a homologous nature of desensitization. REA/001, an ETA/ETB receptor antagonist, abolished IRL 1620-induced dilatation of the basilar artery. BQ 123, a selective ETA receptor antagonist, inhibited constriction in response to ET-1, but did not affect dilator responses of the basilar artery to IRL 1620. Both NG-nitro-L-arginine methyl ester and NG-nitro-L-arginine, inhibitors of nitric oxide synthase, produced marked inhibition of dilator responses of the basilar artery to IRL 1620 without inhibiting vasodilator responses to sodium nitroprusside. Indomethacin did not inhibit vasodilatation in response to IRL 1620. These findings suggest that activation of ETB receptors produces dilatation of the basilar artery in vivo. Dilator responses of the basilar artery to activation of ETB receptors are dependent on production of nitric oxide.

Animals↗
PubMed1996

Transluminal angioplasty for arteriosclerotic disease of the distal vertebral and basilar arteries.

OBJECTIVE: Percutaneous transluminal angioplasty (PTA) for the distal vertebral and basilar artery is now being performed in selected patients with haemodynamically significant lesions of the posterior cerebral circulation. Its effect and overall results were examined. PATIENTS AND METHODS: A balloon dilatation catheter specifically developed for these procedures, with a 2.0-3.5 mm balloon diameter, at 6 atmospheres of pressure, was used. Angioplasty was performed in 12 patients (including six whose initial results have been reported) with angiographically documented stenotic lesions involving either the intracranial vertebral artery (C1-C2 portion) or the basilar artery, and satisfying the following criteria: (1) clinical symptoms suggestive or consistent with a transient ischaemic attack refractory to medical treatment, or small infarction of the posterior circulation; and (2) angiographically documented stenosis greater than 70%. Two of 12 patients had complete thrombosis of the distal vertebral and basilar artery and PTA was performed after successful intra-arterial thrombolysis. RESULTS: Successful results, without complications, were obtained in eight patients, with complete resolution of vertebrobasilar ischaemic symptoms. Immediate complications occurred in four patients including two with vessel dissection, and two with thromboembolism. The two patients with acute arterial dissection were reoperated but developed small infarctions with permanent neurological deficits. The two patients with thromboembolic complication showed transient neurological deficit. The overall stenosis ratio decreased from a mean of 84% pretreatment to 44% after the angioplasty procedure. Restenosis occurred in two patients. Long term clinical follow up in 11 patients who survived more than six months showed resolution of ischaemic symptoms after PTA in all except for one with a restenosis who had recurrent transient ischaemic attacks. CONCLUSION: Transluminal angioplasty may be an effective procedure to treat vertebrobasilar ischaemia secondary to high grade arteriosclerotic disease affecting either the distal vertebral or basilar artery regions that do not respond to medical treatment.

Acute Disease↗
PubMed1993

Role of ATP-sensitive K+ channels in CGRP-induced dilatation of basilar artery in vivo.

Stimulation of adenylate cyclase appears to activate ATP-sensitive K+ channels in the basilar artery. We tested the hypothesis that calcitonin gene-related peptide (CGRP), which increases intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels, activates ATP-sensitive K+ channels and thereby causes vasodilatation. Using a cranial window in anesthetized rats, we examined responses of the basilar artery to CGRP in vivo. We also examined responses of the artery to another vasoactive peptide, vasoactive intestinal peptide (VIP). Topical application of CGRP (10(-11) to 10(-8) M) increased diameter of the basilar artery. Responses of the basilar artery to CGRP were almost abolished by a CGRP1 receptor antagonist, CGRP-(8-37). Vasodilatation in response to VIP was much smaller than that produced by CGRP. Dilator responses of the basilar artery to 10(-9) and 10(-8) M CGRP were inhibited by glibenclamide (10(-6) M), a selective inhibitor of ATP-sensitive K+ channels, by 69 +/- 19 and 41 +/- 9%, respectively. NG-nitro-L-arginine methyl ester (10(-5) M), an inhibitor of nitric oxide synthase, did not attenuate dilator response to 10(-8) M CGRP but inhibited responses to 10(-9) M CGRP by 34 +/- 12%. Indomethacin did not alter dilator responses to CGRP. These findings suggest that a minor component of CGRP-induced dilatation of the basilar artery is mediated by endothelium-derived relaxing factor. Vasodilatation in response to CGRP appears to be mediated primarily by direct activation of CGRP1 receptors on vascular muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

Direct angioplasty of the basilar artery in baboons.

The lower portion of the basilar artery is a site of significant disease, both aneurysmal and stenotic, but has been considered inaccessible via traditional surgical approaches. A baboon model was used to evaluate the feasibility of a direct surgical reconstruction via a transoral-transclival approach, utilizing temporary occlusion of the basilar artery. An arteriotomy was performed and either repaired primarily or a venous patch graft was sutured in place. All animals survived the surgery; one suffered fatal postoperative upper airway obstruction, but the other four were neurologically intact at the time of death. Patency at the site of repair was confirmed both angiographically and histologically. We conclude that temporary clamping in conjunction with direct reconstruction of the basilar artery is feasible in this primate model. Future studies will focus on further applications of this technique.

Animals↗
PubMed1997

Superoxide dismutase partially restores impaired dilatation of the basilar artery during diabetes mellitus.

The goal of this study was to test the hypothesis that administration of superoxide dismutase restores nitric oxide synthase-mediated dilatation of the basilar artery during diabetes mellitus. We measured the diameter of the basilar artery in vivo in nondiabetic and diabetic rats (streptozotocin; 50-60 mg/kg i.p.) in response to nitric oxide synthase-dependent agonists (acetylcholine and bradykinin) and a nitric oxide synthase-independent agonist (nitroglycerin) before and during application of superoxide dismutase. Topical application of acetylcholine (1.0 and 10 microM) and bradykinin (1.0 and 10 microM) produced dose-related dilatation of the basilar artery in nondiabetic and diabetic rats. However, the magnitude of vasodilation produced by acetylcholine and bradykinin was significantly less in diabetic rats. Topical application of nitroglycerin (0.1 and 1.0 microM) produced similar dose-related dilatation of the basilar artery in nondiabetic and diabetic rats. Treatment with superoxide dismutase (150 U/ml) did not alter baseline diameter of the basilar artery in nondiabetic and diabetic rats. However, topical application of superoxide dismutase partially restored nitric oxide synthase-dependent dilatation of the basilar artery in diabetic rats towards that observed in nondiabetic rats. Superoxide dismutase did not alter dilatation of the basilar artery in nondiabetic rats. These findings suggest that impaired nitric oxide synthase-dependent dilatation of the basilar artery during diabetes mellitus may be related, in part, to enhanced release of oxygen-derived free radicals.

Acetylcholine↗
PubMed2001

Role of Na(+)/H(+) exchanger in dilator responses of rat basilar artery in vivo.

We tested the hypothesis that activation of Na(+)/H(+) exchanger is involved in dilator responses of the basilar artery to endothelium-dependent vasodilators in vivo. Using a cranial window in anesthetized rats, we examined responses of the basilar artery to acetylcholine and bradykinin. Topical application of acetylcholine and bradykinin increased diameter of the basilar artery in a concentration-related manner. Because N(G)-nitro-L-arginine, an inhibitor of nitric oxide synthase, almost abolished vasodilator responses to acetylcholine and bradykinin, vasodilatation produced by the agonists appears to be mediated primarily by nitric oxide. 5-N,N-Hexamethyleneamiloride, an inhibitor of Na(+)/H(+) exchanger, did not affect baseline diameter of the basilar artery, but inhibited vasodilatation in response to acetylcholine and bradykinin, without affecting vasodilatation produced by sodium nitroprusside. FR183998, another inhibitor of Na(+)/H(+) exchanger, also attenuated acetylcholine-induced dilatation of the basilar artery without affecting vasodilatation in response to sodium nitroprusside. Monomethylamine hydrochloride, which produces intracellular alkalinization, enhanced acetylcholine-induced dilatation of the basilar artery in the presence of 5-N,N-hexamethyleneamiloride. These results suggest that intracellular alkalinization produced by activation of Na(+)/H(+) exchanger may enhance nitric oxide production in the basilar arterial endothelium and thereby contribute to dilator responses of the artery in vivo.

Acetylcholine↗
PubMed1997

Treatment of dissecting basilar artery aneurysm by flow reversal.

Dissecting aneurysm of the basilar artery is a rare but increasingly recognized entity, with a frequently fatal or morbid outcome. Unlike the well established proximal occlusion and trapping approaches to vertebral artery dissections, surgical intervention for basilar lesions has been limited to wrapping techniques for arterial wall reinforcement. We report a case of midbasilar dissecting aneurysm successfully treated by clipping the proximal basilar artery below the level of the anterior inferior cerebellar arteries, allowing retrograde flow via the posterior communicating arteries to provide continued basilar perfusion. With the growing recognition of basilar dissection and pseudoaneurysm formation there is a need for improved therapeutic options. We suggest that definitive treatment can be achieved using the principle of proximal occlusion and flow reversal, and review the pertinent literature on basilar artery dissection.

Aortic Dissection↗
PubMed1997

Relaxant effects of vasodilator peptides on isolated basilar arteries from stroke-prone spontaneously hypertensive rats.

1. The relaxant of vasodilator peptides were examined in ring preparations of basilar arteries from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats. 2. Vasoactive intestinal peptide and peptide histidine isoleucine produced similar endothelium-independent relaxations in basilar arteries from WKY rats and SHRSP. Calcitonin gene-related peptide (CGRP) elicited endothelium-independent relaxations in both groups and the CGRP-induced relaxation was greater in SHRSP than in WKY rats. Substance P and neurokinin A did nor relax basilar arteries from either group. 3. Both WKY rat and SHRSP basilar arteries were relatively insensitive to atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide. 4. Bradykinin (BK) potently relaxed basilar arteries with endothelium, but BK produced contractions in endothelium-rubbed arteries in both WKY rats and in SHRSP. There was no significant difference in the relaxant response to BK between WKY rat and SHRSP arteries. 5. Adrenomedullin (AM) produced endothelium-independent relaxations in both groups and the relaxant response to AM was significantly greater in SHRSP than in WKY rats. 6. Human CGRP(8-37;mumol/L), a CGRP receptor antagonist, significantly inhibited both relaxant responses induced by CGRP and AM in WKY rats and in SHRSP arteries. 7. Among various peptides tested, the responses to CGRP and AM were higher in basilar arteries from SHRSP than in those from WKY rats. The relaxation produced by AM may be via CGRP receptors in WKY rat and SHRSP basilar arteries.

Adrenomedullin↗
PubMed1993

Endothelium-dependent contraction produced by acetylcholine and relaxation produced by histamine in monkey basilar arteries.

The present experiments were carried out to investigate endothelium-dependence of the responses to ACh, arachidonic acid and histamine in monkey basilar arteries. As we reported previously (1), ACh (10(-7) M) and arachidonic acid (5 x 10(-7) M) caused endothelium-dependent contraction (EDC) in both monkey and canine basilar arteries. The endothelium-derived contracting factor (EDCF) is probably TXA2, since the EDC was attenuated by a cyclooxygenase inhibitor (aspirin, 5 x 10(-5) M), thromboxane A2 (TXA2) synthetase inhibitors (OKY-046, 10(-5) M; RS-5186, 10(-6) M) and TXA2 antagonists (ONO-3708, 10(-8) M; S-145, 5 x 10(-9) M). Histamine caused endothelium-dependent relaxation (EDR) in monkey basilar arteries and EDC in canine basilar arteries. The EDR in monkey basilar arteries was attenuated by nitric oxide synthetase inhibitor, NG-monomethyl-L-arginine (L-NMMA) in a concentration-dependent manner and the EDC in canine basilar arteries was attenuated by aspirin, TAX2 synthetase inhibitors and TXA2 antagonists. The EDR and EDC were antagonized by tripelennamine (10(-6) M) but not by cimetidine (10(-5) M), indicating that they are mediated by H1-receptors. From these results, we suggest that in the monkey basilar artery, either there are two types of endothelium, an EDCF type for ACh and arachidonic acid and an EDRF type for histamine, or there is single type of endothelium with two types of signalling processes, one for EDC and one for EDR.

Acetylcholine↗
PubMed2004

Vestibular evoked myogenic potentials in basilar artery migraine.

OBJECTIVES/HYPOTHESIS: Because the sacculocollic reflex is a descending pathway passing through the territory of basilar artery, the aim of the study was to investigate whether hypoperfusion affects this pathway by applying vestibular evoked myogenic potential (VEMP) testing in patients with basilar artery migraine. STUDY DESIGN: A prospective study from May 2000 to April 2002. METHODS: Twenty patients were diagnosed as having basilar artery migraine according to the criteria of the International Headache Society and literature. Eight were male and 12 were female patients, and their ages ranged from 9 to 48 years (mean age, 40 y). Each patient underwent a battery of audio-vestibular tests. RESULTS: Electronystagmography disclosed abnormal eye tracking test in six patients (30%), and there were abnormal optokinetic nystagmus test results in nine patients (45%). Caloric test revealed canal paresis in seven patients, directional preponderance in four patients, and normal responses in nine patients (45%). Vestibular evoked myogenic potential testing disclosed absent vestibular evoked myogenic potentials in seven patients and delayed vestibular evoked myogenic potentials in two patients, with one patient showing absent vestibular evoked myogenic potentials on one side and delayed vestibular evoked myogenic potentials on the other side. The remaining 10 patients (50%) had bilateral normal vestibular evoked myogenic potentials. Five patients had preserved both caloric and VEMP test responses, six patients displayed absent caloric and VEMP test responses, and the remaining nine patients had either abnormal caloric test responses or abnormal vestibular evoked myogenic potentials, exhibiting a nonsignificant relationship between caloric test responses and vestibular evoked myogenic potentials. Relief of headache and vertigo was achieved after 3 months of medication. Ten asymptomatic patients with either absent or delayed vestibular evoked myogenic potentials before treatment underwent follow-up VEMP test, and nine patients (90%) displayed normal vestibular evoked myogenic potentials bilaterally. CONCLUSION: Vestibular evoked myogenic potential testing evaluates the sacculocollic reflex, which descends through the lower brainstem. Some patients with basilar artery migraine have absent or delayed vestibular evoked myogenic potentials, presumably because the descending pathway from the saccule through the brainstem to cranial nerve XI is interrupted, which is attributed to hypoperfusion in the territory of the basilar artery. After 3 months of medication, recovery of normal vestibular evoked myogenic potentials in an asymptomatic patient indicates reversible ischemia in the territory of the basilar artery.

Adolescent↗
PubMed2001

Basilar artery vasculitis secondary to sphenoid sinusitis--case report.

A 35-year-old male presented with basilar artery vasculitis secondary to sphenoid sinusitis manifesting as rapidly deteriorating symptoms including consciousness disturbance and right hemiparesis. Computed tomography (CT) on admission showed sphenoid sinusitis without intracranial lesion. Emergency angiography demonstrated basilar artery stenosis. The neurological deterioration was considered to be caused by ischemia of the perforating arteries branching from the stenotic portion of the basilar artery. The patient was treated with urokinase infusion through a microcatheter just proximal to the stenosis 3 hours after the onset of the symptoms. His consciousness level and right hemiparesis markedly improved immediately after the procedure. Magnetic resonance (MR) imaging on day 5 revealed that extension of the sphenoid sinusitis into the prepontine cistern had formed an abscess which was attached to the clivus. The basilar artery was embedded in the abscess at the angiographic stenosis. Cerebrospinal fluid (CSF) analysis showed white blood cell count of 601/mm3 with 82% neutrophils, 89.2 mg/dl protein, and 31 mg/dl glucose. No causative organism in the CSF could be identified by smear or culture. Early MR imaging and CSF examination are recommended when patients present with both ischemic symptoms involving the basilar artery and opacification of the sphenoid sinus on CT to identify basilar artery vasculitis secondary to sphenoid sinusitis.

Adult↗
PubMed1994

[Percutaneous transluminal angioplasty for progressing stroke caused by severe basilar artery stenosis: case report].

We encountered one case of progressing stroke caused by severe basilar artery stenosis. The patient was treated with emergent percutaneous transluminal angioplasty (PTA) with satisfactory results. A 54 year-old woman was admitted 15 minutes after the sudden onset of rt. hemiparesis, rt. hemidysesthesia, dysarthria and consciousness disturbance. CT scan on admission showed no abnormal findings. The consciousness level of the patient deteriorated rapidly from JCS 1 to JCS 20 within 30 minutes from the ictus. An emergent angiogram revealed severe basilar artery stenosis at its middle portion and poorly developed collateral circulation. One hour after the stroke occurred, PTA was performed. Using a 3mm diameter balloon catheter, we introduced the balloon into the stenotic lesion and inflated it 6 times from 4 atm to 8 atm pressure. The patient recovered immediately on the operating table improving from JCS 20 to JCS 1. Rt. hemiparesis also improved. Follow-up MRI showed a small area of ischemic change in the brain stem, but no large infarction appeared. The patient was discharged with no neurosurgical deficits after 30 days of PTA. PTA for basilar artery stenosis is still a controversial subject. One reason is the risk of basilar artery perforating branches occlusion by balloon catheter and the other is the difficulty of introducing a flexible balloon catheter into the basilar artery beyond the acute angulation of the vertebral artery. If those two problems were solved, PTA would be the first-choice therapy for basilar artery stenosis in both acute and chronic stages.

Acute Disease↗
PubMed1989

Evidence for the presence of 5-HT1-like receptors in rabbit isolated basilar arteries.

The 5-hydroxytryptamine (5-HT) receptor mediating contraction of rabbit isolated endothelium denuded basilar artery has been investigated. 5-HT and a variety of 5-HT receptor agonists contracted rabbit isolated basilar artery with a rank order of agonist potency: 5-carboxamidotryptamine (5-CT) greater than 5-HT greater than GR43175. None of these agonists relaxed rabbit isolated basilar artery when tone was elevated with prostaglandin F2alpha. The contractile response to both 5-HT and GR43175 was resistant to antagonism by GR38032, phentolamine, (+/-)-cyanopindolol and yohimbine. Ketanserin (100 nM) and mesulergine (100 nM) produced small significant rightward shifts of C-E curves to 5-HT with respective concentration-ratio shifts of 5.7 (1.5-21.0 95% confidence interval and 2.89 (1.1-7.6 95% confidence interval). GR43175-induced contraction was resistant to antagonism by ketanserin however the maximum response to GR43175 was significantly reduced in the presence of mesulergine, with no change in EC50. Methiothepin was a potent antagonist of the contractile actions of both 5-HT and GR43175, with respective pA2 values against each agonist of 10.3 and 9.9. The slope of the Schild regression for methiothepin against 5-HT-induced contraction was significantly less than unity. Methiothepin (100 nM) had no effect on the contractile response to the thromboxane A2 mimetic U-46619. It is concluded that 5-HT and GR43175 contract rabbit isolated basilar artery by activating a 5-HT1-like receptor. In addition 5-HT may activate a population of 5-HT2 receptors producing a further contraction of rabbit isolated basilar artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Variant aneurysms of the fenestrated basilar artery.

Two cases of aneurysm occurring on a fenestrated basilar artery are reported. One patient had a saccular aneurysm in the typical location at the vertebrobasilar junction at the proximal end of the fenestrated basilar segment. The aneurysm sac projected dorsally into the brain stem. The other patient had a blister-like aneurysm distal to a fenestration of the terminal basilar artery. The development of a distal aneurysm on a fenestrated basilar artery is predictable based on the reported morphology of the vessel wall in this vascular anomaly.

Adult↗