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PubMed1986

Selective hemoglobin inhibition of endothelium-dependent vasodilation of rabbit basilar artery.

The effect of hemoglobin on endothelium-dependent vasodilation of the isolated rabbit basilar artery was examined using an isometric tension recording method. Acetylcholine (ACh) (10(-7) - (10(-4) M) evoked a dose-dependent vasodilation of isolated rabbit basilar artery previously contracted by 10(-6) M serotonin. This vasodilating action disappeared after removal of the endothelium. The ACh-induced vasodilation of rabbit basilar artery is thought to be strictly endothelium-dependent. Hemoglobin (10(-7) - 10(-5) M) inhibited this ACh-induced endothelium-dependent vasodilation conditional upon the dose. Adenosine triphosphate (ATP, 10(-7) - 10(-4) M) also relaxed isolated rabbit basilar artery already contracted by 10(-6) M serotonin. This vasodilating action was slightly inhibited by adenosine antagonist, 8-phenyltheophylline (8-PT), and markedly attenuated by removal of the endothelium. This ATP-induced vasodilation is thought to be composed of ATP itself (endothelium-dependent) and ATP degradation products (endothelium-independent) such as adenosine monophosphate or adenosine. Hemoglobin markedly inhibited ATP-induced vasodilation, but there still remained a small vasodilation, which was blocked by 8-PT. Papaverine-induced vasodilation was not affected by removal of the endothelium, and hemoglobin did not inhibit the papaverine-induced vasodilation. These results suggest that rabbit basilar artery has endothelium-dependent vasodilating mechanisms induced by ACh and ATP, and that hemoglobin selectively blocks the endothelium-dependent vasodilation. This finding may relate to the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage: there is a possibility that the presence of hemoglobin released from lysed erythrocytes inhibits the endothelium-dependent vasodilation of cerebral arteries; furthermore, the endothelial degeneration following subarachnoid hemorrhage may impair the vasodilating mechanisms of cerebral artery smooth-muscle cells.

Acetylcholine↗
PubMed1991

Effects of CD-349, a dihydropyridine derivative, on contraction induced by vasoactive agents in canine basilar artery after subarachnoid hemorrhage.

We investigated the effects of CD-349, a dihydropyridine derivative, on contraction induced by vasoactive agents in canine basilar artery after subarachnoid hemorrhage (SAH). Ca(2+)-induced contraction of basilar arterial strips preincubated with serotonin (5-HT, 3x10(-6)M) was potentiated in strips from SAH. However, Ca(2+)-induced contraction of arterial strips which were depolarized with isotonic K+ (64mM) was attenuated in strips from SAH. These Ca(2+)-induced contractions of the basilar arteries preincubated with 5-HT and K+ from both control and SAH dogs were significantly inhibited by CD-349 and nicardipine, both dihydropyridine derivatives. 5-HT contracted the basilar arterial strips in a concentration-dependent manner; however, the maximal contraction of the basilar arterial strips to 5-HT was enhanced in SAH. Endothelium-dependent relaxation in response to substance-P was attenuated in SAH when compared to that in control dogs. Early treatment with CD-349 (1 or 2mg/kg/day, i.m.) for 1 week reversed not only the enhanced contraction of the basilar artery in response to 5-HT but also the impairment of endothelium-dependent relaxation in response to substance-P in SAH. It is expected that CD-349 may be a useful agent for the treatment of cerebrovascular diseases such as SAH.

Animals↗
PubMed1986

Relationship between receptors mediating serotonin (5-HT) contractions in the canine basilar artery to 5-HT1, 5-HT2 and rat stomach fundus 5-HT receptors.

The receptors responsible for contraction to serotonin (5-HT) in the canine basilar artery have not been definitively established to date. Several selective 5-HT2 receptor antagonists (spiperone, ketanserin and LY53857) did not inhibit markedly 5-HT-induced contractions in the canine basilar artery in doses higher than required for substantial inhibition of 5-HT2 receptor-mediated responses. These data suggest that the receptors mediating 5-HT-induced contractions in the basilar artery are not 5-HT2 receptors. Using a series of 5-HT antagonists with relatively high affinity at 5-HT1 sites, over a 1000-fold difference occurred in their ability to block 5-HT receptors in the canine basilar artery, in spite of the similar and high affinity of the antagonists at 5-HT1 binding sites. These data support the contention that 5-HT receptors in the canine basilar artery are not 5-HT1 receptors as defined by ligand binding studies in brain cortical membranes. Similarity of the contractile effects of 5-HT in the rat stomach fundus and in the basilar artery coupled to the previous observations that receptors mediating 5-HT-induced contractions in the fundus were not 5-HT1, 5-HT1A, 5-HT1B or 5-HT2 led us to consider the possibility that 5-HT receptors in the canine basilar artery may resemble those in the rat stomach fundus. The affinity of several 5-HT antagonists determined in the canine basilar artery correlated extremely well (correlation coefficient = 0.96) with the affinities obtained for the same antagonists in the rat stomach fundus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effect of diabetes mellitus on response of the basilar artery to activation of ATP-sensitive potassium channels.

Our goal was to determine whether responses of the basilar artery to activation of ATP-sensitive potassium channels are altered during diabetes mellitus. We measured changes in diameter of the basilar artery in vivo in non-diabetic and diabetic rats (streptozotocin; 50-60 mg/kg i.p.) in response to activation of ATP-sensitive potassium channels using aprikalim (RP 52891) and levcromakalim (BRL 38227). Aprikalim (1.0 microM) dilated the basilar artery in non-diabetic rats by 27 +/- 6%, but by only 11 +/- 3% in diabetic rats (means +/- S.E.; P < 0.05). Levcromakalim (1.0 microM) dilated the basilar artery in non-diabetic rats by 45 +/- 11%, but by only 20 +/- 5% in diabetic rats (P < 0.05). Nitroglycerin (1.0 microM) dilated the basilar artery by 20 +/- 5% in non-diabetic rats and 17 +/- 2% in diabetic rats (P > 0.05). Thus, impaired dilatation of pial arterioles in diabetic rats in response to aprikalim and levcromakalim is not related to a non-specific effect of diabetes mellitus on vasodilatation. The findings of the present study suggest that ATP-sensitive potassium channels are functional in the rat basilar artery in vivo and are altered during diabetes mellitus.

Adenosine Triphosphate↗
PubMed1999

Vasodilator action in the nitroxylated cyanoamidine derivative, KRN2391, in rabbit basilar artery.

KRN2391 is a cyanoamidine derivative with a pyridine ring and a nitroxyl group. This gives the molecule a dual pharmacological action as both an ATP-sensitive K channel (K(ATP)) opener and an organic nitrate. In cerebrovascular disease with endothelial dysfunction, such a compound could be advantageous to prevent the negative consequences of a reduced synthesis of endogenous nitric oxide and endothelium-derived hyperpolarizing factor. The objective of this study was to characterise the vasodilator action of KRN2391 in a cerebral artery. As shown in the rabbit basilar artery contracted by endothelin-1 KRN2391 elicited a concentration-dependent relaxation. KRN2391 was unable to relax arteries contracted by a 60 mM K solution. The KRN2391-induced relaxation of endothelin-1-contracted arteries was unaffected by N(G)-nitro-L-arginine (0.1 mM), indomethacin (10 microM) or removal of the endothelium. The guanylate cyclase inhibitors ODQ (10 microM) and LY53583 (10 microM), and the cGMP phosphodiesterase inhibitor zaprinast (10 microM) each had no effect on the KRN2391-induced relaxation. Glibenclamide (1 microM), a blocker of K(ATP), caused a rightward shift of the concentration-response curve for KRN2391. The relaxation induced by the prototype K(ATP) opener levcromakalim was inhibited to a similar extent by glibenclamide. Addition of ODQ or LY53583, or the calcium-sensitive K channel blockers apamin (0.1 microM) and charybdotoxin (0.1 microM) in the presence of glibenclamide did not produce a significant further inhibition of the KRN-induced relaxation. KRN2391 (10 microM) did not influence the content of cGMP in the basilar artery, whereas the nitric oxide donor 3-morpholino-sydnonimine (0.1 mM) increased the cGMP level three-fold. Thus, KRN2391 is an effective vasodilator of the rabbit basilar artery, acting mainly through opening of KATP . The nitro-moiety of the molecule does not seem to contribute to the relaxant effect in this artery.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1991

Role of the basilar artery in regulation of blood flow to the brain stem in rats.

Large arteries contribute to the regulation of cerebral blood flow. The goal of this study was to examine the effects of changes in diameter of the basilar artery on blood flow to the brain stem. We measured blood flow with laser-Doppler flowmetry in anesthetized rats. The topical application of 10(-6) M serotonin, which selectively constricts large arteries, reduced diameter of the basilar artery by 47 +/- 5% (mean +/- SEM, n = 6) but did not alter blood flow to the ventral brain stem (change in blood flow -2 +/- 5%). The topical application of 10(-8) M vasopressin, which affects both large and small vessels, decreased blood flow by 33 +/- 4% (n = 6). In rats with spontaneous vasomotion, the basilar artery showed rhythmic changes in diameter at a frequency of 4.0 +/- 0.1 cycles/min and an amplitude of 20 +/- 1% of mean diameter (n = 6). Blood flow to the ventral brain stem cycled at the same frequency as and in phase with changes in diameter of the basilar artery, with an amplitude of 15 +/- 1%. We conclude that constriction of the basilar artery may occur with no change in brain stem perfusion. The distinct changes in blood flow during spontaneous vasomotion suggest that vasomotion occurs in intraparenchymal arterioles as well as in the basilar artery.

Animals↗
PubMed2004

Basilar artery to bilateral posterior cerebral artery 'Y stenting' for endovascular reconstruction of wide-necked basilar apex aneurysms: report of three cases.

Endovascular reconstruction of basilar artery (BA) apex aneurysms has been augmented by adjunctive techniques such as balloon and stent assistance. We present three cases of a wide-necked BA apex aneurysm involving the bilateral P1 segments of both posterior cerebral arteries (PCAs) treated by placement of BA to PCA stents bilaterally in a 'Y' configuration to reconstruct the BA apex for effective coil embolization. Three patients (aged 70, 65 and 37 years) with wide-necked basilar artery aneurysms presented for endovascular treatment. All aneurysms had necks that involved the bilateral P1 segments. Each patient was deemed an appropriate candidate for endovascular reconstruction. Patients were pretreated with clopidogrel (75 mg) and aspirin (325 mg) each day for 3 days prior to the procedure. Following induction of general anesthesia, access to the right femoral artery was obtained by placement of a 6F sheath. Intravenous heparin was administered to achieve an activated coagulation time (ACT) of approximately 300 seconds. A 6F guide catheter was placed within the left vertebral artery (VA) in two patients, the right VA in a third. Utilizing over-the-wire (OTW) technique, a microcatheter was advanced into the left P2-P3 junction of the PCA. A 300-cm 0.014-inch microwire was passed through the microcatheter into the distal PCA and the microcatheter was removed. In each case, two neuroform stents were prepared (SMART Therapeutics Inc., San Leandro, CA) and advanced OTW into the PCA with the most acute angle relative to the BA. The initial stent placed was 20 mm in length and was deployed from the P1 segment into the BA. The microwire was pulled retrograde into the BA apex, then advanced though the stent struts and into the right PCA. A second stent, 15 mm in length, was advanced OTW through the struts of the previously placed stent. It was then deployed from the P1 into the BA where it overlapped the first stent, resulting in a stent-in-stent 'Y' configuration at the BA apex. A microcatheter was advanced OTW into the BA apex aneurysm and coil embolization proceeded in the usual fashion. Following the procedure, each patient was maintained in the neurosurgical intensive care unit (NICU). All remained neurologically intact. The two elderly patients were discharged to home the morning following the procedure. The third patient suffered an upper GI bleed and was treated an additional 3 days in hospital. Oral clopidogrel (75 mg by mouth) and aspirin (325 mg by mouth) were continued daily for 4 weeks. The 'Y' stent configuration for reconstruction of the BA apex is a safe effective technique in patients with wide-necked BA aneurysms.

Adult↗
PubMed2006

Isolated IVth (trochlear) nerve palsy due to basilar artery dolichoectasia.

BACKGROUND: Dolichoectasia (elongation, dilatation and tortuosity) of the basilar artery can cause an isolated cranial neuropathy. The trigeminal nerve and facial nerve are most frequently affected. Dysfunction of one of the ocular motor cranial nerves due to basilar artery dolichoectasia is uncommon, and an isolated IVth (trochlear) nerve palsy has not been previously described in the literature. HISTORY AND SIGNS: Two men, ages 70 and 59 years, respectively, presented with vertical diplopia due to a IVth nerve palsy. In one patient, the onset of the IVth nerve palsy was painless and gradual and in the other patient, the onset was acute and associated with periorbital pain. Neuroimaging in both patients revealed pathological tortuosity of the basilar artery around the midbrain and displacement of the artery toward the side of the affected trochlear nerve. THERAPY AND OUTCOME: The patients were observed clinically. One patient had gradual worsening of his palsy for three and one-half years then suffered a stroke. The second patient whose IVth nerve palsy had an acute onset experienced spontaneous resolution of his palsy but later developed dysfunction of other cranial nerves. CONCLUSIONS: Basilar artery dolichoectasia should be considered in the differential diagnosis of an isolated IVth nerve palsy. The clinical course may be variable, and the prognosis is not always benign.

Aged↗
PubMed2004

The carotid-oculomotor window in exposure of upper basilar artery aneurysms: a cadaveric morphometric study.

OBJECTIVE: The carotid-oculomotor window remains the traditional deep window in the exposure of aneurysms of the upper basilar artery. Although several techniques have been described to expand this window, few morphometric studies document either the degree of its expansion or its contribution to the exposure of the basilar artery. We review the microsurgical anatomy of the carotid-oculomotor window, describe expansion techniques, and analyze morphometrically the contribution of each step (i.e., extradural anterior clinoidectomy, mobilization of the internal carotid artery [ICA], and posterior clinoidectomy) to the expansion of the window and/or exposure of the artery. METHODS: Ten formalin-fixed, alcohol-preserved, cadaver heads injected with pigmented silicone were prepared for bilateral dissection. The vertebrobasilar system was injected with pigmented silicone mixed with barium (1:1), rendering it radiopaque. After completing a frontotemporal-orbitozygomatic craniotomy, we performed dissection in two stages: Stage I consisted of a conventional transsylvian exposure of the upper basilar artery through the carotid-oculomotor window; and Stage II added anterior clinoidectomy, ICA mobilization, and posterior clinoidectomy. A clip was applied to the lowest accessible point of the basilar trunk at each stage. Measurements obtained during each stage included: 1). the transverse carotid-oculomotor distance, that is, anteriorly between the oculomotor foramen and ICA, and posteriorly between the oculomotor nerve and ICA; and 2). the exposed length of the basilar artery, as seen under the microscope and on angiograms. RESULTS: Measurements were obtained before and after the addition of anterior clinoidectomy, mobilization of the ICA, and posterior clinoidectomy. Increases in expansion of the window and exposure of the upper basilar artery were documented as percentages of the control values. The anterior carotid-oculomotor distance averaged 7.1 mm (range, 5-10 mm) and 10.1 mm (range, 7-15 mm) before and after the additional surgical steps to expand the window, respectively. The posterior carotid-oculomotor distance averaged 12.7 mm (range, 9-18 mm) and 16.1 mm (range, 11-22 mm) before and after the additional surgical steps to expand the window, respectively. The exposed length of the basilar artery from the bifurcation to the clip was 4.2 mm (range, 1-13 mm) before expansion and 7 mm (range, 3-15 mm) after expansion. CONCLUSION: Anterior clinoidectomy and ICA mobilization increased the carotid-oculomotor space 44% anteriorly and 28% posteriorly. Posterior clinoidectomy increased the exposed length of the basilar artery by 69%. Superficial wide field exposure, expansion of the carotid-oculomotor window, and increased exposure of the upper basilar artery facilitate both visualization of the aneurysm for clip application and the use of proximal vascular control as an adjunct to basilar aneurysm surgery.

Basilar Artery↗
PubMed1993

Effect of norepinephrine on rat basilar artery in vivo.

In anesthetized rats, we used a cranial window to examine effects of topical norepinephrine on diameter of the basilar artery in vivo. Topical application of norepinephrine increased the diameter of the basilar artery. NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, inhibited vasodilatation to acetylcholine but did not attenuate dilator responses to norepinephrine. Indomethacin also did not attenuate vasodilatation in response to norepinephrine. Dilatation of the basilar artery to norepinephrine was inhibited by propranolol and the beta 1-antagonist atenolol but not by the beta 2-antagonist butoxamine. Thus dilatation of the basilar artery in response to norepinephrine is produced by activation of beta 1-receptors and is not mediated by endothelium-derived relaxing factor or prostanoids. Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, partially inhibited vasodilatation in response to norepinephrine. Forskolin, a direct activator of adenylate cyclase, also increased the diameter of the basilar artery, and glibenclamide attenuated the dilatation. Thus dilatation of rat basilar artery in response to norepinephrine is mediated, in part, by activation of ATP-sensitive K+ channels, and activation of these K+ channels may be achieved by an adenosine 3',5'-cyclic monophosphate-dependent mechanism.

Animals↗
PubMed1999

Endovascular stenting of an acutely thrombosed basilar artery: technical case report and review of the literature.

OBJECTIVE AND IMPORTANCE: The goal of this report was to describe the successful percutaneous endovascular use of a Gianturco-Roubin-2 coronary stent in the treatment of an acute atherothrombotic occlusion of the basilar artery. To our knowledge, the percutaneous endovascular deployment of an intra-arterial stent for the treatment of an acute atherothrombotic occlusion of the basilar artery and the percutaneous endovascular placement of a Gianturco-Roubin-2 stent in the basilar artery have not been previously reported. CLINICAL PRESENTATION: An 83-year-old man presented with a recurrent, transient, locked-in syndrome resulting from a lower basilar artery occlusion caused by vertebrobasilar thrombosis superimposed on severe proximal basilar artery atheromatous stenosis. INTERVENTION: After successful superselective intra-arterial thrombolysis of the vertebrobasilar clot, balloon angioplasty of the underlying basilar artery stenosis was performed, without significant angiographic improvement. Percutaneous endovascular deployment of a Gianturco-Roubin-2 coronary stent of 4-mm diameter was subsequently performed, with excellent angiographic results. CONCLUSION: The patient made a very good neurological recovery but unfortunately died as a result of cardiogenic shock and sepsis. Detailed neuropathological follow-up results are presented; stent patency was revealed in the postmortem examination. The anatomic and pathophysiological considerations of basilar artery stent placement for the treatment of acute basilar artery occlusion related to atherosclerotic stenosis are discussed.

Acute Disease↗
PubMed1995

Enhanced responses of the basilar artery to activation of endothelin-B receptors in stroke-prone spontaneously hypertensive rats.

We tested the hypothesis that responses of the basilar artery to selective activation of endothelin-B receptors are altered during chronic hypertension. Using a cranial window in anesthetized rats, we examined responses of the basilar artery to a selective endothelin-B receptor agonist, IRL 1620, in stroke-prone spontaneously hypertensive rats (SHRSP). Under control conditions, baseline basilar artery diameter was smaller in SHRSP (196 +/- 8 microns [mean +/- SEM]) than in normotensive Wistar-Kyoto rats (WKY) (245 +/- 9 microns, P < .05). Topical application of IRL 1620 (10(-8) mol/L) dilated the basilar artery by 27 +/- 5% in WKY and 56 +/- 4% in SHRSP (P < .05). Dilatation of the basilar artery in response to sodium nitroprusside was similar in WKY and SHRSP. In contrast, acetylcholine-induced vasodilatation in SHRSP was markedly impaired. NG-Nitro-L-arginine methyl ester and NG-nitro-L-arginine, inhibitors of nitric oxide synthase, inhibited IRL 1620-induced vasodilatation in WKY. Neither NG-nitro-L-arginine methyl ester nor indomethacin attenuated vasodilatation produced by IRL 1620 in SHRSP. The major finding is that dilator responses of the basilar artery to selective activation of endothelin-B receptors are paradoxically enhanced in SHRSP compared with WKY. Dilator responses of the basilar artery to endothelin-B receptor activation are mediated by endothelium-derived relaxing factor in WKY. In contrast, responses to activation of endothelin receptors in SHRSP do not depend on the production of nitric oxide or prostanoids.

Acetylcholine↗
PubMed2004

Effects of pH on vascular tone in rabbit basilar arteries.

Effects of pH on vascular tone and L-type Ca2+ channels were investigated using Mulvany myograph and voltage-clamp technique in rabbit basilar arteries. In rabbit basilar arteries, high K+ produced tonic contractions by 11+/-0.6 mN (mean+/-S.E.,n=19). When extracellular pH (pHo) was changed from control 7.4 to 7.9 ([alkalosis]o), K+-induced contraction was increased to 128+/-2.1% of the control (n=13). However, K+-induced contraction was decreased to 73+/-1.3% of the control at pHo 6.8 ([acidosis] o, n=4). Histamine (10 microM) also produced tonic contraction by 11+/-0.6 mN (n=17), which was blocked by post-application of nicardipine (1 microM). [alkalosis]o and [acidosis]o increased or decreased histamine-induced contraction to 134+/-5.7% and 27+/-7.6% of the control (n=4, 6). Since high K+- and histamine-induced tonic contractions were affected by nicardipine and pHo, the effect of pHo on voltage-dependent L-type Ca2+ channel (VDCCL) was studied. VDCCL was modulated by pHo: the peak value of Ca2+ channel current (IBa) at a holding of 0 mV decreased in [acidosis]o by 41+/-8.8%, whereas that increased in [alkalosis]o by 35+/-2.1% (n=3). These results suggested that the external pH regulates vascular tone partly via the modulation of VDCC in rabbit basilar arteries.

Animals↗
PubMed1982

Analysis of the 5-hydroxytryptamine induced contraction of the human basilar arterial strip compared with the rat aortic strip in vitro.

1) Experiments were performed to investigate the nature of the contraction produced by 5-hydroxytryptamine in the human basilar arterial strip in vitro and to compare it with that produced in the rat aortic strip in vitro. 2) The human basilar arterial strip was found to be significantly more sensitive to 5-HT compared to the rat aortic strip. 3) Methysergide, cyproheptadine and methergoline were competitive, selective antagonists against 5-HT on the rat aorta with pA2 values of 7.97, 8.76 and 9.49 respectively. In contrast 5-HT was antagonised by these agents in a manner which was not competitive on the human basilar artery. Both 5-HT and NA were antagonised by BW 501 C67 (alpha-anilino-N-2-m-chlorphenoxy propylacetamide hydrochloride) in a manner which was not competitive on both rat aortic and human basilar arterial strips. 4) Phentolamine (10(-7) to 10(-5) M) was found to be a competitive antagonist against noradrenaline on both the rat aortic strip (pA2 6.9) and the human basilar arterial strip (pA2 7.3). Phentolamine at 10(-5) M shifted the 5-HT curve on the human basilar artery to the right with a reduction in maximum response. 5) Methysergide (10(-9) to 10(-4) M) was found to possess contractile activity on some human basilar arterial strips, the maximum response being approximately 60% of that produced by 5-HT. Phentolamine at 10(-5) M shifted the dose-response curve to methysergide to the right with a slight reduction in the maximum response obtained. 6) The results from this study suggest that the receptor(s) mediating 5-HT-induced contraction of the human basilar artery may be different from the classical "D-receptor" which mediates contraction to 5-HT on the rat aorta.

Animals↗
PubMed2006

[Fibromuscular dysplasia of the basilar artery presenting as cerebral infarction in a young female].

We reported a 20-year-old woman with fibromuscular dysplasia (FMD) of the basilar artery presenting multiple cerebral infarctions. A sudden onset of consciousness disturbance and right hemiparesis was experienced. A neurological examination on day 2 revealed an absence of light and corneal reflexes on the left side, homonymous left upper quadrant anopsia and right hemiparesis with Babinski sign: she was also somnolent. On head MRI, multiple high signal intensity lesions were seen in the right occipital lobe, bilateral thalami and left pons on T2- and diffusion weighted images. Brain angiogram revealed the string of beads sign of the basilar artery, suggesting FMD. Neurological deficits gradually improved in the 2 months that followed, leaving slight hemiparesis and homonymous left upper quadrant anopsia In the following 3 years, no recurrence was seen with aspirin (81 mg/day). FMD in the head and neck usually affects extracranial segments of the carotid and vertebral arteries, while FMD of the basilar artery is extremely rare. To the best of our knowledge, 12 cases with FMD of the basilar artery have been reported; of these, 11 were symptomatic and 5 died. Since FMD of the basilar artery has poor prognosis, attention needs to be paid for FMD in young adults as a differential diagnosis of cerebral infarction in the territory of the basilar artery.

Adult↗
PubMed2004

Inward rectifier potassium channels in the basilar artery during chronic alcohol consumption.

BACKGROUND: The goals of this study were to determine whether chronic alcohol consumption alters potassium channel-mediated reactivity in the basilar artery and to determine a potential mechanism that might account for the effects of alcohol on the basilar artery. METHODS: Sprague-Dawley rats were fed liquid diets with or without alcohol for 2 to 3 months. We measured diameter of the basilar artery in response to potassium channel inhibitors and activators. Protein level of inward rectifier potassium channel subunit Kir2.1 in the basilar artery was determined by Western blot. RESULTS: Topical application of glibenclamide (1 and 10 microM) significantly constricted the basilar artery at high dose; iberiotoxin (10 and 100 nM), 4-AP (0.1 and 1 mM), and BaCl2 (1 and 10 microM) produced dose-related constriction in both non-alcohol-fed and alcohol-fed rats. However, the magnitude of constriction in response to BaCl2 was significantly less in alcohol-fed rats compared with non-alcohol-fed rats. Topical application of KCl (1 and 3 mM), cromakalim (0.1 and 0.3 microM), and NS1619 (10 and 30 microM) induced dose-related dilation in non-alcohol-fed and alcohol-fed rats. However, the magnitude of vasodilation in response to KCl was significantly less in alcohol-fed rats compared with non-alcohol-fed rats. In addition, Kir2.1 protein level in the basilar artery was significantly reduced in alcohol-fed compared with non-alcohol-fed rats. CONCLUSIONS: These findings suggest that chronic alcohol consumption reduces expression of inward rectifier potassium channels and inhibits KIR channel-mediated dilation in the basilar artery.

Alcohol Drinking↗
PubMed1988

Quantitative analysis of reversible dysfunction of brain-stem midline structures caused by disturbance of basilar artery blood flow with the auditory brain-stem responses.

To clarify the effects of disturbances in basilar artery blood flow, basilar artery angiospasm was induced in 2 cats and 4 guinea pigs and auditory brain-stem responses (ABRs) were continuously recorded preceding, during and following the angiospasm. The angiospasm caused specific ABR changes in that waves II (P2-N2) and III (P3-N3) were attenuated without any corresponding amplitude reduction of P4. Those changes were equivalent following stimulation of either ear. Moreover, the ABR changes gradually recovered within 5 h. On the basis of the animal experiments, 52 patients with subarachnoid hemorrhage, supratentorial tumor showing increased intracranial pressure or hydrocephalus were selected for repeated ABR examinations. ABR abnormalities similar to those observed in the animal experiment were obtained especially from the patients exhibiting grade 3 or 4 symptomatology with subarachnoid hemorrhage. In these cases, the wave III to wave IV-V amplitude ratio was significantly decreased. In some cases the ABR abnormalities and the wave III to wave IV-V amplitude ratio recovered as the clinical course improved. These results support the conclusion that specific ABR changes (wave III to wave IV-V amplitude ratio) reflect transient ischemic dysfunction of the midline portion of the brain-stem caused by disturbances of basilar artery blood flow.

Adolescent↗
PubMedDate not supplied

Anatomy of segmental duplication in the human basilar artery. Possible site of aneurysm formation.

Segmental duplications of the basilar artery, previously reported exclusively as anatomical variations, owe their clinical interest to the possible association with aneurysms localized at the junctions of the fenestrated segments. The morphological characteristics of 5 cases of basilar artery segmental duplication without aneurysms, found at autopsy, are reported. In 3 of these the proximal junction of the fenestrated segment was studied with scanning electron microscopy and morphometry. In all cases the tunica media of the medial wall of the 2 branches showed a progressive thinning towards the junctions of the fenestrated segments and a small muscular gap at their apex. The limited medial defect might be embryologically ascribed to the persistence of the morphological individuality of the tunica media of the 2 branches at the point where the fusion of the primitive longitudinal neural arteries stopped. The review of the literature shows that the morphology of the junctions of the fenestrated segments is in conformity with that of the intracranial arterial bifurcations. For this reason the basilar artery fenestration exposes to the blood flow a new distal bifurcation where the same etiologic factors that are still under discussion in the origin of saccular intracranial aneurysms may be active.

Aged↗