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At least 289 records · Page 16Linked to original sources
PubMed1989

Effects of prostanoids on human and rabbit basilar arteries precontracted in vitro.

The effect of a range of prostanoids on human and rabbit basilar arteries precontracted in vitro in the presence of the thromboxane receptor-blocking drug AH23848B was investigated. On the rabbit basilar artery and in the presence of AH23848B the thromboxane A2 mimetic U-46619 produced further concentration-related contractions of the tissue. All other prostaglandins (except ICI81008 and PGF2 alpha which had no effect) produced concentration-related relaxations with the rank order of relaxant potency being PGE2 greater than Iloprost greater than PGI2 = PGE1 = 16,16-dimethyl PGE2 = PGD2. On the human basilar artery PGI2 and iloprost produced concentration-related relaxations with iloprost being more potent than PGI2. At high concentrations both these compounds produced reduced relaxant responses. All other prostanoids (except ICI81008 and PGD2 which had no effect) contracted the tissue, the rank order of contractile potency being 16,16-dimethyl PGE2 greater than PGE2 greater than PGF2 alpha = PGE1 greater than U46619 much greater than ICI81008 and PGD2. It is concluded that the human basilar artery possesses two contractile prostanoid receptors, a TP receptor and one which may be of the EP-type in addition to a prostanoid receptor mediating relaxation which may be of the IP-type. The prostanoid receptor(s) mediating relaxation of the rabbit in vitro basilar artery is difficult to determine. The relevance of the observations to cerebrovascular disorders such as migraine and vasospasm is discussed.

Animals↗
PubMed1996

The vasomotor effects of 5-hydroxytryptamine on equine basilar arteries in vitro.

The vasomotor effects of 5-hydroxytryptamine (5-HT) on isolated equine basilar arteries were studied. 5-HT induced contractions of equine basilar arteries in a concentration-dependent manner, with a pEC50 value (with 95% confidence limits) of 7.35 (7.08-7.62). Similar results were obtained with endothelium-denuded basilar arteries. Contractions were not competitively inhibited by the 5-HT2 receptor antagonist ketanserin at low concentrations of 5-HT. Conversely, at high concentrations of 5-HT, contractions were inhibited by ketanserin in a concentration-dependent manner, with a pA2 value of 8.91 (8.62-9.20). The 5-HT1 and 5-HT2 receptor antagonist methiothepin shifted the concentration-response curve of 5-HT downwards and to the right in a concentration-dependent manner. In the presence of 10(-6) mol/L ketanserin, however, methiothepin antagonized 5-HT-induced contractions competitively with a pA2 value of 7.95 (7.59-8.31). The 5-HT3 receptor antagonist MDL 72222 had no effect on 5-HT-induced contractions. The findings of this study indicate that 5-HT1 and 5-HT2 receptors are located in equine basilar arterial smooth muscle cells, and that stimulation of these receptors results in contraction.

Animals↗
PubMed1992

Role of protein kinase C in constrictor responses of the rat basilar artery in vivo.

1. The goal of this study was to determine the effects of activation and inhibition of protein kinase C on the rat basilar artery in vivo. 2. The diameter of the basilar artery was measured through a craniotomy in rats anaesthetized with pentobarbitone sodium (50 mg kg-1, I.P., supplemented with 20 mg kg-1 h-1). Diameters were measured under control conditions and during topical application of various agonists, both alone and in the presence of antagonists. 3. Serotonin (5-HT) produced concentration-related constriction of the basilar artery (baseline diameter = 234 +/- 9 microns, mean +/- S.E.M.), which was inhibited by the 5-HT2 receptor antagonist LY53857. 4. Sphingosine (10(-6) M), a protein kinase C inhibitor which binds to the regulatory site of protein kinase C, inhibited the response to 10(-8) M-serotonin (-19 +/- 2% before vs. -3 +/- 2% during sphingosine, P less than 0.05). In contrast, constrictor responses to prostaglandin F2 alpha to (PGF2 alpha; 10(-6) M) were not inhibited by sphingosine (-16 +/- 2% before vs. -18 +/- 2% during sphingosine, P greater than 0.05). 5. H-7 (10(-9) M), another protein kinase C inhibitor, which binds to the catalytic site of protein kinase C, also inhibited constriction of the basilar artery in response to serotonin, but not prostaglandin F2 alpha. 6. Phorbol 12,13-dibutyrate (PDBu, 10(-8) M), which activates protein kinase C, produced slowly developing constriction of the basilar artery. PDBu-induced vasoconstriction (-33 +/- 2%) was attenuated by sphingosine (-11 +/- 4% during sphingosine, P less than 0.05) and H-7 (-1.5 +/- 5% during H-7, P less than 0.05). 7. In summary, activation of protein kinase C appears to mediate vasoconstrictor responses of the basilar artery to serotonin, but not PGF2 alpha.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1998

Treatment with dimethylthiourea prevents impaired dilatation of the basilar artery during diabetes mellitus.

The goal of this study was to test the hypothesis that the synthesis/release of hydroxyl radical accounts for impaired nitric oxide synthase-dependent 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 ip) in response to nitric oxide synthase-dependent agonists (acetylcholine and substance P) and a nitric oxide synthase-independent agonist (nitroglycerin). Reactivity of the basilar artery was measured in untreated nondiabetic and diabetic rats and in nondiabetic and diabetic rats treated with a daily intraperitoneal injection of dimethylthiourea (DMTU; 50 mg/kg). Injection of DMTU was started 48 h after injection of streptozotocin and was continued throughout the diabetic period (3-4 wk). Topical application of acetylcholine (0.1, 1.0, and 10 microM) and substance P (0.1 and 1.0 microM) produced similar dilatation of the basilar artery in untreated and DMTU-treated nondiabetic rats. In untreated diabetic rats, the magnitude of vasodilation produced by acetylcholine and substance P was significantly less than in untreated nondiabetic rats. However, in DMTU-treated diabetic rats, dilatation of the basilar artery in response to acetylcholine and substance P was similar to that observed in nondiabetic rats. Dilatation of the basilar artery in response to nitroglycerin was similar in untreated and DMTU-treated nondiabetic and diabetic rats. These findings suggest that impaired nitric oxide synthase-dependent dilatation of the basilar artery during diabetes mellitus may be related to the synthesis/release of hydroxyl radical.

Acetylcholine↗
PubMed1992

Reverse flow in the intracranial arteries--the possible significance of comparative flow in the anterior cerebral and the basilar arteries.

Four infants with reverse flow patterns of the intracranial arteries are reported. Two with severe brain damage, had a reverse flow pattern in the anterior cerebral artery, which was recorded during the recovery stage from cardiac arrest. The other two patients showed a reverse flow pattern in the basilar artery and had a good prognosis. Reverse flow in the anterior cerebral artery suggests severe brain damage, but that in the basilar artery does not.

Basilar Artery↗
PubMed1976

Experimental alterations in cyclic adenosine monophosphate concentrations in the cat basilar artery.

Levels of cyclic adenosine monophosphate (AMP) in the basilar artery and in circulating blood of cats were determined after the production of spasm by topical application of blood to the vessel and following treatment with agents known to alter cyclic AMP. Isoproterenol, known to stimulate adenyl cyclase, and aminophylline, a phosphodiesterase inhibitor, were studied alone and in combination. Cyclic AMP of the basilar artery fell from a mean control value of 43 to 26 pmoles per milligram of protein following the production of vasospasm. Intravenous administration of isoproterenol alone and in combination with aminophylline produced dilatation of the basilar artery, which was associated with a marked rise in the cyclic AMP concentration in the vessel. The finding that cerebral vasospasm is associated with a fall and vasodilation with a rise in cyclic AMP concentration supports the hypothesis of an active role for cyclic nucleotides in the regulation of cerebrovascular smooth muscle tone.

Aminophylline↗
PubMed2001

Arachidonate dilates basilar artery by lipoxygenase-dependent mechanism and activation of K(+) channels.

Dilatation of cerebral arterioles in response to arachidonic acid is dependent on activity of cyclooxygenase. In this study, we examined mechanisms that mediate dilatation of the basilar artery in response to arachidonate. Diameter of the basilar artery (baseline diameter = 216 +/- 7 micrometer) (means +/- SE) was measured using a cranial window in anesthetized rats. Arachidonic acid (10 and 100 microM) produced concentration-dependent vasodilatation that was not inhibited by indomethacin (10 mg/kg iv) or N(G)-nitro-L-arginine (100 microM) but was inhibited markedly by baicalein (10 micrometerM) or nordihydroguaiaretic acid (NDGA; 10 microM), inhibitors of the lipoxygenase pathway. Dilatation of the basilar artery was also inhibited markedly by tetraethylammonium ion (TEA; 1 mM) or iberiotoxin (50 nM), inhibitors of calcium-dependent potassium channels. For example, 10 microM arachidonate dilated the basilar artery by 19 +/- 7 and 1 +/- 1% in the absence and presence of iberiotoxin, respectively. Measurements of membrane potential indicated that arachidonate produced hyperpolarization of the basilar artery that was blocked completely by TEA. Incubation with [(3)H]arachidonic acid followed by reverse-phase and chiral HPLC indicated that the basilar artery produces relatively small quantities of prostanoids but large quantities of 12(S)-hydroxyeicosatetraenoic acid (12-S-HETE), a lipoxygenase product. Moreover, the production of 12-HETE was inhibited by baicalein or NDGA. These findings suggest that dilatation of the basilar artery in response to arachidonate is mediated by a product(s) of the lipoxygenase pathway, with activation of calcium-dependent potassium channels and hyperpolarization of vascular muscle.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

Inducible cyclooxygenase expression in canine basilar artery after experimental subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Inducible cyclooxygenase (COX-2) has been found to play a pathological role in cerebral insult. We investigated the expression of COX-2 in the basilar artery after experimental subarachnoid hemorrhage (SAH). METHODS: In a canine "two-hemorrhage" model of SAH, the basilar arteries were obtained on day 2 after a cisternal injection of autologous blood or on days 4, 6, 7, or 9 after the second injection. Basilar arteries also were obtained 12 hours after intracisternal injection a cytokine: interleukin (IL)-1 beta (0.03 microgram), IL-6 (3 micrograms), or IL-8 (10 micrograms). Western blotting with a polyclonal anti-COX-2 antibody was performed in these arteries. RESULTS: COX-2 protein was not demonstrated in the basilar artery in control animals without SAH. However, it was expressed in the basilar artery on days 2, 4, 6, and 7 after blood injection but not on day 9. Intracisternal injection of IL-1 beta, IL-6, or IL-8 also induced COX-2 in the basilar artery. CONCLUSIONS: COX-2 expression was detected in basilar arterial tissue in both acute and chronic stages after SAH. Elevation of inflammatory cytokines after SAH may be involved in the induction of COX-2, which may produce sufficient quantities of eicosanoids to affect hemodynamics after SAH.

Animals↗
PubMed2004

Mechanisms underlying diabetes enhancement of endothelin-1-induced contraction in rabbit basilar artery.

The influence of alloxan-induced diabetes on the reactivity of rabbit basilar artery to endothelin-1 was examined. Endothelin-1 induced concentration-dependent contraction of basilar arteries that was higher in diabetic than in control rabbits. Endothelium removal produced a higher enhancement of the endothelin-1-induced contraction in control than in diabetic rabbits. N(G)-nitro-L-arginine (L-NOArg) enhanced the maximal contraction induced by endothelin-1 in control rabbits and potentiated this response in diabetic rabbits. Endothelin ETA receptor antagonist, cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123), inhibited endothelin-1-induced contraction in both rabbit groups. Endothelin ETB receptor antagonist, 2,6-Dimethylpiperidinecarbonyl-gamma-Methyl-Leu-Nin-(Methoxycarbonyl)-D-Trp-D-Nle (BQ-788), enhanced endothelin-1-induced contraction in control rabbits and decreased the potency of endothelin-1 in diabetic rabbits. Sodium nitroprusside-induced relaxation of basilar arteries was lower in diabetic than in control rabbits. These results suggest that mechanisms underlying rabbit basilar artery hyperreactivity to endothelin-1 include decreased endothelial modulation of endothelin-1-induced contraction, with impaired endothelial endothelin ETB receptor activity; decreased sensitivity to nitric oxide (NO) in vascular smooth muscle; and enhanced participation of muscular endothelin ETA and ETB receptors.

Animals↗
PubMed2000

Magnetic resonance angiography evaluation of basilar artery stenosis in patients with vertebrobasilar insufficiency.

To assess the usefulness of evaluating basilar arterial flow by magnetic resonance angiography (MRA), MRA results for patients with vertebrobasilar insufficiency (VBI) were compared with those for age-matched individuals with no vestibular disorders. The presence of stenosis in the basilar artery, its severity and the presence of complications associated with atherosclerosis in the two groups were statistically compared. Analyses revealed significant differences in the incidence of stenosis, its severity, and the incidence of complications between the two groups. These findings suggest that MRA is valuable for the estimation of vertebrobasilar hemodynamics. MRA evaluation of basilar artery stenosis appears to be suitable for identifying a high-risk group among VBI patients, since basilar artery stenosis can result in serious disabilities.

Aged↗
PubMed2004

Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis.

OBJECTIVE: To define predictors of recanalisation and clinical outcome of patients with acute basilar artery occlusions treated with local intra-arterial thrombolysis (IAT). METHODS: Vascular risk factors, severity of the neurological deficit graded by the National Institutes of Health stroke scale (NIHSS), and radiological findings were recorded at presentation. Outcome was measured using the modified Rankin scale (mRS) three months later and categorised as favourable (mRS 0-2), poor (mRS 3-5), or death (mRS 6). RESULTS: 40 patients were studied. Median NIHSS on admission was 18. Mean time from symptom onset to treatment was 5.5 hours (range 2.3 to 11). Outcome was favourable in 14 patients (35%) and poor in nine (23%); 17 (42%) died. There were two symptomatic cerebral haemorrhages (5%). Recanalisation of the basilar artery was achieved in 32 patients (80%); it was complete (TIMI grade 3) in 20% and partial (TIMI grade 2) in 60%. In multivariate logistic regression analysis, low NIHSS score on admission (p = 0.002) and vessel recanalisation (p = 0.005) were independent predictors of favourable outcome. Recanalisation occurred more often with treatment within six hours of symptom onset (p = 0.003) and when admission computed tomography showed a hyperdense basilar artery sign (p = 0.007). In a univariate model, quadriplegia (p = 0.002) and coma (p = 0.004) were associated with a poor outcome or death. CONCLUSIONS: Low baseline NIHSS on admission and recanalisation of basilar artery occlusions predict a favourable outcome after intra-arterial thrombolysis. Early initiation of IAT and the presence of a hyperdense basilar artery sign on CT were associated with a higher likelihood of recanalisation.

Acute Disease↗
PubMed1993

Auditory phenomena during transcranial Doppler insonation of the basilar artery.

During transcranial Doppler insonation of the basilar artery, 15 normal subjects heard high-frequency tones similar to tinnitus. The pitch of the tones equated with the PRF, and intensity equated with loudness. Alteration of pulse length did not change the tones heard, and the effect was highly dependent on probe position and direction. This is an example of ultrasonography acting as a sensory stimulus. The exact mechanism and implications of this effect will need to be clarified by further investigation. Although this phenomenon is not proved to be harmful, it would seem prudent to use the minimum transmitted power necessary to obtain a satisfactory signal from the basilar artery.

Acoustics↗
PubMed1988

Effect of removal of the endothelium on vasocontraction in canine and rabbit basilar arteries.

The effect of endothelium removal on the contractile responses to KCl, hemoglobin, serotonin (5-HT), norepinephrine (NE), prostaglandin (PG)F2 alpha, PGD2, and PGE2 was investigated in canine and rabbit basilar arteries by an isometric tension-recording method. In canine basilar arteries, endothelium removal elevated the dose-response curves to 5-HT, PGF2 alpha, and PGD2, and PGE2, but not to KCl, hemoglobin, or NE. In rabbit basilar arteries, on the other hand, removal of the endothelium elevated the dose-response curves to 5-HT, NE, PGF2 alpha, and PGD2, but not to KCl or hemoglobin. Neither contractile nor inhibitory response was elicited by PGE2 in rabbit basilar arteries. Contraction induced by 5-HT and NE following endothelium removal had a much more pronounced effect in rabbit basilar arteries than in canine basilar arteries. These results suggest that, following endothelium removal, abolition of the spontaneous release of endothelium-derived relaxing factor is the most probable mechanism of the enhanced vasocontraction. Since endothelial damage results from subarachnoid hemorrhage, the aforementioned mechanism of vasocontraction enhancement may play a role in the pathogenesis of cerebral vasospasm.

Animals↗
PubMed1991

Recombinant tissue plasminogen activator in two patients with basilar artery occlusion.

Two patients with angiographically proved basilar artery occlusion were treated with systemic recombinant tissue plasminogen activator (rtPA) according to protocol. The first patient was in a locked-in state and gradually deteriorated. On repeat angiography the basilar artery remained occluded. He died and necropsy revealed a pontine haemorrhagic infarction. The second patient, who was comatose and with decerebrate posturing, made a remarkable recovery. Angiography showed reperfusion. Therapy was initiated in the first patient after six hours and in the second after two hours. Treatment with rtPA is promising but probably not feasible for every patient. Success may depend on duration of occlusion and composition of occluding thrombus.

Adult↗
PubMed1989

The selective potentiation of noradrenaline-induced tone by Bay K 8644 in the rabbit basilar artery.

A number of studies indicate that relative to the maximal tone possible, for example, to histamine, noradrenaline produces only weak contractile responses in the rabbit basilar artery. Various factors, including a limited number of alpha-adrenoceptors, have been proposed to account for the reduced response to noradrenaline. We examined the effect of the Ca2+-channel activator, Bay K 8644 (0.1 and 1.0 nM) on dose-response curves to noradrenaline, histamine, calcium (Ca2+) and potassium (K+) in ring preparations of rabbit basilar artery and central ear artery. These concentrations of Bay K 8644 (0.1 and 1.0 nM) increased the magnitude of tension developed by noradrenaline (contractility) in the basilar artery, but did not alter its sensitivity (ED50) to the adrenergic vasoconstrictor. Bay K 8644 (0.1 and 1.0 nM) did not alter the contractility or sensitivity to histamine or K+ of the rabbit basilar artery. When dose-response curves to Ca2+ were made in K+-depolarized rabbit basilar artery rings, Bay K 8644 (0.1 and 1.0 nM) dose-dependently augmented tone generated by readmission of Ca2+. Bay K 8644 (0.1 and 1.0 nM) did not alter responses to noradrenaline, histamine, or K+ in rabbit central ear artery preparations. These results are compatible with a voltage-dependent mechanism of action of Bay K 8644 in the rabbit basilar artery, which may be partially depolarized in the resting state. We propose that in addition to other factors, the contractile response of rabbit basilar arteries is limited by a weak or inefficient coupling of alpha-adrenoceptors to Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Giant fusiform aneurysm of the basilar artery: consideration of its pathogenesis.

BACKGROUND: We tried to determine the pathogenesis of a fusiform aneurysm of the basilar artery based on the findings of two patients who had pontine infarctions due to thrombosis within the aneurysm. CASE REPORT: The patients were female, aged 75 and 62 years. At autopsy of the first case, the dilated basilar artery was filled with fresh and old thrombus. The wall was extremely thin on the left side, where a fresh red thrombus was evident, and thick on the right side, where an old white thrombus appeared. The thick wall had a thickened and hyalinized intima, and a deposition of atheromatous plaque disrupted both the internal elastic lamina and muscle layer. The left vertebral artery was atherosclerotic and its lumen was severely compromised, but the right vertebral artery was hypoplastic. On angiogram of the second case, the dilated basilar artery presumably was filled with thrombus on the left side, contralateral to the dilated and tortuous vertebral artery. The left vertebral artery was hypoplastic. CONCLUSION: Atherosclerosis may be the essential factor in the pathogenesis of a fusiform aneurysm of the basilar artery in elderly patients. The disrupted internal elastic lamina and muscle layer may be susceptible to mechanical injury by hemodynamic strain, causing progressive attenuation of the arterial wall. Stenosis of the vertebral artery on the dominant side probably produces a jet stream within the basilar artery on the stenotic side and a stagnant zone on the opposite side, promoting the initial thrombus formation.

Aged↗
PubMed1997

Effect of nitric oxide and potassium channel agonists and inhibitors on basilar artery diameter.

The first goal of this study was to examine the hypothesis that dilatation of the basilar artery in response to activation of ATP-sensitive K+ channels is mediated by nitric oxide (NO). Diameter of the basilar artery (209 +/- 5 microns, mean +/- SE) was measured using a cranial window in anesthetized rats. Aprikalim (a direct activator of ATP-sensitive K+ channels) dilated the basilar artery under control conditions. Inhibition of endogenous NO production with NG-nitro-L-arginine (L-NNA, 10(-4) M) did not alter responses to aprikalim. The second goal was to determine whether vasodilatation in response to NO is dependent on activation of calcium-activated K+ channels. Tetraethylammonium (TEA, 10(-3) M), an inhibitor of calcium-activated K+ channels, did not affect dilator responses to sodium nitroprusside (an NO donor) under control conditions. Responses to nitroprusside (10(-8) and 10(-7) M) were augmented more than twofold during application of L-NNA. In the presence of L-NNA, the augmented portion of the response to nitroprusside was inhibited by TEA and iberiotoxin (5 x 10(-8) M, a highly selective inhibitor of calcium-activated K+ channels), but it was not inhibited by glibenclamide (10(-6) M), an inhibitor of ATP-sensitive K+ channels. These findings suggest that dilator responses of the basilar artery to an activator of ATP-sensitive potassium channels are not mediated by NO. Calcium-activated K+ channels may not normally contribute to dilator responses of the basilar artery to nitroprusside. The effects of TEA and iberiotoxin suggest that when endogenous production of NO is inhibited, sodium nitroprusside causes the opening of calcium-activated K+ channels, contributing to an augmented vasodilator response.

Animals↗
PubMedDate not supplied

Transluminal angioplasty of the vertebral and basilar artery.

Transluminal angioplasty of brachiocephalic vessels for atherosclerotic lesions is now being performed in selected cases. We have thus far treated 17 cases of vertebral artery stenosis and one case of basilar artery stenosis by intravascular balloon dilatation techniques. Clinical presenting symptoms included vertebral basilar insufficiency, repeated transient ischemic attacks (TIAs), and multiple strokes. We performed successful transluminal angioplasty in 16 patients with marked narrowing (greater than 70%) of the dominant vertebral artery from atherosclerosis. One patient with basilar artery stenosis with tandem atherosclerotic lesions was also treated by angioplasty techniques. Repeat angiography at 3- to 12-month intervals has revealed continued patency at the angioplasty site. Complications occurred in our one patient with basilar artery angioplasty, who suffered a brainstem infarction after treatment, and in one patient who had a TIA after bilateral vertebral artery angioplasty. Two other patients had residual vertebral stenosis but remained asymptomatic after the procedure. All other patients who had successful dilatation were asymptomatic at 6 months to 2 years (mean, 15 months) of follow-up. These initial studies indicate that vertebral artery angioplasty may be effective for treating high-grade atherosclerotic lesions and for improving blood flow to the posterior circulation. Angioplasty of the basilar artery is technically more difficult and has a higher degree of risk because of the many perforating branches supplying the brainstem.

Aged↗