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At least 307 records · Page 17Linked to original sources
PubMed1998

Collateral circulation and outcome after basilar artery thrombolysis.

BACKGROUND AND PURPOSE: This study was undertaken to examine the relationship between collateral flow and outcome after local intraarterial thrombolytic treatment for basilar artery thrombosis. METHODS: Twenty-four patients with symptomatic basilar thrombosis were treated with intraarterial urokinase. Angiograms at the time of treatment were analyzed to characterize collateral flow. The number of posterior communicating arteries (PCoAs) and the degree of collateral filling of the basilar artery were then compared with symptom duration before treatment, with Glasgow Coma Scale (GCS) score at the time of treatment, with 90-day modified Rankin score, and with 90-day survival status. RESULTS: Of the 20 patients who had carotid artery injections at the time of the thrombolytic procedure, two had no PCoA, eight had one PCoA, and 10 had two PCoAs. Nine had no collateral opacification of the basilar artery, six had collateral opacification of the distal basilar artery, and five had collateral opacification of the distal and proximal basilar artery. Ninety-day survival was 38%; 25% of patients had good neurologic outcomes. No correlation was found between the number of PCoAs and symptom duration, pretreatment GCS score, survival, or neurologic outcome. Duration of symptoms before treatment was longer in patients with collateral flow to the basilar artery. Basilar artery collateral flow did not correlate with survival, but it did correlate with neurologic outcome for the 12 patients with middle or distal basilar artery thrombus in whom collateral flow to the basilar artery was assessed (83% with collateral flow had good neurologic outcomes, but only 17% without collateral flow had good outcomes). All six patients with proximal basilar artery thrombus in whom collateral flow was assessed died, independent of the collateral flow observed. CONCLUSION: In symptomatic acute basilar artery thrombosis, neurologic outcome was better after intraarterial thrombolysis in patients who had collateral filling of the basilar artery, except in cases of proximal basilar thrombosis. Patients with collateral filling of the basilar artery also tolerated longer symptom duration.

Basilar Artery↗
PubMed1990

Role of nitric oxide in regulation of basilar artery tone in vivo.

Previous studies have suggested that nitric oxide (NO) may be a major endothelium-derived relaxing factor in peripheral blood vessels. This study tested the hypotheses that 1) formation of NO from L-arginine contributes to basal tone of cerebral arteries in vivo and 2) dilator responses of cerebral arteries to acetylcholine are dependent on formation of NO. Diameter of the basilar artery was measured through a cranial window in anesthetized rats. Under control conditions, topical application of 10 microM NG-monomethyl-L-arginine (L-NMMA, an arginine analogue that inhibits enzymatic formation of NO), constricted the basilar artery by 11 +/- 1% (means +/- SE). L-Arginine (100 microM), which had no effect on baseline diameter, abolished vasoconstriction in response to L-NMMA. L-Arginine did not alter vasodilation during acetylcholine (1 microM) (11 +/- 2 vs. 12 +/- 2%) or vasoconstriction during serotonin (1 nM) (-15 +/- 3 vs. -16 +/- 2%). L-NMMA (5-10 microM) abolished the dilator response of the basilar artery to acetylcholine but did not alter responses to nitroglycerin (0.01 microM) (24 +/- 4 vs. 20 +/- 3%). The inhibitory effect of L-NMMA on the vasodilator response to acetylcholine was prevented by L-arginine. These studies suggest that synthesis of NO from L-arginine influences resting tone of the basilar artery in vivo. Dilatation of the basilar artery to acetylcholine in vivo appears to be dependent on formation of NO from L-arginine.

Acetylcholine↗
PubMed1981

[Fibrinolytic treatment of severe thrombosis of the basilar artery (author's transl)].

Thrombosis of the basilar artery occurred in a 27-year-old woman after physical exercise (bowling). She became deeply unconscious without change so that four days after onset urokinase was administered. The neurological status than markedly improved, with partial regression of the paresis and the cranial nerve deficits, and she became responsive again. Angiography after four-day urokinase administration demonstrated complete recanalisation of the basilar artery. Subsequent rehabilitative measures led to almost complete disappearance of all symptoms. Later neurological tests revealed merely very discrete left hemiparesis, mainly of the arm.

Adult↗
PubMed2000

Effect of endothelin-1 receptor antagonist BQ-123 on basilar artery diameter after subarachnoid hemorrhage (SAH) in rats.

Aim of the study was to quantify cerebral vasospasm in rats after subarachnoid hemorrhage (SAH) by morphometric examination of basilar artery and to evaluate the influence of endothelin receptor blocker BQ-123 on basilar artery constriction. The rat cisterna magna (CM) was cannulated and after 7 days SAH was developed by administration of 100 microl autologic, non-heparinized blood to the CM. The sham subarachnoid hemorrhage was developed by intracisternal administration of 100 microl of artificial cerebrospinal fluid. Endothelin receptor blocker BQ-123 was injected into the CM in a dose of 40 nmol diluted in 50 microl of cerebrospinal fluid 20 min. before SAH, and 24h and 48 h after SAH. After perfusion fixation the brains were removed from the skull and histological preparations of basilar artery were done. The internal diameter and wall thickness of basilar arteries was measured by interactive morphometric method. The most severe vasospasm was found in rats after SAH. The presence of numerous infiltrations composed of neutrophils and macrophages correlated with advanced vasospasm (index of constriction 5 times lower than in normal), suggesting the role of other factors participating in the late phase of vasospasms after SAH. Administration of BQ-123 in the late phase after SAH caused the dilatation of basilar artery. Following the administration of BQ-123 in the late phase (48 h after SAH) the basilar artery dilated, its wall became thinner, and the number of leukocyte infiltrations in the subarachnoid space decreased compared to the values after SAH alone.

Animals↗
PubMed1994

[Anatomical analysis of the basilar artery and its branches with special reference to the arterial anastomosis, and its course and distribution on the pontine ventral surface].

The morphology of the basilar artery and its branches was studied in 52 human brains with special reference to arterial anastomosis, and its course and distribution on the pontine ventral surface. The results were as follows: 1. Main trunk of the basilar artery (1) The average maximum and minimum external diameter was 3.93 +/- 0.76 mm and 3.14 +/- 0.58 mm, and the average length was 35.0 +/- 5.1 mm. (2) Fenestration was observed in one case (1.9%). (3) The shape of flexion was classified into three types: S-shaped (18 cases = 34.6%), inverted S-shaped (29 cases = 55.8%) and straight (5 cases = 9.6%). (4) The average angle of flexion was 32.5 +/- 24.5 degrees. A positive correlation was observed between age and the angle of flexion; the coefficient was 0.31. 2. Branches of the basilar artery (1) The average number of branches from the main trunk of the basilar artery was 22.8 +/- 3.94. The main trunk was divided into three equal portions: the rostral, intermediate and caudal. Of all the branches, 43.9% arose from the rostral portion, 33.3% from the intermediate portion and the remaining 22.8% from the caudal portion. (2) Forty-eight percent of all the branches had an external diameter ranging from 0.35 mm to 0.55 mm, and this size was predominant in the branches from each of the three portions. (3) Of all the branches, 45.4% had a diverging angle between 45 degrees and 90 degrees. This was the predominant range of diverging angle in the intermediate and rostral portions. In the caudal portion, however, the predominant diverging angle tended to range from 0 degrees to 45 degrees. 3. Arterial anastomosis, course and distribution on the pontine ventral surface (1) Ninety-nine anastomoses were found on the pontine ventral surface in 42 cases. Fifty-seven anastomoses (57.5%) were found between pontine branches and 21 (21.3%) between a pontine branch and an anterior inferior cerebellar artery. More anastomoses were found in the median area than in the lateral area. (2) A number of arterial distributions were observed along the basilar sulcus in the middle and lower parts, around the facial and vestibulocochlear radices and around the trigeminal radix. Many branches had a downward distribution along the basilar sulcus in the middle and lower parts, an outward distribution around the facial and vestibulocochlear radices, and a downward or outward distribution around the trigeminal radix.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMedDate not supplied

Endovascular treatment of a giant fusiform aneurysm of the entire basilar artery.

The authors describe a case of fusiform basilar artery aneurysm not amenable to surgical clipping or balloon occlusion with preservation of the parent artery. The aneurysm was treated by balloon occlusion (proximal basilar artery) after test occlusion was well-tolerated; 7-year follow-up showed good results.

Adolescent↗
PubMed1979

Basilar artery occlusion in childhood: report of a case.

Basilar artery occlusion occurred in a 13-year-old boy. Eighteen cases in children reported in the literature were also analyzed. Basilar artery occlusion is more common in males. The main clinical manifestations are disturbance in consciousness, hemiplegia or quadriplegia, and pupillary abnormalitites. The prognosis is better in children than in adults.

Adolescent↗
PubMedDate not supplied

Basilar artery vasospasm after severe head injury: a preliminary transcranial Doppler ultrasound study.

BACKGROUND: Post-traumatic vasospasm after severe head injury is now a well known entity. However, all studies available in the literature have evaluated only the anterior cerebral circulation. We evaluated the incidence of basilar artery vasospasm in patients with severe head injury. METHODS: Basilar artery mean blood flow velocity was measured in 16 patients with severe closed head injury (Glasgow Coma Scale 8 or less) using transcranial Doppler ultrasonography. Ten normal subjects also underwent the same investigation. The patients' age ranged from 5 to 65 years. The study group included 13 males and 3 females. All patients underwent serial CT scans. In 10 patients the blood flow velocity was measured within 72 hours of the injury and in the remaining 6 it was done within 4 days to 3 weeks after the injury. RESULTS: The basilar artery could be insonated easily in all the patients. The depth of insonation ranged from 65-85 mm in adults and 50-60 mm in children (n = 2). The mean blood flow velocity in severely head-injured patients was 47.4 cm/second which was significantly higher than the normal value of 42 cm/second (p < 0.008). Eight of the 14 adults (57%) had a mean blood flow velocity higher than the control value. In 7 (50%) of these the velocity was higher than 60 cm/second. Seven of these 8 patients with a high blood flow velocity had evidence of diffuse brain injury on CT scan. Six of them had effacement of the basal cisterns as a result of diffuse brain oedema. Among the remaining 8 patients who had contusion and haematoma on CT scan, only 2 had a high blood flow velocity in the basilar artery. CONCLUSION: Basilar artery blood flow velocity is higher in patients with severe head injury. Patients with diffuse brain injury have a particularly high velocity. Thus, it may be an easy method to assess the severity of head injury. The temporal profile of basilar artery vasospasm needs to be established in severely head-injured patients to assess its clinical utility.

Adolescent↗
PubMed2002

Characterization of Ca2+ channels involved in endothelin-1-induced contraction of rabbit basilar artery.

This study attempted to characterize Ca2+ channels involved in endothelin-1-induced contraction of rabbit basilar artery using whole-cell patch-clamp and measurement of intracellular free Ca2+ concentration. Endothelin-1 activates two types of Ca2+-permeable nonselective cation channels (NSCC-1 and NSCC-2) and a store-operated Ca2+ channel (SOCC) in addition to the voltage-operated Ca2+ channel (VOCC). These channels can be discriminated using Ca2+ channel blockers, SK&F 96365 and LOE 908. Tension study was conducted to clarify the Ca2+ channels involved in endothelin-1-induced contraction of basilar artery. Endothelin-1-induced basilar artery contraction is fully dependent on extracellular Ca2+ influx. Based on sensitivity to nifedipine, an L-type VOCC blocker, VOCCs have a minor role in endothelin-1-induced contraction. Both LOE 908 and SK&F 96365 inhibit endothelin-1-induced contraction in a concentration-dependent manner, and their combination abolished it. The median inhibitory concentrations of these blockers for endothelin-1-induced contraction correlated well with those of the endothelin-1-induced [Ca2+]i responses. Thus, the inhibitory action of these blockers on endothelin-1-induced contraction may be mediated by blockade of NSCC-1, NSCC-2, and the SOCC. Extracellular Ca2+ influx through NSCC-1, NSCC-2, and SOCC may be essential for endothelin-1-induced basilar artery contraction.

Animals↗
PubMed1993

Basilar artery occlusion following yoga exercise: a case report.

Basilar artery occlusion developed in a 34 year old woman 2 months after adopting unusual neck postures during yoga practice. On angiography, her basilar artery was filled with intraluminal clot while the vertebral arteries were normal. We postulate that a severe reduction in blood flow and possibly an intimal tear triggered thrombosis of the vertebral artery and that the final stroke mechanism was artery-to-artery embolism.

Adult↗
PubMed1992

Effect of hematocrit variations on cerebral blood flow and basilar artery diameter in vivo.

Despite observations that pial arterioles constrict with decreased blood viscosity or hemodilution, several investigators have found an inverse relationship between cerebral blood flow (CBF) and hematocrit (Hct) under physiological conditions. To investigate whether this is due to a dilation of the more proximal large cerebral arteries, in vivo responses of CBF and basilar artery to hemodilution and hemoconcentration were studied in 21 anesthetized normal cats, using a closed clival window model. An inverse correlation between Hct and CBF was found, but CBF responses were smaller than previously reported data suggest. Varying Hct between 60 and 120% of baseline caused CBF to vary between 140 and 90%, approximately. Moderate hemodilution was associated with a significant decrease (-4.4%) in basilar artery diameter (P less than 0.05), but other Hct manipulations had no consistent effect on basilar artery diameter. It is concluded that dilation of large cerebral arteries cannot account for the decreased cerebrovascular resistance following hemodilution but that a disproportionate reduction of in vivo viscosity must be responsible. Pial arteriolar constriction after hemodilution therefore probably reflects a normal autoregulatory adjustment of vasomotor tone to altered blood rheology, whereas changes in large artery caliber may serve to modulate microvascular pressure.

Animals↗
PubMed1992

Mechanism of contractile responses to bradykinin in canine basilar arteries.

This study was undertaken to investigate the role of endothelium in the modulation of vascular responses to bradykinin and to elucidate the receptor types and mechanism of action of bradykinin in isolated basilar artery. The results showed a contractile response to bradykinin in basilar artery. This contractile response to bradykinin was partially modulated by endothelium in a dose-dependent manner. In addition, both des-Arg9-[Leu8]bradykinin and [d-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin significantly antagonized the responses to bradykinin. However, the blocking effect and the apparent affinity of [d-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin (pA2 = 9.6 +/- 0.4) were greater than those with des-Arg9-[Leu8]bradykinin (pA.2 = 7.8 +/- 0.3). These results suggest that two apparently distinct types of BK receptors may exist in basilar arteries. Furthermore, the contractile response to bradykinin in basilar artery was significantly inhibited by 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (10(-5) M), H-7 (10(-5) M) and TMB-8 (10(-5) M), but not by indomethacin (10(-5) M) or nordihydroquariaretic acid (10(-5) M). On the other hand, nifedipine, Ca(2+)-free medium, EGTA and Ca(2+)-free medium/EGTA significantly reduced the bradykinin-induced contraction, indicating that part of the contractile response of basilar artery to bradykinin is dependent on extracellular Ca2+. In conclusion, the mechanism of the contractile responses to bradykinin in basilar artery may involve increased intracellular Ca2+ levels acting on the BK1 and BK2 receptor, followed by activation of the phosphoinositide pathway and receptor-mediated Ca2+ channel.

Animals↗
PubMed2002

Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery.

The modulation of serotonin (5-HT(1B/1D)) receptor-induced vascular contractility by histamine and U-46619 was compared in the rabbit basilar artery and saphenous vein. In the saphenous vein, histamine (5 x 10(-7) M) significantly increased the potency (from pEC(50) of 6.0 to 6.8) and efficacy (from 52.3% to 88.2%) of sumatriptan. Likewise, U-46619 (5 x 10(-9) M) also increased the potency (from pEC(50) of 5.9 to 6.6) and efficacy (from 51.8% to 92.1%) of sumatriptan in the saphenous vein. In contrast, equieffective concentrations of histamine (10(-7) M) and U-46619 (3 x 10(-9) M) failed to amplify contraction to sumatriptan in the basilar artery. Contraction to sumatriptan was inhibited by nitrendipine (10(-7) M) in the basilar artery but not in the saphenous vein, suggesting that different contractile signaling mechanisms are operating in these tissues. Furthermore, U-46619- and thrombin-induced contractility in the basilar artery were also not amplified by histamine, suggesting that lack of amplification of contraction in the basilar artery was not restricted to sumatriptan but was rather a characteristic of this cerebral vessel. These data suggest that in the in vivo plasma milieu sumatriptan will more markedly contract the peripheral saphenous vein than the basilar artery, a cerebral blood vessel.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Microsurgical anatomy of the lower basilar artery.

This study was designed to study the microvascular anatomy of the basilar artery between the superior cerebellar artery and the vertebrobasilar junction (i.e. the lower basilar artery). Twenty unfixed brains were injected with silicone rubber solution and studied with a Zeiss OPMI microscope. The length of this segment of the basilar artery was 28.1 + 1.35 mm and its course was straight in 9 (45%) brains, curved in 7 (35%) and tortuous in 4 (20%). The total number of perforators found in 20 brains was 340 with an average of 17 per brain. Of these, 118 (34.7%) were median and 222 (65.2%) were lateral. Median branches had a mean length of 5.8 + 1.25 mm, whereas left and right lateral branches had a mean length of 16 + 1.25 mm and 16 + 1.58 mm respectively.

Autopsy↗
PubMed1991

Inhibition of the acetylcholine-induced relaxation of canine isolated basilar artery by potassium-conductance blockers.

Canine basilar artery rings precontracted with 5-hydroxytryptamine (0.1-0.5 microM) relaxed in the presence of acetylcholine (25-100 microM), sodium nitroprusside (0.1 microM), or stimulation of the electrogenic sodium pump by restoration of extracellular K+ (4.5 mM) after K(+)-deprivation. Acetylcholine-induced relaxation is believed to be caused by the release of endothelium-derived relaxing factor (EDRF) and is prevented by mechanical removal of the endothelium, while relaxations induced by sodium nitroprusside or restarting of the sodium pump are endothelium-independent. Acetylcholine-induced relaxation was selectively blocked by pretreatment of the tissue with the nonselective K+ conductance inhibitors, 4-aminopyridine (4-AP, 3 mM), Ba2+ (1 mM), and tetraethylammonium (20 mM), 4-AP also blocked ACh-mediated relaxation in muscles contracted with elevated external K+. Relaxation of 5-hydroxytryptamine-induced contraction by sodium nitroprusside, or by addition of K+ to K(+)-deprived muscle, was not affected by 4-AP. Relaxation of basilar artery with acidified sodium nitrite solution (containing nitric oxide) was reduced by 4-AP. These results suggest that 4-AP and possibly Ba2+ inhibit acetylcholine-induced endothelium-dependent relaxation by inhibition of the action of EDRF on the smooth muscle rather than through inhibition of release of EDRF. The increase in K+ conductance involved in acetylcholine-induced relaxation is not due to ATP-inhibited K+ channels, as it is not blocked by glyburide (10(-6) M). Endothelium-derived relaxant factor(s) may relax smooth muscle by mode(s) of action different from that of sodium nitroprusside or by hyperpolarization due to the electrogenic sodium pumping.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1996

Protein synthesis and immunoreactivities of contraction-related proteins in smooth muscle cells of canine basilar artery after experimental subarachnoid hemorrhage.

We examined time-dependent changes in protein synthesis and in the immunoreactivities of representative contraction-related structural proteins in smooth muscle cells of canine basilar arteries after experimental subarachnoid hemorrhage (SAH). Protein synthesis was assessed by the percentage of polyribosome-forming ribosomes to total ribosomes (aggregation rate), a morphological index of the activity of protein synthesis. The aggregation rates in prostaglandin F2 alpha-(PGF 2 alpha) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced contracted basilar arteries were 70.0 +/- 7.0% and 71.4 +/- 8.7%, respectively, quite similar to the value in normal basilar artery (73.0 +/- 8.0%). In the single-SAH group with little delayed histological changes in the basilar arteries, the aggregation rate was significantly decreased to 30.5 +/- 6.4% by 24 h after the SAH, and recovered to 52.3 +/- 9.0% and 70.2 +/- 7.6% at 7 and 14 days postSAH, respectively, when the vasospasm was moderately and completely ameliorated. In contrast, in the double-SAH group in which the basilar arteries developed delayed smooth muscle cell death and long-lasting arterial contraction, a significant decrease in the aggregation rate (25.0 +/- 5.0% on day 4) persisted for 14 days. The in vitro incorporation of [3H]-leucine in the basilar arterial cells was also significantly suppressed 4 and 7 days after the initial SAH (1.2 +/- 0.4 and 1.4 +/- 0.3 x 10(3) dpm/mg protein) in the double-SAH group, as opposed to no significant decrease in the basilar artery at 7 days postSAH in the single-SAH group (1.9 +/- 0.6 x 10(3) dpm/mg protein). The immunoreactivity of alpha-smooth muscle actin, a contractile protein, demonstrated by immunohistochemistry and immunoblots, was not altered for up to 14 days even in the double-SAH group, but that of calponin and of h-caldesmon, contraction-inhibiting proteins, was markedly reduced 4-14 days after the initial SAH. Persistent impairment of protein synthesis and relative reduction of immunoreactivities of the contraction-inhibiting proteins were observed in arteries with severe vasospasm and loss of smooth muscle cells, as noted in the double-SAH subjects. These abnormalities may cooperate to cause cerebral arterial narrowing accompanied by degeneration of smooth muscle cells after SAH.

Actins↗
PubMedDate not supplied

High-resolution computed tomography of the basilar artery: 2. Vertebrobasilar dolichoectasia: clinical-pathologic correlation and review.

To better define the clinical significance of vertebrobasilar dolichoectasia, the clinical signs and symptoms and basilar artery parameters of diameter, height, and transverse position were evaluated in two groups of symptomatic patients. Ten patients had isolated involvement of the third, sixth, or seventh cranial nerves. The other 10 patients had multiple neurologic deficits including combinations of compressive cranial nerve deficits, both ischemic and compressive central nervous system deficits, and hydrocephalus. Although significant differences for mean basilar artery diameter and height exist between these two groups, the symptomatology and basilar artery parameters present as a spectrum. A symptomatic patient with a normal-caliber, but tortuous, basilar artery is more likely to have isolated cranial nerve involvement. Conversely, the patient with marked basilar artery dilatation (ectasia) is far more likely to present with multiple compressive or ischemic neurologic deficits. Conventional angiography in patients with dilated basilar arteries carries a significant risk for brainstem ischemia. Most authors agree that when vertebrobasilar dolichoectasia has been demonstrated by computed tomography, additional angiography, if required at all, should be performed by digital subtraction techniques.

Adult↗
PubMed1990

Ionic mechanisms in spontaneous vasomotion of the rat basilar artery in vivo.

1. The goal of this study was to examine ionic mechanisms that modulate spontaneous rhythmic changes in vascular calibre or 'vasomotion' in the basilar artery in vivo. 2. Diameter of the basilar artery was measured through a craniotomy in anaesthetized rats under control conditions and during topical application of antagonists or alteration in the ionic composition of artificial cerebrospinal fluid (CSF). 3. Both Ca2(+)-free CSF and the Ca2+ channel blocker, nimodipine, produced moderate dilatation of the basilar artery and abolished vasomotion. Increasing the concentration of Ca2+ in CSF from 1.7 to 5.0 mM did not affect the frequency of vasomotion, although the amplitude was increased slightly. 4. Both K(+)-free CSF and ouabain produced mild to moderate vasoconstriction and abolished vasomotion. In contrast, increasing the concentration of K+ in CSF produced vasodilatation of the basilar artery and decreased or abolished vasomotion depending on the degree of vasodilatation. 5. Tetrodotoxin had no effect on vasomotion. 6. These results suggest that vasomotion of the basilar artery in vivo is dependent on extracellular Ca2+ and K+, and on the activity of Na(+)-K(+)-ATPase, and not dependent on Na+ channel.

Animals↗