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L-arginine restores dilator responses of the basilar artery to acetylcholine during chronic hypertension.

The objective of this study was to test the hypothesis that administration of L-arginine, a substrate for nitric oxide synthase, restores acetylcholine-induced dilatation of the basilar artery in chronically hypertensive rats. Basilar artery diameter was measured through a cranial window in anesthesized stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) aged 6 to 7 months (adult) and 12 months (older adult). Under control conditions, baseline basilar artery diameter was smaller in SHRSP (adult, 239 +/- 30 micron; older adult, 198 +/- 13 micron) (mean +/- SE) than in WKY (adult, 261 +/- 10 micron; older adult, 259 +/- 7 micron) (P <.05 versus SHRSP). Topical application of acetylcholine (10(-5) mol/L) produced dilatation of the basilar artery in WKY, which was impaired in both adult and older SHRSP (P <.05). Topical L-arginine (10(-3) mol/L for 30 minutes) did not affect responses to acetylcholine in adult SHRSP but enhanced vasodilatation in response to acetylcholine (10(-5) mol/L) in older SHRSP without affecting responses to sodium nitroprusside. In contrast, D-arginine did not affect acetylcholine-induced vasodilatation in older SHRSP. These results suggest that impaired dilatation of the basilar artery in response to acetylcholine in older SHRSP is restored toward normal by L-arginine, a substrate for nitric oxide synthase.

Acetylcholine↗

Comparison of vasorelaxants in human basilar arteries and umbilical arteries.

The vasodilatation produced by adenosine, sodium nitrite, and papaverine was compared on isolated human basilar arteries and umbilical arteries precontracted with 30 mM KCl or submaximal concentrations of serotonin and prostaglandin F2 alpha. The basilar artery was far more sensitive to the vasodilators than the umbilical vessel. Papaverine, for instance, was 133 times more effective (EC50 = 3.9 x 10(-6) M) in basilar arteries precontracted with KCl than it was in the umbilical artery (EC50 = 5.2 x 10(-4) M) and all dilators inhibited by at least 95% basilar arteries precontracted with serotonin or prostaglandin F2 alpha. In contrast, umbilical arteries precontracted with KCl or prostaglandin F2 alpha failed to relax significantly to adenosine and sodium nitrite at concentrations that exceeded 10(-3) M, and contractions elicited by serotonin were inhibited by less than 40%. The results support the concept that physiological mechanisms responsible for dilation in most vessels are deficient in the umbilical artery and that the deficiency may be related to the role this atypical vessel plays in closure of the extracorporeal circulation at birth.

Basilar Artery↗

Intraoperative angiography and temporary balloon occlusion of the basilar artery as an adjunct to surgical clipping: technical note.

The direct surgical treatment of intracranial aneurysms is not always possible, especially in posterior circulation aneurysms. This is usually because of their complex anatomy and location next to the skull base and brain stem, where proximal vascular control is usually not attainable. Four patients at our institution underwent intraoperative transfemoral catheterization of the basilar artery with a nondetectable endovascular balloon for proximal control of the basilar artery. The flow control in the basilar artery was excellent and facilitated the surgery. Before surgery, each patient underwent the placement of a 10-cm 8-French femoral introducer sheath and were taken to the operating room where they were placed in a supine position and a subtemporal or pterional craniotomy was performed. After the initial exposure and before aneurysm manipulation, a nondetachable silicone balloon catheter was passed through an introducer catheter and was placed into the rostral basilar artery, using flow direction, microguidewires, and angiographic "road-mapping" techniques. In two patients, temporary basilar occlusion was used to collapse the aneurysm and to facilitate clip placement. In the third patient, intraoperative aneurysm rupture occurred and was controlled by temporary basilar artery occlusion. Using intraoperative angiography, complete aneurysm obliteration and vessel patency was confirmed in all four patients. All patients made a complete recovery except for initial postoperative third nerve palsies in three patients. This technique achieves intraoperative control of the basilar artery proximal to an aneurysm by the use of a nondetachable occlusive balloon in the basilar artery. An added benefit is the ease with which intraoperative angiography can be obtained in this context.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Evidence against serotonin as a vasoconstrictor neurotransmitter in the rabbit basilar artery.

It has been suggested recently that serotonergic nerves distinct from the known adrenergic innervation are present in cerebral blood vessels. We have confirmed that serotonin is present in the wall of rabbit cerebral arteries using a high-performance liquid chromatography technique, with levels in the basilar artery of 0.27 +/- 0.04 microgram/g wet wt. Furthermore, adrenergic denervation in vitro with 6-hydroxydopamine, while substantially reducing norepinephrine content, did not alter serotonin levels in the basilar artery. However, it was not possible to demonstrate specific accumulation of [3H]serotonin into distinct serotonergic nerves. Both the basilar artery and ear artery (which has been shown not to be innervated with serotonergic nerves) accumulated [3H]serotonin when incubated with a low concentration (10(-8) M). However, [3H]serotonin accumulation was reduced markedly in 6-hydroxydopamine-treated vessels as well as in the presence of the norepinephrine uptake blocker, desmethylimipramine. Furthermore, pretreatment with the serotonin uptake blocker, fluoxetine, did not inhibit selectively [3H]serotonin accumulation in the basilar artery. Thus, the majority of [3H]serotonin accumulation can be attributed to adrenergic nerves. The possibility that serotonergic nerves contribute to the neurogenic constrictor response of the rabbit basilar artery was also tested. Adrenergic denervation with 6-hydroxydopamine in vitro abolished the constrictor response to transmural nerve stimulation completely, but levels of endogenous serotonin were not affected. Thus, although the presence of endogenous serotonin in cerebral arteries has been confirmed, this substance does not appear to contribute to the neurogenic vasoconstriction seen in this vessel.

Animals↗

A ruptured aneurysm at the distal end of the basilar artery fenestration associated with multiple fenestrations of the vertebrobasilar system: case report.

BACKGROUND: An aneurysm at the fenestrated basilar artery usually arises at the proximal end of the fenestration, with few exceptions. We failed to reveal any case of aneurysm at this site associated with multiple fenestrations of the vertebrobasilar system. CASE REPORT: This 62-year-old male was admitted to our hospital 1 day after a sudden onset of headache. CT scan showed subarachnoid hemorrhage, and angiogram revealed an aneurysm at the distal end of the fenestrated basilar artery in association with two other fenestrations of the vertebrobasilar system. The limb of the basilar artery fenestration was trapped tightly with one clip through the transcondylar approach. Postoperative course was uneventful, and postoperative angiogram showed complete disappearance of the aneurysm. CONCLUSION: An extremely rare case of an aneurysm at the distal end of the fenestrated basilar artery in association with multiple fenestrations of the vertebrobasilar system is reported. The coexistence of vertebral artery fenestration and the fenestration of the vertebrobasilar junction may give a clue to the mechanism of occurrence of basilar artery fenestration.

Aneurysm, Ruptured↗

[Basilar artery thrombosis (author's transl)].

Arteriosclerosis is the most common cause of basilar artery thrombosis. Rarely basilar occlusions are observed after cerebral concussion and hyperextension of the neck; occasionally they are founded in craniocervical dysplasia, arteritis and hypercoagulability of blood.--Clinical data and differential diagnostic aspects are demonstrated in 4 own cases and the present literature. Characteristics of clinical symptomatology are discussed with respect to the sites of predilection in distal and proximal part of basilar artery. Angiography examination is the most important diagnostic method and shows prognostic indications by demonstration of collaterals.--The treatment consists of inhibition of blood viscosity, reduction of perifocal edema and stabilization of blood-pressure.

Adult↗

[A case of basilar artery occlusion successfully treated with tissue plasminogen activator].

This case concerns a stroke in the basilar artery territory that was successfully treated with a tissue plasminogen activator (t-PA). A 44-year-old man suddenly lost consciousness. It took fifty minutes to arrive to our hospital after the onset. On admission, his consciousness was in a coma state. A head CT revealed normal findings but a cerebral angiography showed complete occlusion in the basilar artery. We gave 240,000 units t-PA intravenously for 60 minutes. The intravenous t-PA dramatically improved his state of consciousness. After treatment, the brain CT scan showed low-density areas in the left occipital area and right pons. The cerebral angiography showed arterial sclerosis in the basilar artery. There was no parenchymal hemorrhage or hemorrhagic infarction in the patient. The hitherto reports showed the intravenous infusion of t-PA may be particular value in patients with thromboembolic occlusion in the middle cerebral artery. In contrast, our results support its efficacy in strokes in the basilar artery territory.

Adult↗

The actions of sodium nitroprusside and diltiazem on calcium-, potassium- and histamine-induced contractile responses in isolated rabbit basilar artery, aorta, taenia coli and tracheal smooth muscle.

The effects of sodium nitroprusside (NaNP) and diltiazem on CaCl2-,KCl- and histamine-induced contractile responses were studied in isolated rabbit basilar artery, aorta, taenia coli and trachea. NaNP reduced CaCl2-induced maximal contractions in basilar artery and aorta, but little affected those in taenia coli and trachea. NaNP reduced histamine-induced maximal contraction markedly in aorta but slightly in basilar artery and taenia coli. The reduction in aorta was reversed by increasing CaCl2 contraction in bathing medium. NaNP inhibited histamine-induced contractions of basilar artery, aorta and taenia coli in Ca-free medium. Diltiazem reduced CaCl2-induced maximal contractions in basilar artery and aorta, whilst it caused a parallel shift of concentration-response curves for CaCl2 to the right in taenia coli and trachea. diltiazem reduced histamine-induced maximal contractions in basilar artery and taenia coli. These reductions were reversed by increasing CaCl2 concentration in bathing medium. Diltiazem strongly inhibited histamine-induced contraction of taenia coli in Ca-free medium. The effects of NaNP and diltiazem on KCl-induced contractions both in normal (Ca; 2.5 mM) and in high Ca (Ca; 12.5 mM) media were also studied. From the results obtained in this study, the actions of NaNP and diltiazem were considered to vary with the type of smooth muscle or the condition eliciting contraction. Their possible mechanisms were discussed in this paper.

Animals↗

Occlusion of the basilar artery. A clinical and pathological study of thirteen autopsied cases.

The present report dealt with thirteen autopsied cases of basilar artery occlusion. The age of the patients ranged from fifty one to seventy six years with a mean age of fifty six years, and there were eleven males and two females. Basilar artery occlusion was found in one in every 160 autopsies. The average length of the clinical course of the disease was five months. Many patients had a history of hypertension, diabetes mellitus, and cerebrovascular attacks. The neurological signs and symptoms of basilar artery occlusion extremely varied and were complicated. In our series, occular bobbing, palatal myoclonus, Foville syndrome, and Millard - Gubler syndrome are significant. Arteriosclerotic thrombosis is the most important etiologic factor. The site of occlusion was most frequently encountered in the lower third of the basilar artery. Areas of softening were prominent in the midbrain and the pons. In the cerebellum, softenings were present particularly in the areas supplied by the superior cerebellar artery. Infarcts in the thalamus and the temporo-occipital lobes supplied by the posterior cerebral artery were observed very frequently. The distribution of softening was related to the site of occlusion of the basilar artery and the collateral circulation through the Willis ring.

Aged↗

L-Arginine does not restore dilatation of the basilar artery during diabetes mellitus.

The goal of this study was to test the hypothesis that administration of L-arginine, a substrate for the synthesis of nitric oxide, restores endothelium-dependent dilatation of the basilar artery during diabetes mellitus. We measured the diameter, of the basilar artery in vivo in nondiabetic and diabetic (streptozotocin; 50-60 mg/kg i.p.) rats in response to endothelium-dependent agonists (acetylcholine and bradykinin) and an endothelium-independent agonist (nitroglycerin) before and during application of L-arginine. Topical application of acetylcholine (1.0 and 10 muM) and bradykinin (1.0 and 10 microM) produced dilatation in nondiabetic rats of the basilar artery which was impaired in diabetic rats. Topical application of nitroglycerin (0.1 and 1.0 microM) produced similar dilatation of the basilar artery in nondiabetic and diabetic rats. Topical application of L-arginine (0.1 and 3 mM) did not enhance dilatation of the basilar artery in response to acetylcholine and bradykinin in diabetic rats. Thus, impairment of dilatation of the basilar artery in diabetic rats in response to acetylcholine and bradykinin appears to be related to a mechanism unrelated to the availability of L-arginine for nitric oxide synthase.

Acetylcholine↗

Aneurysms of the basilar artery trunk.

Ten cases of basilar artery trunk aneurysms are reported; nine were operated on by a middle subtemporal approach and one by a pterional transsylvian technique. The middle subtemporal approach facilitated clipping of aneurysms located as deep as 25 mm below the posterior clinoid process as seen on the lateral views of the angiogram, such that the junction of the vertebral arteries was visible in most cases. The authors emphasize the usefulness of direct retraction of the trigeminal nerve, the pons, and the aneurysm itself; occasionally, drilling off the pyrimidal edge is also valuable. Surgical results were satisfactory in seven cases and poor in one; two patients died.

Adult↗

Ibuprofen or ozagrel increases NO release and l-nitro arginine induces TXA(2) release from cultured porcine basilar arterial endothelial cells.

The vascular resting tone of the porcine basilar artery appears to be mostly maintained by a balance between spontaneously released nitric oxide (NO) from endothelial cells and thromboxane (TX) A(2) from endothelial and smooth muscle cells. However the precise role of the interaction between the above two substances in the control of vascular tone is unclear. We attempted to clarify the interaction between NO and TXA(2) using cultured porcine basilar arterial endothelial cells. The cultured endothelial cells produced NO spontaneously, while TXB(2) (a stable metabolite of TXA(2)) production remained below the detection limit. Ibuprofen (a COX inhibitor) and ozagrel (a TXA(2) synthetase inhibitor) significantly increased the spontaneous production of NO, which was not affected by 1400W (an iNOS inhibitor). l-Nitro arginine (a NOS inhibitor) significantly induced TXB(2) production. These results suggest that NO may inhibit COX or TXA(2) synthetase, and that therefore inhibition of NOS might disinhibit COX or TXA(2) synthetase, subsequently inducing TXA(2) production. On the other hand, as TXA(2) and other contractility-related prostaglandin(s) may inhibit NOS, therefore the inhibition of COX or TXA(2) synthetase might disinhibit NOS, and then increase the spontaneous production of NO in porcine basilar arterial endothelial cells.

Animals↗

Simulated microgravity enhances vasoconstrictor responsiveness of rat basilar artery.

Recently, hypertrophy and increased myogenic tone of brain vessels have been observed in rats after simulated microgravity. It is expected that simulated microgravity may also induce hyperreactivity of brain vessels. To test this hypothesis, Sprague-Dawley rats were subjected to a 4-wk tail-suspended hindlimb unloading (TS) to simulate the cardiovascular deconditioning effect of microgravity. After 4 wk, the vasoreactivity of isolated basilar arterial rings from TS rats to both receptor- and non-receptor-mediated vasoconstrictors, such as KCl, arginine vasopressin, or 5-hydroxytryptamine (5-HT), and vasodilators such as ACh, thrombin, adenosine, or sodium nitroprusside were examined and compared with those from simultaneous control (Cn) rats. In the first part of this study, it was found that the maximal isometric contractile responsiveness evoked by vasoconstrictors such as KCl, arginine vasopressin, or 5-HT was enhanced in basilar arterial rings from TS rats, whereas vasodilatory responsiveness to vasodilators showed no significant difference between TS and Cn rats. In the second part of this study, it was found that removal of the endothelium had no effects on the contractile responsiveness to 5-HT in basilar arterial rings from TS rats but enhanced markedly the responsiveness in basilar arterial rings from Cn rats to an extent comparable with that of TS rats. Application of tetraethylammonium also had no effects on the contractile response to 5-HT in basilar arterial rings from TS but significantly increased the responsiveness of basilar arterial rings from Cn rats with endothelium intact. These results showed that 4-wk simulated microgravity enhanced the vascular contractile responsiveness of basilar arterial rings to both receptor- and non-receptor-mediated vasoconstrictors, and the enhancement of 5-HT-induced contraction in TS rat basilar arteries was due to an impairment of endothelium-dependent mechanism. These results suggest that endothelium-derived hyperpolarizing factors are responsible for this endothelium-dependent attenuating modulatory mechanism in contractile responsiveness of rat basilar arteries to 5-HT.

Animals↗

[A case of basilar artery fenestration with recurrent attacks of vertebrobasilar insufficiency].

Fenestration of basilar artery is an uncommon vascular anomaly that is usually an incidental product on autopsy or angiography. None of the cases in the literature had clinical symptoms associated with this anomaly except for subarachnoid hemorrhage when accompanied with saccular aneurysm. We report a rare case of the basilar artery fenestration associated with clinical symptoms without any aneurysm. A 71-years-old male, who had been treated for labile hypertension and had had recurrent attacks of vertigo, nausea, sometimes diplopia or unsteady gait, for 5 years, was referred to our hospital on Sept. 13, 1985. One day prior to admission, he suddenly felt diplopia and vertigo and unsteady gait. His family noticed he was dysarthric. On admission, he was alert and normotensive. He complained of dysesthesia on the right half of the perioral region and his right fingers. A neurological examination showed a mild weakness and hyperactive deep tendon reflexes on his right leg. His motor coordination was almost normal, but he was unsteady when he stood on one foot with his eyes closed. Laboratory examinations were normal except for an elevated serum uric acid level. A chest x-ray film showed a sclerotic change of aorta and mild cardiomegaly. Left ventricular hypertrophy was observed on his ECG. His CT scans showed multiple lacunae and mild brain atrophy. On cerebral angiography, his basilar artery (BA) had a fenestration almost in its total length that divided the BA, like a duplication, into two components with a smaller diameter than normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Electroencephalograms in basilar artery migraine.

Nine cases of 'basilar artery migraine' (BAM) have been recorded. In 8 cases, excess of beta activity was observed during the attacks and disappeared in less than 3 days. The inter-ictal EEGs were normal. Drug ingestion was excluded each time. These EEG patterns are different from those which have been reported in the literature, i.e., transitory posterior abnormal slow waves. However, case no.1 is in agreement with the literature. The expression 'BAM' probably covers different syndromes which are further discussed.

Adolescent↗

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

The present experiments were carried out to investigate the endothelium dependence of the responses to acetylcholine (ACh), arachidonic acid, and histamine in monkey basilar arteries. ACh and arachidonic acid caused endothelium-dependent contraction (EC) in both monkey and canine basilar arteries. The endothelium-derived contracting factor (EDCF) was probably thromboxane A2 (TxA2), as the EDC was attenuated by a cyclooxygenase inhibitor, TxA2 synthetase inhibitors, and TxA2 antagonists. On the other hand, histamine caused endothelium-dependent relaxation (EDR) in monkey and EDC in canine basilar arteries. The EDR in monkey basilar arteries was attenuated by a nitric oxide synthase inhibitor. The EDR and EDC were antagonized by tripelennamine but not by cimetidine, 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 a single type of endothelium with two types of signalling processes (one for EDC and one for EDR).

Acetylcholine↗

Evidence for the existence of 5-hydroxytryptamine receptors, which are not of the 5-HT2 type, mediating contraction of rabbit isolated basilar artery.

In the rabbit isolated basilar artery the contractile action of 5-hydroxytryptamine (5-HT) was little affected by high concentrations of ketanserin (1.0 X 10(-6) M) indicating that 5-HT-receptors other than those of the 5-HT2-type were involved. The contractile action of 5-HT was mimicked by methysergide and 5-carboxamidotryptamine (5-CT) with equipotent concentration ratios (5-HT = 1) of about 22 and 0.6 respectively. This profile is characteristic of that in the dog saphenous vein which contains a 5-HT receptor type that may be described as '5-HT1-like'.

Animals↗