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At least 253 records · Page 14Linked to original sources
PubMed1996

[Traumatic basilar artery dissection presenting with "locked-in" syndrome: report of a case].

We encountered a case of traumatic basilar artery dissection presenting with "locked-in" syndrome. A 46-year-old-man fell approximately 2 meters and landed in an inverted position. He was admitted to our hospital after 4 days. He was in coma on admission, and neurological examination revealed that his pupils were 2 mm in size and reactive, the corneal reflex of both sides was absent, the pharyngeal reflex was absent, and quadriplegia was present. CT and MRI showed infarction at the ventral portion of the pons. 3D-CT and CT using a bone algorithm showed fractures of the upper clivus, the left petrous bone, and the left occipital condyle. Angiography showed a pearl and string sign at the upper basilar artery. It is suggested that the cause of the infarction of the ventral portion of the pons was the occlusion of the perforating arteries due to the basilar artery dissection, and the mechanism of the basilar artery dissection was the hyperextension or hyperflexion of the basilar artery by the movement of the brain stem caused by the traumatic impact. Repeated angiography revealed gradual improvement. Eventually he freed himself from the "locked-in" syndrome.

Basilar Artery↗
PubMed1991

Flow-mediated dilatation of the basilar artery in vivo.

Flow-mediated dilatation has been described mainly in peripheral conduit arteries. The goal of this study was to examine mechanisms and functional implications of flow-mediated dilatation in large cerebral arteries in vivo. Vessel diameter and velocity of blood flow through the basilar artery were measured using a cranial window in 45 anesthetized rats. Mean blood flow velocity through the basilar artery increased by 94 +/- 8% during unilateral common carotid artery occlusion and 203 +/- 13% during bilateral occlusion. Diameter of the basilar artery increased by 10 +/- 1% during unilateral common carotid artery occlusion and 29 +/- 2% during bilateral occlusion from control diameter of 275 +/- 8 microns. Vasodilatation appeared with a delay of 13 +/- 1 seconds after the onset of the increase in flow velocity. With systemic arterial pressure maintained at baseline levels, pressure in the basilar artery (servonull) decreased initially during carotid occlusion, and during dilatation of the basilar artery, pressure was restored partially toward normal. Indomethacin (10 mg/kg i.v.), topical application of tetrodotoxin (10(-6) M), NG-monomethyl L-arginine (5 x 10(-6) M), tetraethylammonium chloride (10(-2) M), glibenclamide (10(-5) M), SKF 525A (3 x 10(-5) M), and ouabain (10(-5) M) had no effect on flow-mediated dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effect of diabetes mellitus on responses of the basilar artery in rats to products released by platelets.

BACKGROUND AND PURPOSE: Aggregation and adherence of platelets to vascular endothelium are increased during diabetes mellitus, and thus responses of cerebral arteries to products released by platelets may have important implications for the pathogenesis of stroke during diabetes. The goal of this study was to determine whether responses of the basilar artery to products released by platelets are altered during diabetes. METHODS: A craniotomy was performed over the ventral medulla to expose the basilar artery. Diameter of the basilar artery was measured using intravital microscopy in nondiabetic and diabetic (50-60 mg/kg i.p. streptozotocin) rats in response to adenosine 5'-diphosphate, serotonin, and the thromboxane analogue U-46619. RESULTS: Topical application of 10 and 100 microM adenosine 5'-diphosphate produced only minimal changes in diameter of the basilar artery that were similar in nondiabetic and diabetic rats (p greater than 0.05). At 0.01, 0.1, and 1.0 microM serotonin produced dose-related constriction of the basilar artery that was similar in nondiabetic and diabetic rats (p greater than 0.05). At 0.1 and 1.0 microM U-46619 also produced similar dose-related constriction of the basilar artery in nondiabetic and diabetic rats (p greater than 0.05). CONCLUSIONS: These findings suggest that responses of the basilar artery to products released by platelets are not altered by diabetes mellitus. Thus, it does not appear that alterations in reactivity of the basilar artery to products released by platelets contribute to the pathogenesis of stroke during diabetes.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1987

Analysis of the mechanism of action of bradykinin on human basilar artery in vitro.

Bradykinin (BK) initially produced concentration-related relaxations of human basilar artery in vitro. Concentration-effect curves constructed at 2 h intervals to BK over an 8 h period were reproducible. The rank order of potency of three kinins on the human basilar artery was found to be BK greater than methionyl-lysyl-BK greater than des-Arg9-BK. The B2-receptor antagonist Thi5,8, D-Phe7-BK but not the B1-receptor antagonist des-Arg9-Leu8-BK selectively blocked BK-induced relaxations of the human basilar artery. The relaxant effects of bradykinin and acetylcholine but not papaverine were attenuated after removal of the endothelium or treating the tissues with BW755C. Indomethacin was without effect. Concentration-effect curves to angiotensin I were markedly attenuated by captopril at a concentration which had no effect on BK, angiotensin II or 5-hydroxytryptamine responses. It is concluded that BK induced relaxations of the human basilar artery are mediated via activation of a B2 receptor and the response is dependent upon the release of a factor present in the endothelium. Angiotensin converting enzyme is present in the human basilar artery and is important for the conversion of angiotensin I to angiotensin II but apparently not for the degradation of BK. It is likely that other kininases are present and active in the tissue.

Acetylcholine↗
PubMedDate not supplied

Basilar artery occlusion: clinical and radiological correlation.

Twenty patients with basilar artery occlusion and three patients with bilateral vertebral artery occlusions have been studied. The clinical data at the time of the ictus and the long-term follow-up data have been correlated with the site and extent of the basilar artery occlusion and the type of collateral flow. Patients with hypertension and with coma at the outset have a grave prognosis. The presence of surface collateral flow may not indicate adequate perfusion of the paramedian penetrating branches of the basilar artery or the thalamoperforating branches of the posterior communicating or posterior cerebral arteries. It is these vessels which supply the territory regulating the level of consciousness and containing some of the control mechanisms for respiratory function.

Adult↗
PubMed1984

[Doppler sonogram in basilar artery thromboses].

We have investigated 6,380 patients with directional c-w Doppler sonography within the last 3 1/2 years, and have suspected obstruction of the basilar artery or of both distal vertebral arteries in 7 cases. Either bilateral sonographic silence or an absent diastolic flow component of the vertebral arteries were employed as criteria in the sonographic evaluation. Angiography of the vertebro-basilar system, performed in 6 cases, confirmed the diagnoses: basilar artery occlusion was found in 4 patients, 1 patient revealed tight stenosis of the basilar artery in its entire length, and 1 patient exhibited occlusion of both distal vertebral arteries. Three further basilar artery occlusions were detected by means of angiography despite initially negative Doppler sonography within the same period of time; 1 of those patients, however, met the above criteria for basilar artery occlusion upon sonographic reevaluation on the following day. Thus, we believe that directional c-w Doppler sonography is very useful in the diagnosis of basilar artery obstruction.

Adult↗
PubMed1989

5-HT1-like receptors mediate 5-hydroxytryptamine-induced contraction of human isolated basilar artery.

1. The 5-hydroxytryptamine (5-HT) receptor mediating contraction of endothelium denuded human basilar artery has been characterized in vitro. 2. 5-HT and a variety of 5-HT agonists contracted human isolated basilar artery with a rank order of agonist potency, 5-carboxamidotryptamine (5-CT) greater than 5-HT identical to methysergide greater than GR43175 much greater than 8-OHDPAT much greater than 2-methyl-5-HT. The maximum response produced by these agonists differed. 3. None of the agonists relaxed human basilar artery when tone was elevated with prostaglandin F2 alpha, indeed further contraction was seen. 4. The contractile responses of human basilar artery to 5-HT and the selective 5-HT1-like agonist GR43175 were highly reproducible whilst those to 5-CT were not. 5. The contractile response to both 5-HT and GR43175 was resistant to antagonism by ketanserin and GR38032, thus excluding activation of 5-HT2 and 5-HT3 receptors. The contractile action of 5-HT and GR43175 was also not antagonized by (+/-)-cyanopindolol, excluding the activation of receptors similar to 5-HT1A and 5-HT1B recognition sites identified in ligand binding studies. 6. In marked contrast, methiothepin was a potent antagonist of the contractile actions of both 5-HT and GR43175, with a pA2 value of 8.8 against both agonists. Methiothepin (100 nM) had no effect on the contractile response to the thromboxane A2-mimetic U46619. 7. We conclude that 5-HT and GR43175 contract the human isolated basilar artery by activating the same receptor type. This receptor appears identical to the 5-HT1-like receptor causing contraction of the dog isolated saphenous vein and cerebral blood vessels from the dog and primate.

Basilar Artery↗
PubMed1998

Constrictor responses of the rat basilar artery during diabetes mellitus.

Diabetes mellitus produces abnormalities of the endothelium and impairs endothelium-dependent dilatation of large and small cerebral blood vessels. However, the effect of diabetes mellitus on cerebral vasoconstriction and the modulatory influence of nitric oxide on cerebral vasoconstriction is unclear. Thus, the first goal of this study was to examine the effect of diabetes mellitus on constrictor responses of the basilar artery in vivo. Our second goal was to examine a potential role for nitric oxide in modulating constrictor responses of the basilar artery. A craniotomy was performed over the ventral medulla to expose the basilar artery. The diameter of the basilar artery was measured using intravital microscopy in nondiabetic and diabetic (3-4 months after injection of streptozotocin; 50-60 mg/kg i.p.) rats in response to angiotensin II, arginine vasopressin, endothelin-1, and the thromboxane analogue, U-46619. Topical application of angiotensin II (10 and 100 nM) produced only minimal changes in diameter of the basilar artery which were similar in nondiabetic and diabetic rats (p>0.05). Arginine vasopressin (0.1 and 1.0 nM), endothelin-1 (10 and 50 nM), and U-46619 (10 and 100 nM) produced marked dose-related constriction of the basilar artery which also was similar in nondiabetic and diabetic rats (p>0.05). Next, we examine whether the synthesis/release of nitric oxide played a role in constriction of the basilar artery in response to the agonists. We found that L-NMMA (1.0 microM) did not alter constrictor responses of the basilar artery in nondiabetic and diabetic rats. Thus, responses of the basilar artery to important vasoactive agonists are not altered by diabetes mellitus. In addition, it does not appear that the synthesis/release of nitric oxide modulates constrictor responses of the basilar artery to angiotensin II, arginine vasopressin, endothelin-1 and U-46619. We suggest that preservation of vasoconstrictor responses, coupled with impaired vasodilator responses, may contribute to the pathogenesis of cerebrovascular abnormalities associated with diabetes mellitus.

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