[Penetrating needling on head points for vertigo caused by vertebral-basilar arterial blood-supply insufficiency].

OBJECTIVE: To observe the differences in therapeutic effect between penetrating needling on head points and acupuncture of syndrome division in the treatment of vertigo caused by vertebral-basilar arterial blood-supply insufficiency. METHODS: Sixty cases of vertigo caused by vertebral-basilar arterial blood-supply insufficiency were divided into 2 groups: a penetrating needling on head points group (group A) and an acupuncture of syndrome division group (group B), 30 cases in each one. In group A, penetrating needling technique was applied from Baihui (GV 20) towards Qianding (GV 21), Shuaigu (GB 8) towards Qubin (GB 7) and Yuzhen (BL 9) towards Tianzhu (BL 10). Electric stimulation was added. In group B, the acupoints were selected according to syndromes. For example, upper disturbance of wind yang: Ganshu (BL 18), Xingjian (LR 2),etc. were selected; upper disturbance of turbid phlegm: Yinlingquan (SP 9), Fenglong (ST 40), etc. were selected; qi and blood deficiency: Baihui (GV 20), Xuehai (SP 10), etc. were selected; liver and kidney yin deficiency: Ganshu (BL 18), Shenshu (BL 23), etc. were selected. Electric stimulation and needling manipulation were conducted on those acupoints. Ten treatments made one session. After continuous 2 sessions of treatment, the efficacy, symptom score and physical sign score were compared between two groups. Transcranial Doppler (TCD) examination was done to observe hemodynamic changes of anterior cerebral artery (ACA), middle cerebral artery (MCA) and posterior cerebral artery (PCA) before and after treatment. RESULTS: The total effective rate in group A was 96.7% (29/30) that was obviously better than 83.3% (25/30) in group B (P<0.05). The scores of vertigo degree, vertigo frequency, duration and accompanied symptoms after treatment were lower obviously as compared with those before treatment in two groups (all P<0.05). The improvements in group A were much significant (all P<0.05). The highest mean velocity(Vm) of bilateral MCA, ACA and PCA were apparently reduced after treatment in two groups (P< 0.05, P<0.01). The improvements in group A were much more apparently (all P<0.05). CONCLUSION: The penetrating needling on head points can effectively relieve vertigo caused by vertebral-basilar arterial blood-supply insufficiency, reduce the attack frequency and improve in its accompanied symptoms. Its clinical efficacy is significantly superior to that in acupuncture of syndrome division group.

Post stroke depression: treatments and complications in a young adult.

Post-stroke depression has been noted to be one of the most frequent complications of stroke with an estimated prevalence of as high as 80%. However, the incidence of stroke in the young is extremely low and evidence based therapy for this complication is quite limited. The case of a 28-year-old woman who experienced a basilar artery vasospasmic stroke resulting in anoxic brain injury to the midbrain and paramedian thalamus is presented, along with a literature review of psychiatric complications of this injury to include post-stroke depression (PSD). Therapeutic modalities such as TCAs, SSRIs, atypical antipsychotics and stimulant medications are also reviewed as these medications may aid in the treatment of such patients but may also contribute to psychiatric sequelae.

[Evaluation of the efficacy of therapeutic physical training in patients with osteochondrosis according to rheoencephalography data].

This paper reports results of clinical and rheoencephalographic examination of 40 middle-age women with cervical osteochondrosis and symptoms of insufficiency of vertebrobasiliar blood circulation. A system of methods for therapeutic physical training has beendeveloped to normalize hemodynamics in the basin of vertebral arteries. The system was tested on 20 patients during a year. It included special physical exercises, massage, and automobilization. The efficiency of therapeutic physical training was evaluated by rheoencephalography. The women involved in the testing reported a marked improvement of the health status. Their rheoencephalograms suggested diminishing of the asymmetry coefficient and beneficial effect of therapeutic physical training on the elastic properties of vertebral arteries. No such changes were documented in a control group of women with osteochondrosis.

Experimental model of brainstem stroke in rabbits via endovascular occlusion of the basilar artery.

BACKGROUND: Basilar artery thrombosis remains a significant clinical problem, and no reproducible animal model has been established to study the stroke within the vertebrobasilar distribution. We report a study designed to pilot test a novel model of brainstem stroke in rabbits, created by selective endovascular occlusion of the basilar artery. METHODS: Basilar artery occlusion was induced in 8 New Zealand white rabbits by injection of the autologous clot through the microcatheter positioned within the distal vertebral artery. Animals were divided into subgroups (I and II) based on the length of produced ischemia (3 and 6 hours, respectively). Magnetic resonance (MR) imaging of the brain and MR angiography of the intracranial vessels were performed before the procedure, and at 3 hours after induced ischemia for groups I and II, with continued imaging up to 6 hours for group II, with diffusion-weighted images acquired approximately every 30 minutes. Animals were killed at the end of the 3-hour (group I) or 6-hour (group II) ischemia time. RESULTS: Brainstem stroke was successfully induced in all animals, with pathological changes documented in all cases. The earliest changes of ischemia on MR diffusion-weighted images were identified at only 4.5 hours of basilar artery occlusion. CONCLUSION: These results suggest that a reproducible model of brainstem stroke can be induced in rabbits using selective endovascular occlusion of the basilar artery. The availability of such a model, integrated with state-of-the-art imaging techniques, holds promise for preclinical investigations of emergent therapeutic approaches in stroke.

Forty-six cases of vertebrobasilar insufficiency treated by acupuncture plus intravenous infusion of ligustrazine.

OBJECTIVE: To observe the therapeutic effect of acupuncture plus Ligustrazine on vertebrobasilar insufficiency (VBI) by transcranial Doppler (TCD) sonography. METHODS: 86 VBI patients including 56 cases of low flow rate velocity type (LFVT) and 30 cases of high flow velocity type (HFVT) were randomly divided into Ligustrazine group (26 LFRT and 14 HFVT) and acupuncture plus Ligustrazine group (30 LFVT and 16 HFVT). The blood flow velocity (BFV) of vertebral artery (VA) and basilar artery (BA) in systole before and after treatment was measured with TCD and therapeutic effects were evaluated after 10 days' treatment in the two groups. RESULTS: In the acupuncture plus Ligustrazine group, the total effective rate was 93.3% and 88.5% in cases of LFVT and HFVT respectively, and BFV of VA and BA increased in LFVT patients while that in HFVT patients decreased significantly (P<0.05 or P<0.01). CONCLUSION: Owing to its dual regulation on blood flow of VA and BA, the therapeutic effect of acupuncture plus Ligustrazine was better than that of simple Ligustrazine.

Recovery in a patient with locked-in syndrome.

BACKGROUND AND PURPOSE: Sildenafil citrate has been shown to enhance neurogenesis, angiogenesis, synaptogenesis, and neurological outcome by augmentation of cyclic guanosine monophosphate (cGMP) levels in animal models of ischemic stroke. Whether sildenafil citrate may be helpful for recovery in human stroke is unknown at this time. METHODS: A 41-year-old woman with locked-in syndrome due to pontine infarction began receiving 150 mg of oral sildenafil citrate daily on a compassionate use basis in August 2003 and continues treatment at this time. Magneto-encephalography (MEG) was performed at 12 and 17 months after stroke. RESULTS: No serious adverse events have occurred. Significant milestone recoveries including standing, use of both arms, talking, and full return of swallowing have occurred, particularly after nine months of treatment. The MEG showed a significantly increased amplitude in the somatosensory cortex. CONCLUSION: Daily use of high dose sildenafil citrate appears to be safe in this patient with stroke resulting in locked-in syndrome. Further studies will be required to establish safety and efficacy.

[Effect of vertebral manipulation therapy on vertebro-basilar artery blood flow in cervical spondylosis of vertebral artery type].

OBJECTIVE: To observe the effect of vertebral manipulation (VM) therapy on vertebro-basilar artery (VBA) blood flow in patients with cervical spondylosis of vertebral artery type (CS-VAT) by transcranial Doppler (TCD) ultrasonic examination. METHODS: One hundred and fifty patients with CS-VAT were randomized into the VM group (n = 100) and the acupuncture group (n = 50), and treated for ten times as one therapeutic course. Changes of the contraction peak, the end-diastolic and average blood flow velocity of VBA before and after treatment in the two groups were observed and compared by TCD. RESULTS: Vp, Vd, Vm of LVA, RVA and BA in the two groups after treatment were all lowered, showing significant difference, excepting Vp of VBA in the acupuncture group, when compared with before treatment (P< 0.05 or P <0.01). Comparison between the two groups after treatment showed significant difference in Vp and Vm of LVA, Vp, Vd and Vm of RVA, Vp and Vm of VBA respectively (P<0.05, P <0.01). CONCLUSION: VM therapy in treating patients with CS-VAT shows therapeutic effect superior to VA therapy, which could significantly improve VBA blood flow.

Diffusion-weighted magnetic resonance imaging in symptomatic vertebrobasilar atherosclerosis and dissection.

BACKGROUND: Acute multiple brain infarction (AMBI) pattern on diffusion-weighted imaging (DWI) is associated with arterial and cardiac sources of embolism. The DWI characteristics of patients with stroke due to vertebrobasilar arterial dissection and atherosclerotic disease have not been reported in detail. OBJECTIVE: To describe the DWI stroke patterns in patients with posterior circulation occlusive disease to determine mechanisms of ischemia. DESIGN: Retrospective analysis of infarct patterns in patients with symptomatic vertebrobasilar disease. SETTING: Large community-based teaching hospital. PATIENTS: Patients admitted with stroke due to vertebrobasilar disease were identified retrospectively. Patients were included if DWI was obtained within 7 days of symptom onset. MAIN OUTCOME MEASURE: Infarct patterns were analyzed according to established templates of vascular territories. RESULTS: Eleven patients with vertebral dissection and 39 patients with atherothrombosis were identified. An AMBI pattern was present in 8 (72%) of 11 patients with arterial dissections and 25 (64%) of 39 patients with atherosclerotic disease (P = .48). Distal embolism to the terminal branches of the basilar artery occurred with equal frequency in both groups and was found in half of all cases. Isolated thalamic infarction did not occur. Pontine infarction was noted in 2 (18%) of 11 patients with dissections and 18 (46%) of 39 patients with atherosclerosis (P = .09). Cerebellar border zone involvement was found in 14 (36%) of 39 patients with atherosclerosis and 4 (37%) of 11 patients with dissections (P = .6). CONCLUSIONS: Large arterial disease is frequently associated with AMBI in the posterior circulation. The incidence of AMBI was comparable to that reported in the anterior circulation. This DWI study supports the importance of embolism as the main mechanism of infarction in patients with vertebrobasilar occlusive disease. On the basis of our experience, large-vessel vertebrobasilar disease rarely causes isolated small-vessel thalamic infarction.

Doppler ultrasonography of the vertebrobasilar circulation in patients with sudden sensorineural hearing loss.

BACKGROUND: The etiology of sudden sensorineural hearing loss (SSNHL) is still unclear and is most probably diverse. OBJECTIVE: To determine the relationship between vertebrobasilar circulation and hearing in patients with SSNHL treated with pentoxifylline. DESIGN: Case-control study of 32 consecutive patients with SSNHL. METHODS: Patients with onset of SSNHL within 72 hours were treated with pentoxifylline infusions for 10 days. Transcranial Doppler (TCD) ultrasonography of vertebrobasilar circulation and hearing levels were examined at the onset of SSNHL (before treatment), after 10 days of therapy, and after 3 months. MAIN OUTCOME MEASURES: Hearing levels and TCD ultrasonographic findings at the onset of SSNHL, after 10 days, and after 3 months. RESULTS: Patients with SSNHL had more frequent pathologic TCD ultrasonographic findings compared with a normal population. Thirteen patients with SSNHL had normal TCD ultrasonographic findings, eight had borderline findings, and six had pathologic findings, and in five patients, initially, pathologic TCD ultrasonographic findings improved during therapy. Patients with normal TCD ultrasonographic findings had an average hearing improvement of 17 dB, whereas patients with borderline and pathologic TCD ultrasonographic findings had 3 and 0 dB of average hearing improvement, respectively. The greatest improvement (28 dB) was noticed in patients who showed improvement in TCD ultrasonographic findings. CONCLUSION: Although the number of patients is small, our results led to the conclusion that SSNHL has vascular etiology, at least in some patients. Consequently, the therapy for SSNHL should depend on etiology; that is, vasoactive medications should be reserved for patients with supposed vascular etiology. TCD ultrasonography could have a role in the decision regarding the optimal treatment of SSNHL.

The influence of noradrenergic blockade on vasospasm and the quantity of cerebral dopamine beta-hydroxylase following subarachnoid haemorrhage in rabbits.

BACKGROUND: The aim of this study of experimental subarachnoid haemorrhage (SAH) and exclusion of the sympathetic nervous system (SNS) in rabbits was to find out if changes in the central noradrenergic areas of the hypothalamus and brain stem could be ascertained, in parallel with measurement of the intensity of chronic cerebral vasospasm in the basilar arteries. METHODS: Histologic specimens were prepared by perfusion fixation on day 8 after the SAH. The spastic effect of experimentally induced SAH in New Zealand rabbits was investigated: firstly, using our previously developed method for measuring the corrugation coefficient (CC) of the vessel intima on precisely defined locations of the basilar artery (BA) with the aid of computer image analysis; and secondly, by immunohistochemical assessment of the concentration and localization of dopamine beta-hydroxylase (DBH), using anti-DBH, at precisely defined sites of the hypothalamus and brain stem of the same rabbit. RESULTS: The intima of the BA, assessed by CC, was significantly less corrugated and had significantly less DBH in group A (the control group without SAH and without additional interventions; mean CC = 1.192, P = 0.004; median DBH = 0.50, P = 0.044), in group C (SAH and alpha-blocker phenoxybenzamine; mean CC = 1.142, P = 0.000; median DBH = 0.75, P = 0.001), and in group D (SAH and cervical gangliectomy; mean CC = 1.210, P = 0.003; median DBH = 0.50, P = 0.002) compared with group B (rabbits with SAH and without medication). Group B showed a significantly more intensive accumulation of DBH (median DBH = 1.15) and, according to the CC (mean CC = 1.369), more intensive corrugation of the intima of BA than all other groups. The correlation between CC and DBH for all the rabbits (groups A, B, C and D together) was significantly positive (Spearman Rho = 0.470; p = 0.010). CONCLUSIONS: The results of this study demonstrated: firstly, an intensive excitatory influence of SAH on the quantity of DBH in central noradrenergic areas in the hypothalamus and brain stem; secondly, a very effective influence of peripheral and systemic sympathetic exclusion on lowering the quantity of central sympathetic DBH; thirdly, that the changes in the BA of individual rabbits occur simultaneously with corresponding changes in DBH-containing neurons, thus suggesting the likelihood of SNS involvement in the pathogenesis of post-SAH vasospasm in rabbits.

Prevention of experimental cerebral vasospasm by intracranial delivery of a nitric oxide donor from a controlled-release polymer: toxicity and efficacy studies in rabbits and rats.

BACKGROUND AND PURPOSE: A reduction in the local availability of nitric oxide (NO) may play a role in the etiology of chronic cerebral vasospasm after subarachnoid hemorrhage (SAH). We investigated the toxicity and efficacy of a locally delivered NO donor from a controlled-release polymer in preventing experimental cerebral vasospasm in rats and rabbits, respectively. METHODS: Diethylenetriamine/NO (DETA/NO) was incorporated into controlled release ethylene-vinyl acetate (EVAc) polymers. Twenty-eight rats were used in a dose-escalation toxicity study to establish a maximally tolerated dose of DETA/NO-EVAc polymer. In the efficacy experiment, 20 rabbits were assigned to 4 experimental groups (n=5 per group): sham operation; SAH only; SAH+empty EVAc polymer; and SAH+DETA/NO-EVAc polymer. Treatment was initiated 30 minutes after blood deposition. Basilar artery lumen patency was assessed 72 hours after hemorrhage to evaluate the efficacy of DETA/NO in preventing cerebral vasospasm. RESULTS: In the toxicity study, a dose of 3.4 mg/kg was identified as the LD(20) (dose with 20% mortality during the study period) of this DETA/NO formulation. Brain histology revealed hemorrhage and ischemic changes at the implantation site associated with high concentrations of DETA/NO. In the efficacy study, treatment with DETA/NO-EVAc polymer resulted in a significant decrease in basilar artery vasospasm compared with no treatment (93.0+/-4.9% versus 71.4+/-11.9%; P=0.035) or compared with treatment with blank EVAc polymer (93.0+/-4.9% versus 73.2+/-6.4%; P=0.003). CONCLUSIONS: Local delivery of DETA/NO prevents vasospasm in the rabbit basilar artery. Local delivery of DETA/NO via polymers is a safe and effective strategy for preventing cerebral vasospasm after SAH in this model.

High-dose methylprednisolone prevents vasospasm after subarachnoid hemorrhage through inhibition of protein kinase C activation.

We have previously shown that the inflammatory process after subarachnoid hemorrhage causes vasospasm. The efficacy of methylprednisolone by suppression of the inflammatory process has been reported, although pharmacological mechanisms have not been clarified. The purpose of this study was to investigate the pharmacological mechanism of methylprednisolone on vasospasm. Using the 'two-hemorrhage' canine model, progression of angiographic vasospasm was assessed in nontreated and treated groups with methylprednisolone. Methylprednisolone 10 mg kg-1 was injected i.v. after the first injection of blood, and the same dose was injected every 12 h until day 7. Protein kinase C (PKC) activity of canine basilar arteries in both groups was measured during the course of vasospasm. In the isometric tension study, the effect of methylprednisolone on tensions induced by phorbol 12-myristate 13-acetate (PMA), or high-K+ solution, was also evaluated. Methylprednisolone significantly reduced severity of vasospasm. In the treated group, PKC activity was not enhanced compared with the nontreated group at any point. Methylprednisolone inhibited tonic tension induced by PMA, but not that induced by high-K+ solution. We conclude that methylprednisolone prevents severity of vasospasm through inhibition of PKC activation, but does not work as a Ca2+ channel blocker.

Effect of EGb-761 on vasospasm in experimental subarachnoid hemorrhage.

Based on the previously suggested hypothesis that the generation of free radicals leading to lipid peroxidation is involved in the genesis of vasospasm and vasculopathy following subarachnoid hemorrhage, the therapeutic effect of EGb 761 as an antioxidant on experimental vasospasm and vasculopathy was evaluated in a double hemorrhage dog model of chronic cerebral vasospasm. For this study 14 dogs were randomly assigned to two groups, a control and a Ginkgo biloba group. The control group was only administered saline in a volume equivalent to a dose of 100 mgEGb 761/kg while the treatment group was given 100 mg EGb 761/kg. The diameter of the basilar artery decreased from 1.95 +/- 0.16 mm at day 0 to 1.11 +/- 0.07 mm at day 8 in the control group, while in the treatment group the vessel diameter decreased from 2.01 +/- 0.17 mm at day 0 to 1.72 +/- 0.16 mm at day 8. These results correspond a decrease in vessel diameter of 15.1% in the treatment group and of 43.1% in the control group (P < 0.05). Histopathological studies of the specimens obtained from basilar arteries showed that pathological signs of proliferative vasculopathy, including narrowing of the vessel lumen, corrugation of the lamina elastica and subendothelial thickening, were present in all the animals in the control group, while they could not be demonstrated in the Ginkgo biloba group. These results suggest that Ginkgo biloba may have a protective effect against subarachnoid hemorrhage-induced vasospasm and vasculopathy as a result of antioxidants.

The role of transcranial Doppler sonography in the identification of patients at risk of cerebral and brainstem ischemia.

OBJECTIVE: To review the literature pertaining to transcranial Doppler (TCD) examination of the anterior and posterior cerebral circulation. This paper focuses on the application of TCD as a screening modality for vertebral artery-induced brainstem ischemic events. DATA SOURCES: A Medline literature search was performed. Key terms included; transcranial Doppler, vertebral artery dissection, neck trauma, stroke and vertebrobasilar system. DATA EXTRACTION: The studies examined TCD techniques that monitor the hemodynamics of the circle of Willis. Papers pertaining to vertebral artery trauma and resulting brainstem injury were included. The validity and reproducibility of these procedures were also reviewed. CONCLUSION: TCD procedures provide hemodynamic data pertaining to intra-arterial vertebrobasilar stenosis and extra-arterial mechanical compression of the vertebral arteries. During cervical spine positional testing, brainstem symptoms may be correlated with TCD documented perfusion deficits. TCD increases the sensitivity of the standard positional test.

[Paramedian thalamo-mesencephalic infarct con triphasic waves]. / Infarto talamomesencefálico paramediano con ondas trifásicas.

Triphasic waves are usually associated with metabolic encephalopathies but have been reported in patients with other etiologies. The pathophysiology of this EEG pattern remains poorly understood, although they have been attributed to lesion in the connections between the thalamus and cortex. We report a case of top-of-the-basilar artery occlusion with selective paramedian thalamic-mesencephalic infarct in which triphasic waves were evident on the EEG during clinical hypersomnia. To our knowledge this is the first reported case of triphasic waves with selective paramedian thalamomesencephalic infarct. We conclude that triphasic waves are a nonspecific manifestation of diencephalic dysfunction, probably of the paramedian thalamomesencephalic reticular system.

[Syndromes involving rostral occlusion of the basilar artery: a preliminary study and proposal for a new clinical and neuro- radiological classification]. / Síndromes por oclusión rostral de la arteria basilar: estudio preliminar y propuesta de una nueva clasificación cliniconeurorradiológica.

Occlusion of the top of the basilar artery causes infarctions in supra- and infra-tentorial regions (thalamus, occipito-temporal lobes, rostral trunk and cerebellum) with characteristic clinical and radiological manifestations. We studied 17 patients with this syndrome whose clinical data and neurological images led us to classify them into four groups: type I (2 patients, 12%), showing mainly alterations in consciousness and ocular motricity, and bilateral thalamic infarction; type II (6 patients, 35%), with campimetric manifestations and uni- or bilateral ischemia of the occipito-temporal lobes; type III (5 patients, 29%), with associated corticospinal deficits and lacunar images in the rostral brainstem; and type IV (4 patients, 24%) with symptoms of and neuro-images revealing lesions in the cerebellum. The proposed classification is an attempt to facilitate diagnosis by neuro-imaging and to group patients according to prognosis.

Hyperventilation-induced cerebral ischemia in panic disorder and effect of nimodipine.

Basilar artery blood flow was measured by transcranial Doppler ultrasonography before and during hyperventilation in nine patients with panic disorder and nine normal comparison subjects. The hyperventilation-induced decrease in basilar artery blood flow was significantly greater in patients with panic attacks than in comparison subjects. Two patients with decreases in basilar flow greater than 80% were successfully treated with nimodipine, a centrally active calcium channel blocker.

Effect of nicardipine on basilar artery vasoactive responses after subarachnoid hemorrhage.

The effect of the dihydropyridine calcium antagonist, nicardipine, on the vasoactive responses of the basilar artery was investigated after subarachnoid hemorrhage (SAH). Forty-five rabbits were separated into one control group and four groups receiving SAH (nine animals each). The SAH was induced by injecting 5 ml of autologous arterial blood into the cisterna magna. SAH animals were subjected to one of the following: 1) no treatment; 2) intravenous (i.v.) saline infusion (vehicle); 3) i.v. infusion of low-dose nicardipine (0.01 mg/kg/hr), or 4) i.v. infusion of high-dose nicardipine (0.15 mg/kg/hr). The i.v. infusions were started immediately after SAH and continued for 48 hours. Serotonin (5-HT) (10(-8) to 10(-5) mol/L) was used to evoke dose-dependent vasoconstriction of isolated rings of the basilar artery 2 days after SAH. Acetylcholine (ACh) (10(-8) to 10(-4)) and adenosine-triphosphate (ATP) (10(-8) to 10(-4) mol/L) were applied after maximal contraction with 5-HT, evoke a dose-dependent vasodilatation. Compared with controls, in animals subjected to SAH serotonin caused similar or slightly larger contractions; nicardipine infusion did not decrease the amount of contraction observed after SAH. ACh and ATP caused significantly less dilatation in animals submitted to SAH than in controls. After high-dose nicardipine, ACh- and ATP-induced dilatations were significantly more pronounced (57% and 68% of initial contractile tone) than in the other animals receiving SAH (36%-39% and 45%-55%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of vascular supersensitivity in hypercholesterolemia.

We have characterized in vitro, for the first time, the phenomenon of acute interaction between hypercholesterolemia and cerebrovascular function. We then used this model to investigate a number of mechanisms for the interaction. Rabbits fed a diet supplemented with 2% cholesterol developed hypercholesterolemia over 4 weeks with no histologically detectable atherosclerosis. This absence of anatomic change was reflected in normal biophysical elastic responses to graded radial stretch and normal optimum tension for responses to exogenous K+ in the selected arteries. However, basilar arteries removed from cholesterol-fed rabbits showed abolished myogenic responses to radial stretch and decreased median effective doses for added norepinephrine. These potentiated constrictor responses to norepinephrine were significantly correlated with increased plasma cholesterol concentration. A mechanism related to the opening of membrane calcium channels may be responsible for the supersensitivity.