The hemodynamic effects of internal carotid artery stenosis and occlusion

Mendelow, AD; Graham, David I.; Tuor, Ursula I.; Fitch, W.

doi:10.3171/jns.1987.66.5.0755

Cited by 21 publications

(15 citation statements)

References 29 publications

(3 reference statements)

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“…7,9 -12 An abrupt drop in blood pressure or cardiac output has been postulated as a hemodynamic mechanism that acts as a risk factor for stroke evolution in the area with reduced vasoreactivity. 6,13,14 However, it has not been determined whether a vasodilatory deficit as detected by measurement of CO 2 or acetazolamide can actually lead to a decrease in blood flow when the blood pressure or cardiac output falls in such? patients.…”

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confidence: 99%

Posthyperventilatory Steal Response in Chronic Cerebral Hemodynamic Stress

Nariai

Senda

Ishii

et al. 1998

Stroke

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Background and Purpose-The alteration of regional cerebral blood flow (CBF) during and after hyperventilation was measured using positron emission tomography (PET) to determine the circulatory response induced by daily respiratory changes in the cerebral area under chronic hemodynamic stress. Methods-Three normal volunteers and 12 patients with an obstruction of major cerebral arteries underwent PET measurements of the CBF after an injection of H 2 15 O: (1) in the resting condition, (2) during hyperventilation (HV scan), (3) 1 to 3 minutes after hyperventilation (post-HV scan), (4) during the inhalation of 5% CO 2 , and (5) after an injection of acetazolamide. Eleven patients also underwent a 15 O gas study to measure CBF, oxygen extraction fraction (OEF), and cerebral blood volume (CBV). Results-(1) In 9 patients, the CBF value in the post-HV scan was lower than that in the HV scan in 1 or more regions in the area of the obstructed arteries, although the PaCO 2 level during the post-HV scan was higher than that during the HV scan in all patients. All control regions in the patients and in the normal volunteers showed an elevated CBF in the post-HV scan compared with the HV scan. (2) The negative post-HV response (posthyperventilatory steal) was prominent in 4 patients with moyamoya vessels and in another 5 patients with atherosclerotic disease who had PET evidence of hemodynamic stress (elevated CBV or OEF). (3) The regional pre-to post-HV change in CBF was significantly correlated with the CBF responses to acetazolamide and CO 2 . Conclusions-Vasodilatation after the termination of hyperventilation in the normal areas induces a steal response in the cerebral area suffering from hemodynamic stress and may cause profound hypoperfusion in everyday situations. This phenomenon may be important to our understanding of the clinical symptoms and the natural course of chronic cerebral occlusive disease bearing hemodynamic stress. (Stroke. 1998;29:1281-1292.)

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confidence: 99%

Posthyperventilatory Steal Response in Chronic Cerebral Hemodynamic Stress

Nariai

Senda

Ishii

et al. 1998

Stroke

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“…38 Our principal aim was to determine if hypotension of a degree that is normally well tolerated produces focal cerebral infarction when there is also occlusion of the extracranial arteries. Our study reported previously 13 chosen because previous studies had shown that brain damage occurred only when the cerebral perfusion pressure was decreased rapidly to <25 mm Hg and was sustained at this value for at least 15 minutes. 14 - 37 In group 1 MABP was reduced to 28 mm Hg and CBF to 28.5±5.0 ml/100 g/min, that is, to a level not expected to produce ischemic damage.…”

Section: Discussionmentioning

confidence: 99%

“…Mean arterial blood pressure (MABP) was simultaneously monitored through the opposite femoral artery, and the level of MABP was strictly maintained throughout the 10 minutes of the xenon-133 CBF measurement between predetermined limits ("bins" of 10 mm Hg) depending upon the initial baseline blood pressure after occlusion. 13 Blood gas tensions were measured to ensure normoxia and normocapnia.…”

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Neuropathologic consequences of internal carotid artery occlusion and hemorrhagic hypotension in baboons.

Graham

Mendelow

Tuor

et al. 1990

Stroke

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We studied eight anesthetized and physiologically monitored adult baboons (Papio cyanoctphalus); four were subjected to hemorrhagic hypotension alone and four to hemorrhagic hypotension plus unilateral carotid artery occlusion. Cerebral blood flow was measured using xenon-133, the electroencephalogram was recorded using silver-silver chloride epidural electrodes, and histologic examination was carried out after perfusion-fixation. In the baboons subjected to hypotension alone (mean arterial blood pressure of 28 mm Hg) cerebral blood flow was 28.5±5.0 ml/100 g/min, whereas in the baboons subjected to hypotension plus unilateral carotid artery occlusion it was 21.8±1.8 ml/100 g/min at a mean arterial blood pressure of 27 mm Hg. There was no ischemic damage in the former group, but in the latter group there was necrosis in the arterial boundary zones of three baboons and in the distribution of the middle cerebral artery in one. We conclude that, when combined with hypotension, unilateral carotid artery occlusion may lead to hemodynamic ischemia accentuated in the arterial boundary zones of the ipsilateral cerebral hemisphere. (Stroke 1990^1:428-434) T here is a well-known association between occlusion of the internal carotid artery (ICA) and cerebral infarction.1 -5 One of the patterns of ischemic brain damage seen after ICA occlusion is infarction along the boundary zone between the territories of the anterior cerebral artery (ACA) and middle cerebral artery (MCA).5 -8 This pattern is the consequence of a rapid and considerable reduction in cerebral perfusion pressure. -9When ischemic brain damage occurs along the arterial boundary zones, the critical factor is a reduction in the availability of tissue oxygen, usually because of a local reduction in cerebral blood flow (CBF). Because permanent occlusion of one or more of the large arteries in the neck may be symptomless, 9 the aim of our study was to determine if hypotension of a degree that is normally well tolerated produces focal ischemic damage, particularly in the arterial boundary zones, when combined with occlusion of one ICA. Materials and MethodsEight adult baboons (Papio cyanocephalus) weighing 7-16 kg were divided into two groups. Group 1 From the Wellcome Surgical Institute, University of Glasgow, Glasgow, Scotland.Address for correspondence: Professor D.I. Graham, Department of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Govan Road, Glasgow, G51 4TF Scotland, UK Received April 12, 1989; accepted October 17, 1989. (control baboons, n=4) was subjected to hemorrhagic hypotension alone, and Group 2 (occlusion baboons, n=4) was subjected to hemorrhagic hypotension plus unilateral carotid artery occlusion. The baboons were prepared in a manner identical to that established in our laboratory.10 Briefly, the animals were sedated with 10 mg i.m. phencyclidine hydrochloride, anesthetized with 15 mg/kg thiopental sodium, intubated, and connected to a positive-pressure ventilator supplied with a mixture of 70% N 2 O and 30% ...

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“…They found that classification varied widely: 81% of infarctions were considered territorial when the maximal definition was used, compared to 19% were when the minimal map was used. Second, while global hypotension may result in cortical infarctions bilaterally in the border zone territories between MCA and anterior and posterior cerebral artery territories, particularly in the presence of severe carotid occlusive disease [32, 33], many of the strokes in this location are embolic in nature [34,35,36]. Hennerici et al [15] reviewed the CT scans of a large cohort of 800 stroke patients.…”

Section: Discussionmentioning

confidence: 99%

Patterns of Infarction in Hemodynamic Failure

Derdeyn¹,

Carpenter

Videen

et al. 2007

Cerebrovasc Dis

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Background and Purpose: The mechanism of stroke in patients with atherosclerotic occlusive disease and hemodynamic failure may be primarily hemodynamic or a combination of hemodynamic and embolic factors. The purpose of this study was to investigate the clinical and imaging features of stroke in these patients. Methods: Eleven patients with complete atherosclerotic carotid artery occlusion and increased oxygen extraction fraction measured in the hemisphere distal to the occlusion developed an ischemic stroke during the observation phase of a prospective study of cerebral hemodynamics and stroke risk. The medical and study records related to the endpoint event for these 11 patients were reviewed. Records were reviewed for evidence of associated hypotension and for specific details of the neurological deficit. Infarct location was characterized, based on review of imaging and clinical features, as: (1) middle cerebral artery (MCA) core; (2) possible cortical border zone, or (3) internal border zone. Results: One patient had a retinal infarction; the remaining 10 had MCA territory strokes. Six of the 10 infarctions occurred in the MCA core territory. Two of these 6 were fatal hemispheric events. One of the 10 infarctions occurred in the cortical border zone region. Two of the remaining 3 infarctions were localized to the internal border zone. One was indeterminate. Conclusions: The clinical features and radiological patterns of stroke in many patients with hemodynamic impairment failure and carotid occlusion are most consistent with large artery thromboembolic stroke. These data suggest a synergistic effect between embolic and hemodynamic mechanisms for large artery thromboembolic stroke.

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The hemodynamic effects of internal carotid artery stenosis and occlusion

Cited by 21 publications

References 29 publications

Posthyperventilatory Steal Response in Chronic Cerebral Hemodynamic Stress

Posthyperventilatory Steal Response in Chronic Cerebral Hemodynamic Stress

Neuropathologic consequences of internal carotid artery occlusion and hemorrhagic hypotension in baboons.

Patterns of Infarction in Hemodynamic Failure

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