Effect of carotid artery surgery on cerebral blood flow: Clinical and experimental studies. Bryan Jennett, J. Douglas Miller and A. Murray Harper. 243 × 165 mm. Pp. 172 + viii. Illustrated. 1976. Amsterdam: Excerpta Medica. Dfl. 75. US $29.95

1977 ◽  
Vol 64 (8) ◽  
pp. 608-608
Author(s):  
H. H. G. Eastcott
2004 ◽  
Vol 96 (5) ◽  
pp. 1875-1878 ◽  
Author(s):  
Seham Mustafa ◽  
O. Thulesius ◽  
H. N. Ismael

Clinical and experimental studies indicate that hyperthermia can cause heatstroke with cerebral ischemia and brain damage. However, no study has examined the direct effects of heating carotid artery smooth muscle and tested the hypothesis that hyperthermia induces arterial vasoconstriction and, thereby, decreases cerebral blood flow. We recorded isometric tension of rabbit carotid artery strips in organ baths during stepwise temperature elevation. The heating responses were tested at basal tone, in norepinephrine- and KCl-precontracted vessels, and after electrical field stimulation. Stepwise heating from 37°C to 47°C induced reproducible graded contraction proportional to temperature. The responses could be elicited at basal tone and in precontracted vessels. Heating decreased the contractile responses to norepinephrine and electrical field stimulation but increased contraction to KCl. These responses were not eliminated by pretreatment with the neuronal blocker tetrodotoxin. Our results demonstrate that heating carotid artery preparations above 37°C (normothermia) induced a reversible graded vasoconstriction proportional to temperature. In vivo this reaction may lead to a decrease in cerebral blood flow and cerebral ischemia with brain damage as in heatstroke. The heating-induced contraction is not mediated by a neurogenic process but is due to altered transcellular Ca2+ transport. Cooling, in particular of the neck area, therefore, should be used in the treatment of heatstroke.


1995 ◽  
Vol 3 (2) ◽  
pp. 84-86
Author(s):  
Praveen Kumar Neema ◽  
Kurur Sankaran Neelakandhan ◽  
Kottilil Mohandas ◽  
Hemant Digambar Waikar ◽  
Ganapati Potti

Use of intraluminal shunts is an established method for augmenting cerebral blood flow during carotid artery surgery. However, many undesirable complications such as embolization of atheromatous plaque and scuffing of the intima have been described after their use. We describe a simplified shunt, which provides sufficient cerebral blood flow and is devoid of the various known complications.


2015 ◽  
Vol 129 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Nia C.S. Lewis ◽  
Kurt J. Smith ◽  
Anthony R. Bain ◽  
Kevin W. Wildfong ◽  
Tianne Numan ◽  
...  

Diameter reductions in the internal carotid artery (ICA) and vertebral artery (VA) contribute to the decline in brain blood with hypotension. The decline in vertebral blood flow with hypotension was greater when carbon dioxide was low; this was not apparent in the ICA.


Neurosurgery ◽  
2002 ◽  
Vol 50 (5) ◽  
pp. 996-1005 ◽  
Author(s):  
Randolph S. Marshall ◽  
Ronald M. Lazar ◽  
William L. Young ◽  
Robert A. Solomon ◽  
Shailendra Joshi ◽  
...  

Neurosurgery ◽  
2001 ◽  
Vol 48 (2) ◽  
pp. 436-440 ◽  
Author(s):  
Colin P. Derdeyn ◽  
DeWitte T. Cross ◽  
Christopher J. Moran ◽  
Ralph G. Dacey

Abstract OBJECTIVE AND IMPORTANCE The presence of reduced blood flow and increased oxygen extraction fraction (OEF) (misery perfusion) in the hemisphere distal to an occluded carotid artery is a proven risk factor for subsequent stroke. Whether angioplasty of intracranial stenosis is sufficient to reverse this condition has not been documented. CLINICAL PRESENTATION A 67-year-old man exhibited progressive right hemispheric ischemic symptoms despite maximal antiplatelet and antithrombotic therapy. Angiography demonstrated focal 80% stenosis of the supraclinoid segment of the ipsilateral internal carotid artery. TECHNIQUE 15O positron emission tomographic measurements of cerebral blood flow and OEF were made before and after transfemoral percutaneous angioplasty. OEF values measured before angioplasty were elevated in the middle cerebral artery distal to the stenosis. Angioplasty reduced the degree of luminal stenosis to 40% (linear diameter). OEF values measured 36 hours after angioplasty were normal. CONCLUSION Angioplasty of intracranial stenosis can restore normal cerebral blood flow and oxygen extraction, despite mild residual stenosis after the procedure. Hemodynamic measurements may be useful for the identification of patients with the greatest potential to benefit from angioplasty.


1965 ◽  
Vol 68 (11) ◽  
pp. 1466-1471
Author(s):  
KENJIRO YANAGINO ◽  
NOBUO TAKASUGA ◽  
SANETOMI EGUCHI ◽  
TAKASHI FUKUSA

2014 ◽  
Vol 65 (4) ◽  
pp. 352-359 ◽  
Author(s):  
Santanu Chakraborty ◽  
Reem A. Adas

Purpose Neurologic determination of death or brain death is primarily a clinical diagnosis. This must respect all guarantees required by law and should be determined early to avoid unnecessary treatment and allow organ harvesting for transplantation. Ancillary testing is used in situations in which clinical assessment is impossible or confounded by other factors. Our purpose is to determine the utility of dynamic computed tomographic angiography (dCTA) as an ancillary test for diagnosis of brain death. Materials and Methods We retrospectively reviewed 13 consecutive patients with suspected brain death in the intensive care unit who had dCTA. Contrast appearance timings recorded from the dCTA data were compared to findings from 15 controls selected from patients who presented with symptoms of acute stroke but showed no stroke in follow-up imaging. Results The dCTA allows us to reliably assess cerebral blood flow and to record time of individual cerebral vessels opacification. It also helps us to assess the intracranial flow qualitatively against the flow in extracranial vessels as a reference. We compared the time difference between enhancement of the external and internal carotid arteries and branches. In all patients who were brain dead, internal carotid artery enhancement was delayed, which occurred after external carotid artery branches were opacified. Conclusion In patients with suspected brain death, dCTA reliably demonstrated the lack of cerebral blood flow, with extracranial circulation as an internal reference. Our initial results suggest that inversion of time of contrast appearance between internal carotid artery and external carotid artery branches at the skull base could predict a lack of distal intracranial flow.


2020 ◽  
Author(s):  
Joseph P Archie

AbstractIntroductionIn patients with 70% to 99% diameter carotid artery stenosis cerebral blood flow reserve may be protective of future ischemic cerebral events. Reserve cerebral blood flow is created by brain auto-regulation. Both cerebral blood flow reserve and cerebrovascular reactivity can be measured non-invasively. However, the factors and variables that determine the availability and magnitude and of reserve blood flow remain poorly understood. The availability of reserve cerebral blood flow is a predictor of stroke risk. The aim of this study is to employ a hemodynamic model to predict the variables and functional relationships that determine cerebral blood flow reserve in patients with significant carotid stenosis.MethodsA basic one-dimensional, three-unit (carotid, collateral and brain) energy conservation fluid mechanics blood flow model is employed. It has two distinct but adjacent blood flow components with normal cerebral blood flow at the interface. In the brain auto-regulated blood flow component cerebral blood flow is maintained normal by reserve flow. In the brain pressure dependent blood flow component cerebral blood flow is below normal because cerebral perfusion pressure is below the lower threshold value for auto-regulation. Patient specific values of collateral vascular resistance are determined from a model solution using clinically measured systemic and carotid arterial stump pressures. Collateral vascular resistance curves illustrate the model solutions for reserve and actual cerebral blood flow as a function of percent diameter carotid artery stenosis and mean systemic arterial pressure. The threshold cerebral perfusion pressure value for auto-regulation is assumed to be 50 mmHg. Normal auto-regulated regional cerebral blood flow is assumed to be 50 ml/min/100g. Cerebral blood flow and reserve blood flow solutions are given for systemic arterial pressures of 80, 90, 100, 110 and 120 mmHg and for three patient specific collateral vascular resistance values, Rw = 1.0 (mean patient value), Rw = 0.5 (lower 1 SD) and Rd = 3.0 (upper 1 SD).ResultsReserve cerebral blood flow is only available when a patients cerebral perfusion pressure is in the normal auto-regulatory range. Both actual and reserve cerebral blood flows are primarily from the carotid circulation when carotid stenosis is less than 60% diameter. Between 60% and 75% stenosis the remaining carotid blood flow reserve is utilized and at higher degrees of stenosis all reserve flow is from the collateral circulation. The primary independent variables that determine actual and reserve cerebral blood flow are mean systemic arterial pressure, degree of carotid stenosis and patient specific collateral vascular resistance. Approximate 16% of patients have collateral vascular resistance greater than 5.0 and are predicted to be at high risk of cerebral ischemia or infarction with progression to severe carotid stenosis or occlusion. The approximate 50% of patients with a collateral vascular resistance less than 1.0 are predicted to have adequate cerebral blood flow with progression to carotid occlusion, and most maintain some reserve. Clinically measured values of cerebral blood flow reserve or cerebrovascular reactivity are predicted to be unreliable without consideration of systemic arterial pressure and degree of carotid stenosis. Reserve cerebral blood flow values measured in patients with only moderate 60% to 70% carotid stenosis are in general too high and variable to be of clinical value, but are most reliable when measured near 80% diameter stenosis and considered as percent of the maximum reserve blood flow. Patient specific measured reserve blood flow values can be inserted into the model to calculate the collateral vascular resistance.ConclusionsPredicting cerebral blood flow reserve in patients with significant carotid stenosis is complex and multifactorial. A simple cerebrovascular model predicts that patient specific collateral vascular resistance is an excellent predictor of reserve cerebral blood flow in patients with significant carotid stenosis. Cerebral blood flow reserve measurements are of limited value without accounting for systemic pressure and actual percent carotid stenosis. Asymptomatic patients with severe carotid artery stenosis and a collateral vascular resistance greater than 1.0 are at increased risk of cerebral ischemia and may benefit from carotid endarterectomy.


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