Hyperthermia-induced vasoconstriction of the carotid artery, a possible causative factor of heatstroke

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.

2015 ◽  
Vol 35 (6) ◽  
pp. 883-887 ◽  
Author(s):  
Francisco Fernandez-Klett ◽  
Josef Priller

Pericytes are mural cells with contractile properties. Here, we provide evidence that microvascular pericytes modulate cerebral blood flow in response to neuronal activity (‘functional hyperemia’). Besides their role in neurovascular coupling, pericytes are responsive to brain damage. Cerebral ischemia is associated with constrictions and death of capillary pericytes, followed by fibrotic reorganization of the ischemic tissue. The data suggest that precapillary arterioles and capillaries are major sites of hemodynamic regulation in the brain.


2021 ◽  
Author(s):  
Joseph P Archie

AbstractIntroductionCarotid artery stenosis related stroke is a major health care concern. Current risk management strategies for patients with asymptomatic carotid stenosis include ultrasound surveillance and occasionally an estimate of cerebral blood flow reserve. Other patient specific hemodynamic variables may be predictive of ischemic stroke risk. This study, based on a cerebral blood flow hemodynamic model, aims to investigate the impact of systemic arterial pressure, collateral vascular resistance and degree of carotid stenosis on cerebral ischemic risk, cerebrovascular blood flow reserve, critical carotid artery stenosis, carotid artery blood flow and carotid stenosis hemodynamics.MethodsThis study uses a three-component (carotid, collateral, brain) energy conservation cerebrovascular fluid mechanics model in combination with the Lassen cerebral blood flow autoregulation model that predicts cerebral blood flow in patients with carotid stenosis. It is a two-phase model, zone A when regional cerebral blood flow is autoregulated at normal values and zone B when cerebral blood flow is below normal and dependent on collateral perfusion pressure. The model solution with carotid artery occlusion defines collateral vascular resistance, with patient specific values calculated from clinical pressure measurements. In addition to cerebral blood flow the model predicts critical stenosis values and carotid and collateral blood flows as a function of systemic arterial pressure and percent diameter stenosis. Carotid stenosis blood flow velocities and energy dissipation are predicted from carotid blood flow solutions.ResultsThe model defines patient specific collateral vascular resistance, cerebral vascular resistance and critical carotid stenosis. It predicts carotid vascular resistance to be non-linearly proportional to area carotid stenosis. Solutions include reserve cerebral blood flow, the carotid and collateral components of cerebral blood flow, criteria for cerebral ischemia and carotid stenosis hemodynamics. Critical carotid stenosis is determined by mean systemic arterial pressure and the Lassen autoregulation threshold cerebral perfusion pressure. Critical stenosis values range from 61% to 76% diameter stenosis when mean systemic arterial pressures are 80mmHg to 120mmHg and the cerebral autoregulation pressure threshold is 50mmHg. When carotid stenosis is less than critical, cerebral blood flow is maintained normal and the ratios of carotid blood flow to collateral blood flow are inversely proportional to the carotid to collateral vascular resistance ratios. At stenosis greater than the critical, carotid blood flow is not adequate to maintain normal cerebral blood flow, cerebral blood flow is primarily collateral flow, all reserve blood flow is collateral and prevention of cerebral ischemia requires adequate collateral flow. Patient specific collateral vascular resistance values less than 1.0 predict normal cerebral blood flow at moderate to severe stenosis. Values greater than 1.0 predicts cerebral ischemia to be dependent on the magnitude of collateral vascular resistance. Systemic arterial pressure is a major determinant of carotid stenosis hemodynamics. Carotid blood flow velocities increase with carotid stenosis and have progressively higher variance depending on collateral blood flow as predicted by collateral vascular resistance. Turbulent flow energy dissipation intensity is similarly inversely proportional to collateral vascular resistance at severe carotid stenosis.ConclusionsCerebral, collateral and carotid blood flow solutions are determined by systemic arterial pressure, collateral vascular resistance and degree of stenosis. Critical carotid stenosis, systemic arterial pressure and collateral vascular resistance are primary determinants of cerebral ischemic risk in patients with significant carotid stenosis.


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.


1989 ◽  
Vol 20 (5) ◽  
pp. 663-669 ◽  
Author(s):  
Carlo Alberto Maggi ◽  
Riccardo Patacchini ◽  
Paolo Santicioli ◽  
Damiano Turini ◽  
Gabriele Barbanti ◽  
...  

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.


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