Regional redistribution of blood flow in the external and internal carotid arteries during acute hypotension

2014 ◽  
Vol 306 (10) ◽  
pp. R747-R751 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Romain Lericollais ◽  
Ai Hirasawa ◽  
Sadayoshi Sakai ◽  
Hervé Normand ◽  
...  

The present study examined to what extent an acute bout of hypotension influences blood flow in the external carotid artery (ECA) and the corresponding implications for blood flow regulation in the internal carotid artery (ICA). Nine healthy male participants were subjected to an abrupt decrease in arterial pressure via the thigh-cuff inflation-deflation technique. Duplex ultrasound was employed to measure beat-to-beat ECA and ICA blood flow. Compared with the baseline normotensive control, acute hypotension resulted in a heterogeneous blood flow response. ICA blood flow initially decreased following cuff release and then returned quickly to baseline levels. In contrast, the reduction in ECA blood flow persisted for 30 s following cuff release. Thus, the contribution of common carotid artery blood flow to the ECA circulation decreased during acute hypotension (−10 ± 4%, P < 0.001). This finding suggests that a preserved reduction in ECA blood flow, as well as dynamic cerebral autoregulation likely prevent a further decrease in intracranial blood flow during acute hypotension. The peripheral vasculature of the ECA may, thus, be considered an important vascular bed for intracranial cerebral blood flow regulation.

2020 ◽  
Vol 129 (4) ◽  
pp. 901-908
Author(s):  
Shigehiko Ogoh ◽  
Takuro Washio ◽  
Julian F. R. Paton ◽  
James P. Fisher ◽  
Lonnie G. Petersen

We investigated whether gravity-induced changes in intracranial pressure influence cerebral blood flow regulation in young men. We recorded extra- and intracerebral blood flow during changes in posture, and data indicate that the external carotid artery may serve as an overflow pathway to prevent cerebral hyperperfusion during increases in cerebral arterial blood pressure.


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.


Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Randolph S Marshall ◽  
MaryKay Pavol ◽  
Ken Cheung ◽  
Isabelle Strom ◽  
Kevin Slane ◽  
...  

Background: Cerebral blood flow (CBF) regulation is a critical element in cerebrovascular pathophysiology, particularly in large vessel disease. Different methods to assess hemodynamics may represent different aspects of blood flow regulation, however, uniquely affecting outcomes and management. We examined 4 different blood-flow related measures in patients with high-grade unilateral carotid disease, assessing asymmetry between the occluded vs non-occluded side, and the correlations among the measures. Methods: Thirty-three patients (age 50-93, 19M) with unilateral 80-100% ICA occlusion but no stroke underwent: 1) quantitative resting CBF using continuous arterial spin labeling (CASL) MRI, 2) mean flow velocity (MFV) in both middle cerebral arteries (MCAs) by transcranial Doppler, 3). Vasomotor reactivity (VMR) in response to 2 minutes of 5% CO2 inhalation, and 4) Dynamic cerebral autoregulation (DCA) using continuous insonation of both MCAs for 10 minutes at depth 56mm with a standard head frame. Phase shift (PS) between spontaneous oscillations in blood pressure (measured with finger photoplethysmography) and MCA MFV at frequencies .06-.12 Hz was calculated for each hemisphere using transfer function analysis. Lower PS indicated worse autoregulation. Paired T-tests and Pearson correlations were used to look for side-to-side differences within each measure, and correlations between measures (SPSS v.22). Results: CASL CBF (p=.001), MFV (p<.001), VMR (p=.008), and DCA (p=.047) all showed significantly lower values on the occluded side. The 4 measures were independent of each other on correlation analysis, even when controlling for age and anterior circle of Willis collateral (correlation coefficients all <0.40, p-values >0.09). Conclusions: These 4 measures showed high sensitivity to the occluded carotid artery, but appear to represent independent aspects of cerebral blood flow (CASL: resting gray matter CBF; MFV: whole-hemisphere CBF; VMR: cerebrovascular reserve, and DCA: homeostatic blood flow regulation) suggesting that any given measure only partially characterizes hemodynamic state. Further investigation will use these 4 measures to predict outcomes including vascular cognitive impairment.


2017 ◽  
Vol 313 (6) ◽  
pp. H1155-H1161 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Gilbert Moralez ◽  
Takuro Washio ◽  
Satyam Sarma ◽  
Michinari Hieda ◽  
...  

The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 μg·kg−1·min−1) and then a high dose (15 μg·kg−1·min−1)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despite increases in cardiac contractility, cardiac output, and arterial pressure with dobutamine, ICA blood flow and conductance slightly decreased from resting baseline during both low- and high-dose infusions. In contrast, ECA blood flow and conductance increased appreciably during both low- and high-dose infusions. Greater ECA vascular conductance and corresponding increases in blood flow may protect overperfusion of intracranial cerebral arteries during enhanced cardiac contractility and associated increases in cardiac output and perfusion pressure. Importantly, these findings suggest that the acute increase of blood perfusion attributable to dobutamine administration does not cause cerebral overperfusion or an associated risk of cerebral vascular damage. NEW & NOTEWORTHY A dobutamine-induced increase in cardiac contractility did not increase internal carotid artery blood flow despite an increase in cardiac output and arterial blood pressure. In contrast, external carotid artery blood flow and conductance increased. This external cerebral blood flow response may assist with protecting from overperfusion of intracranial blood flow.


2021 ◽  
Author(s):  
Alexander T. Friend ◽  
Matthew. Rogan ◽  
Gabriella M. K. Rossetti ◽  
Justin S. Lawley ◽  
Paul G. Mullins ◽  
...  

2013 ◽  
Vol 115 (5) ◽  
pp. 653-659 ◽  
Author(s):  
Anthony R. Bain ◽  
Kurt J. Smith ◽  
Nia C. Lewis ◽  
Glen E. Foster ◽  
Kevin W. Wildfong ◽  
...  

We investigated 1) the regional distribution of cerebral blood flow (CBF), 2) the influence of end-tidal Pco2 (PetCO2) on CBF, and 3) the potential for an extracranial blood “steal” from the anterior brain region during passive hyperthermia. Nineteen (13 male) volunteers underwent supine passive heating until a steady-state esophageal temperature of 2°C above resting was established. Measurements were obtained 1) during normothermia (Normo), 2) during poikilocapnic hyperthermia (Hyper), and 3) during hyperthermia with PetCO2 and end-tidal Po2 clamped to Normo levels (Hyper-clamp). Blood flow in the internal carotid (Q̇ica), vertebral (Q̇VA), and external carotid (Q̇eca) arteries (Duplex ultrasound), blood velocity of the middle cerebral (MCAv) and posterior cerebral (PCAv) arteries (transcranial Doppler), and cutaneous vascular conductance on the cheek (cheek CVC; Doppler velocimetry) were measured at each stage. During Hyper, PetCO2 was lowered by 7.0 ± 5.2 mmHg, resulting in a reduction in Q̇ica (−18 ± 17%), Q̇va (−31 ± 21%), MCAv (−22 ± 13%), and PCAv (−18 ± 10%) compared with Normo ( P < 0.05). The reduction in Q̇VA was greater than that in Q̇ICA ( P = 0.017), MCAv ( P = 0.047), and PCAv ( P = 0.034). Blood flow/velocity was completely restored in each intracranial vessel (ICA, VA, MCA, and PCA) during Hyper-clamp. Despite a ∼250% increase in Q̇ECA and a subsequent increase in cheek CVC during Hyper compared with Normo, reductions in Q̇ICA were unrelated to changes in Q̇ECA. These data provide three novel findings: 1) hyperthermia attenuates Q̇VA to a greater extent than Q̇ICA, 2) reductions in CBF during hyperthermia are governed primarily by reductions in arterial Pco2, and 3) increased Q̇ECA is unlikely to compromise Q̇ICA during hyperthermia.


1983 ◽  
Vol 3 (1) ◽  
pp. 71-77 ◽  
Author(s):  
J. J. Grome ◽  
A. M. Harper

This study was undertaken to measure the effects of serotonin administration on local cerebral blood flow following blood–brain barrier (BBB) disruption with hypertonic urea. Rats were anesthetized with halothane in nitrous oxide and oxygen (70%:30%). In some animals urea (3.5 M) was infused retrogradely through an external carotid catheter, followed after 10 min by serotonin (50 ng kg−1 min−1) or physiological saline. Local cerebral blood flow was measured using the 14C-iodoantipyrine quantitative autoradiographic technique of Sakurada et al. (1978). The administration of saline or urea alone had only minimal effects on local cerebral blood flow. When the BBB was intact, serotonin produced a significant fall in regional blood flow only in the caudate nucleus. Following BBB disruption, however, serotonin produced a marked decrease in local perfusion in a number of discrete brain areas that are supplied by blood from the internal carotid artery. On the other hand, there were increases in local perfusion in areas not supplied by the internal carotid artery.


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