Regional changes in brain blood flow during severe passive hyperthermia: effects of PaCO2 and extracranial blood flow

2013 ◽  
Vol 115 (5) ◽  
pp. 653-659 ◽  
Author(s):  
Anthony R. Bain ◽  
Kurt J. Smith ◽  
Nia C. Lewis ◽  
Glen E. Foster ◽  
Kevin W. Wildfong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Internal Carotid ◽  
Regional Distribution ◽  
Duplex Ultrasound ◽  
External Carotid ◽  
Subsequent Increase ◽  
Intracranial Vessel ◽  
End Tidal ◽  
Passive Hyperthermia ◽  
Cutaneous Vascular Conductance

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.

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 ◽  
...  
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid ◽  
Duplex Ultrasound ◽  
Flow Regulation ◽  
External Carotid ◽  
Peripheral Vasculature ◽  
Abrupt Decrease ◽  
Blood Flow Regulation ◽  
Acute Hypotension

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.

Regional cerebral blood flow in humans at high altitude: gradual ascent and 2 wk at 5,050 m

2014 ◽  
Vol 116 (7) ◽  
pp. 905-910 ◽  
Author(s):  
C. K. Willie ◽  
K. J. Smith ◽  
T. A. Day ◽  
L. A. Ray ◽  
N. C. S. Lewis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Internal Carotid ◽  
Duplex Ultrasound ◽  
Brain Regions ◽  
Interindividual Variation ◽  
Oxyhemoglobin Saturation ◽  
End Tidal ◽  
Carotid And Vertebral Arteries

The interindividual variation in ventilatory acclimatization to high altitude is likely reflected in variability in the cerebrovascular responses to high altitude, particularly between brain regions displaying disparate hypoxic sensitivity. We assessed regional differences in cerebral blood flow (CBF) measured with Duplex ultrasound of the left internal carotid and vertebral arteries. End-tidal Pco2, oxyhemoglobin saturation (SpO2), blood pressure, and heart rate were measured during a trekking ascent to, and during the first 2 wk at, 5,050 m. Transcranial color-coded Duplex ultrasound (TCCD) was employed to measure flow and diameter of the middle cerebral artery (MCA). Measures were collected at 344 m (TCCD-baseline), 1,338 m (CBF-baseline), 3,440 m, and 4,371 m. Following arrival to 5,050 m, regional CBF was measured every 12 h during the first 3 days, once at 5–9 days, and once at 12–16 days. Total CBF was calculated as twice the sum of internal carotid and vertebral flow and increased steadily with ascent, reaching a maximum of 842 ± 110 ml/min (+53 ± 7.6% vs. 1,338 m; mean ± SE) at ∼60 h after arrival at 5,050 m. These changes returned to +15 ± 12% after 12–16 days at 5,050 m and were related to changes in SpO2 ( R2 = 0.36; P < 0.0001). TCCD-measured MCA flow paralleled the temporal changes in total CBF. Dilation of the MCA was sustained on days 2 (+12.6 ± 4.6%) and 8 (+12.9 ± 2.9%) after arrival at 5,050 m. We observed no significant differences in regional CBF at any time point. In conclusion, the variability in CBF during ascent and acclimatization is related to ventilatory acclimatization, as reflected in changes in SpO2.

Dynamic Computed Tomography Angiography in Suspected Brain Death: A Noninvasive Biomarker

2014 ◽  
Vol 65 (4) ◽  
pp. 352-359 ◽  
Author(s):  
Santanu Chakraborty ◽  
Reem A. Adas
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Brain Death ◽  
Internal Carotid ◽  
External Carotid Artery ◽  
External Carotid ◽  
Ancillary Test ◽  
Organ Harvesting

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.

scholarly journals Effect of increases in cardiac contractility on cerebral blood flow in humans

2017 ◽  
Vol 313 (6) ◽  
pp. H1155-H1161 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Gilbert Moralez ◽  
Takuro Washio ◽  
Satyam Sarma ◽  
Michinari Hieda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid ◽  
Cardiac Contractility ◽  
External Carotid Artery ◽  
External Carotid ◽  
High Dose ◽  
Artery Blood Flow

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.

scholarly journals Coupling between arterial and venous cerebral blood flow during postural change

2016 ◽  
Vol 311 (6) ◽  
pp. R1255-R1261 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Takuro Washio ◽  
Hiroyuki Sasaki ◽  
Lonnie G. Petersen ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Blood Flow ◽  
Healthy Subjects ◽  
Internal Carotid ◽  
Jugular Vein ◽  
Venous Drainage ◽  
Postural Change ◽  
Venous Outflow ◽  
Venous Flow ◽  
End Tidal ◽  
The Brain

In supine humans the main drainage from the brain is through the internal jugular vein (IJV), but the vertebral veins (VV) become important during orthostatic stress because the IJV is partially collapsed. To identify the effect of this shift in venous drainage from the brain on the cerebral circulation, this study addressed both arterial and venous flow responses in the “anterior” and “posterior” parts of the brain when nine healthy subjects (5 men) were seated and flow was manipulated by hyperventilation and inhalation of 6% carbon dioxide (CO2). From a supine to a seated position, both internal carotid artery (ICA) and IJV blood flow decreased ( P = 0.004 and P = 0.002), while vertebral artery (VA) flow did not change ( P = 0.348) and VV flow increased ( P = 0.024). In both supine and seated positions the ICA response to manipulation of end-tidal CO2 tension was reflected in IJV ( r = 0.645 and r = 0.790, P < 0.001) and VV blood flow ( r = 0.771 and r = 0.828, P < 0.001). When seated, the decrease in ICA blood flow did not affect venous outflow, but the decrease in IJV blood flow was associated with the increase in VV blood flow ( r = 0.479, P = 0.044). In addition, the increase in VV blood flow when seated was reflected in VA blood flow ( r = 0.649, P = 0.004), and the two flows were coupled during manipulation of the end-tidal CO2 tension (supine, r = 0.551, P = 0.004; seated, r = 0.612, P < 0001). These results support that VV compensates for the reduction in IJV blood flow when seated and that VV may influence VA blood flow.

Changes of carotid and vertebral arteries in patents with arterial hypertension and hepatobiliary pathology

2016 ◽  
Vol 94 (1) ◽  
pp. 39-42
Author(s):  
Vladimir Ya. Polyakov ◽  
Yu. A. Nikolaev ◽  
S. V. Pegova ◽  
T. R. Matsievskaya ◽  
I. V. Obukhov
Keyword(s):  
Blood Flow ◽  
Arterial Hypertension ◽  
Carotid Arteries ◽  
Internal Carotid ◽  
External Carotid ◽  
Experimental Medicine ◽  
Laboratory Diagnostics ◽  
Group 2 ◽  
Internal Carotid Arteries ◽  
Group 1

The study included 1172patients (410 men and 762 women) at the mean age of 60.3±10.4years with grade I-II (stage I-II) arterial hypertension (AH) admitted to the clinic of Institute of Experimental Medicine. The patients were divided into 2 groups based on the results of clinical and laboratory diagnostics. Group 1 (n=525) included patients with AH and hepatobiliary system (HBS) diseases, group 2 (n=647) patients with AH without HBS diseases. The patients group 1 had a thicker intima-media complex of carotid arteries, higher peak systolic bloodflow rate in the internal and vertebral carotid arteries, more pronounced coiling of internal carotid arteries than patients of group 2. Patients with AH and HBS diseases exhibited correlation between blood flow rate in external carotid arteries and atherogenicity coefficient. Duplex scanning of neck vessels of in patients with AH without HBS diseases revealed peculiar changes of the intima-media thickness and hemodynamically significant changes of the blood flow in the internal carotid arteries that may be of prognostic value in this nosological syntropy and require the personified approach to diagnostics, treatment, and prevention of these conditions.

scholarly journals Internal carotid, external carotid and vertebral artery blood flow responses to 3 days of head-out dry immersion

2017 ◽  
Vol 102 (10) ◽  
pp. 1278-1287 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Ai Hirasawa ◽  
Steven de Abreu ◽  
Pierre Denise ◽  
Hervé Normand
Keyword(s):  
Blood Flow ◽  
Vertebral Artery ◽  
Internal Carotid ◽  
External Carotid ◽  
Artery Blood Flow ◽  
Dry Immersion

Internal carotid and vertebral arterial flow velocity in men at high altitude

1987 ◽  
Vol 63 (1) ◽  
pp. 395-400 ◽  
Author(s):  
S. Y. Huang ◽  
L. G. Moore ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
A. J. Micco ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Flow Velocity ◽  
Sea Level ◽  
Internal Carotid ◽  
Hemoglobin Concentration ◽  
Subsequent Increase ◽  
O2 Transport ◽  
Flow Velocities

Cerebral blood flow increases at high altitude, but the mechanism of the increase and its role in adaptation to high altitude are unclear. We hypothesized that the hypoxemia at high altitude would increase cerebral blood flow, which would in turn defend O2 delivery to the brain. Noninvasive Doppler ultrasound was used to measure the flow velocities in the internal carotid and the vertebral arteries in six healthy male subjects. Within 2–4 h of arrival on Pikes Peak (4,300 m), velocities in both arteries were slightly and not significantly increased above sea-level values. By 18–44 h a peak increase of 20% was observed (combined P less than 0.025). Subsequently (days 4–12) velocities declined to values similar to those at sea level. At altitude the lowest arterial O2 saturation (SaO2) and the highest end-tidal PCO2 was observed on arrival. By day 4 and thereafter, when the flow velocities had returned toward sea-level values, hemoglobin concentration and SaO2 were increased over initial high-altitude values such that calculated O2 transport values were even higher than those at sea level. Although the cause of the failure for cerebral flow velocity to increase on arrival is not understood, the subsequent increase may act to defend brain O2 transport. With further increase in hemoglobin and SaO2 over time at high altitude, flow velocity returned to sea-level values.

scholarly journals Regulation of regional cerebral blood flow during graded reflex-mediated sympathetic activation via lower body negative pressure

2018 ◽  
Vol 125 (6) ◽  
pp. 1779-1786 ◽  
Author(s):  
Jasdeep Kaur ◽  
Jennifer R. Vranish ◽  
Thales C. Barbosa ◽  
Takuro Washio ◽  
Benjamin E. Young ◽  
...  
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Internal Carotid ◽  
Lower Body Negative Pressure ◽  
Blood Velocity ◽  
Lower Body ◽  
Sympathetic Activation ◽  
Voluntary Hyperventilation ◽  
End Tidal ◽  
Baseline Diameter

The role of the sympathetic nervous system in cerebral blood flow (CBF) regulation remains unclear. Previous studies have primarily measured middle cerebral artery blood velocity to assess CBF. Recently, there has been a transition toward measuring internal carotid artery (ICA) and vertebral artery (VA) blood flow using duplex Doppler ultrasound. Given that the VA supplies autonomic control centers in the brainstem, we hypothesized that graded sympathetic activation via lower body negative pressure (LBNP) would reduce ICA but not VA blood flow. ICA and VA blood flow were measured during two protocols: protocol 1, low-to-moderate LBNP (−10, −20, −30, and −40 Torr) and protocol 2, moderate-to-high LBNP (−30, −50, and −70 Torr). ICA and VA blood flow, diameter, and blood velocity were unaffected up to −40 LBNP. However, −50 and −70 LBNP evoked reductions in ICA and VA blood flow [e.g., −70 LBNP: percent change (%∆)VA-baseline = −27.6 ± 3.0] that were mediated by decreases in both diameter and velocity (e.g., −70 LBNP: %∆VA-baseline diameter = −7.5 ± 1.9 and %∆VA-baseline velocity = −13.6 ± 1.7), which were comparable between vessels. Since hyperventilation during −70 LBNP reduced end-tidal pressure of carbon dioxide ([Formula: see text]), this decrease in [Formula: see text] was matched via voluntary hyperventilation. Reductions in ICA and VA blood flow during hyperventilation alone were significantly smaller than during −70 LBNP and were primarily mediated by decreases in velocity (%∆VA-baseline velocity = −8.6 ± 2.4 and %∆VA-baseline diameter = −0.05 ± 0.56). These data demonstrate that both ICA and VA were unaffected by low-to-moderate sympathetic activation, whereas robust reflex-mediated sympathoexcitation caused similar magnitudes of vasoconstriction in both arteries. Thus, contrary to our hypothesis, the ICA was not preferentially vasoconstricted by sympathetic activation. NEW & NOTEWORTHY Our study demonstrates that moderate-to-high reflex-mediated sympathetic activation with lower body negative pressure (LBNP) decreases internal carotid artery and vertebral artery blood flow via reductions in both vessel diameter and blood velocity. This vasoconstriction was primarily sympathetically mediated as voluntary hyperventilation alone, to isolate the effect of decreases in end-tidal pressure of carbon dioxide that occurred during LBNP, resulted in a significantly smaller vasoconstriction. In contrast to our hypothesis, these data indicate a lack of heterogeneity between the anterior and posterior cerebral circulations in response to sympathoexcitation.

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