scholarly journals Blood Flow Distribution during Heat Stress: Cerebral and Systemic Blood Flow

2013 ◽  
Vol 33 (12) ◽  
pp. 1915-1920 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Kohei Sato ◽  
Kazunobu Okazaki ◽  
Tadayoshi Miyamoto ◽  
Ai Hirasawa ◽  
...  

The purpose of the present study was to assess the effect of heat stress-induced changes in systemic circulation on intra- and extracranial blood flows and its distribution. Twelve healthy subjects with a mean age of 22±2 (s.d.) years dressed in a tube-lined suit and rested in a supine position. Cardiac output (Q), internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) blood flows were measured by ultrasonography before and during whole body heating. Esophageal temperature increased from 37.0±0.2°C to 38.4±0.2°C during whole body heating. Despite an increase in Q (59±31%, P<0.001), ICA and VA decreased to 83±15% ( P=0.001) and 87±8% ( P=0.002), respectively, whereas ECA blood flow gradually increased from 188±72 to 422±189 mL/minute (+135%, P<0.001). These findings indicate that heat stress modified the effect of Q on blood flows at each artery; the increased Q due to heat stress was redistributed to extracranial vascular beds.

2014 ◽  
Vol 117 (1) ◽  
pp. 46-52 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Kohei Sato ◽  
Kazunobu Okazaki ◽  
Tadayoshi Miyamoto ◽  
Ai Hirasawa ◽  
...  

The purpose of this study was to assess blood flow responses to changes in carbon dioxide (CO2) in the internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) during normothermic and hyperthermic conditions. Eleven healthy subjects aged 22 ± 2 (SD) yr were exposed to passive whole body heating followed by spontaneous hypocapnic and hypercapnic challenges in normothermic and hyperthermic conditions. Right ICA, ECA, and VA blood flows, as well as left middle cerebral artery (MCA) mean blood velocity ( Vmean), were measured. Esophageal temperature was elevated by 1.53 ± 0.09°C before hypocapnic and hypercapnic challenges during heat stress. Whole body heating increased ECA blood flow and cardiac output by 130 ± 78 and 47 ± 26%, respectively ( P < 0.001), while blood flow (or velocity) in the ICA, MCA, and VA was reduced by 17 ± 14, 24 ± 18, and 12 ± 7%, respectively ( P < 0.001). Regardless of the thermal conditions, ICA and VA blood flows and MCA Vmean were decreased by hypocapnic challenges and increased by hypercapnic challenges. Similar responses in ECA blood flow were observed in hyperthermia but not in normothermia. Heat stress did not alter CO2 reactivity in the MCA and VA. However, CO2 reactivity in the ICA was decreased (3.04 ± 1.17 vs. 2.23 ± 1.03%/mmHg; P = 0.039) but that in the ECA was enhanced (0.45 ± 0.47 vs. 0.95 ± 0.61%/mmHg; P = 0.032). These results indicate that hyperthermia is capable of altering dynamic cerebral blood flow regulation.


2016 ◽  
Vol 120 (7) ◽  
pp. 766-773 ◽  
Author(s):  
Kohei Sato ◽  
Anna Oue ◽  
Marina Yoneya ◽  
Tomoko Sadamoto ◽  
Shigehiko Ogoh

We hypothesized that heat stress would decrease anterior and posterior cerebral blood flow (CBF) during exercise, and the reduction in anterior CBF would be partly associated with large increase in extracranial blood flow (BF). Nine subjects performed 40 min of semirecumbent cycling at 60% of the peak oxygen uptake in hot (35°C; Heat) and thermoneutral environments (25°C; Control). We evaluated BF and conductance (COND) in the external carotid artery (ECA), internal carotid artery (ICA), and vertebral artery (VA) using ultrasonography. During the Heat condition, ICA and VA BF were significantly increased 10 min after the start of exercise ( P < 0.05) and thereafter gradually decreased. ICA COND was significantly decreased ( P < 0.05), whereas VA COND remained unchanged throughout Heat. Compared with the Control, either BF or COND of ICA and VA at the end of Heat tended to be lower, but not significantly. In contrast, ECA BF and COND at the end of Heat were both higher than levels in the Control condition ( P < 0.01). During Heat, a reduction in ICA BF appears to be associated with a decline in end-tidal CO2 tension ( r = 0.84), whereas VA BF appears to be affected by a change in cardiac output ( r = 0.87). In addition, a change in ECA BF during Heat was negatively correlated with a change in ICA BF ( r = −0.75). Heat stress resulted in modification of the vascular response of head and brain arteries to exercise, which resulted in an alteration in the distribution of cardiac output. Moreover, a hyperthermia-induced increase in extracranial BF might compromise anterior CBF during exercise with heat stress.


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.


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.


Neurology ◽  
1970 ◽  
Vol 20 (1) ◽  
pp. 1-1 ◽  
Author(s):  
H. J. M. Barnett ◽  
G. Wortzman ◽  
R. M. Gladstone ◽  
W. M. Lougheed

2021 ◽  
Vol 20 (2) ◽  
pp. 45-51
Author(s):  
V. B. Semenyutin ◽  
А. А. Nikiforova ◽  
V. A. Aliev ◽  
G. К. Panuntsev

Introduction. Conventionally, hemodynamic significance of carotid stenosis is characterized with an increased peak systolic velocity up to 230 cm/s, which corresponds to 70 % carotid stenosis. This does not take into account changes of cerebral hemodynamics or collateral circulation, which can be determined by assessment of blood flow distribution in precerebral arteries. Aim – to evaluate blood flow redistribution in precerebral arteries in patients with critical carotid stenosis. Materials and methods. 40 patients (aged 49–80 y. o.) with critical carotid stenosis were studied (13 patients had 70–79 % stenosis, 11 patients – 80–89 %, and 16 patients – 90–99 % stenosis). Flow velocity index in precerebral arteries was determined with duplex scanning (Vivid e, USA), whereas linear blood flow velocity in intracranial arteries – with transcranial Doppler (MultiDop X, Germany). Results. In 60 % of patients, flow velocity index in ipsilateral carotid artery was reliably decreased (p<0.05). In 49 % of patients flow velocity index in contralateral carotid artery and blood flow velocity in contralateral anterior cerebral artery were reliably increased (p<0.05), as well as linear blood flow velocity in the contralateral anterior cerebral artery. Just in 39 % of patients flow velocity index in ipsilateral vertebral artery and linear blood flow velocity in ipsilateral posterior cerebral artery were increased (p<0.05). In 13 % of cases flow velocity index in the external carotid artery was increased (p<0.05). Conclusion. Thus, critical degree of carotid stenosis does not always indicate its hemodynamic significance. Flow velocity index distribution in precerebral arteries can be used as an additional criterion for assessing hemodynamic significance of carotid stenosis and, along with other indicators, should be taken into account when choosing treatment modality.


1969 ◽  
Vol 216 (1) ◽  
pp. 50-55 ◽  
Author(s):  
BS Grimson ◽  
SC Robinson ◽  
ET Danford ◽  
GT Tindall ◽  
Greenfield JC

2001 ◽  
Vol 280 (4) ◽  
pp. R1016-R1022 ◽  
Author(s):  
Joseph J. Smolich

It is unknown if nitric oxide (NO) modulates the relative levels of left (LV) and right (RV) ventricular output, fetal O2 consumption, or blood flow distribution between the body and placenta at midgestation. To address these questions, six fetal lambs were instrumented at 89–96 days gestation (term 147 days), and blood flows were measured with radioactive microspheres 3–4 days later at baseline and after inhibition of NO synthesis with 10 mg/kg (l-NNA10) and 25 mg/kg (l-NNA25) N ω-nitro-l-arginine. LV output fell by 74 ± 15 ml · min−1 · kg−1 atl-NNA10 ( P < 0.005), whereas RV output decreased by 90 ± 18 ml · min−1 · kg−1 atl-NNA10 ( P < 0.02) and by a further 80 ± 22 ml · min−1 · kg−1 atl-NNA25 ( P < 0.05). As a result, RV output exceeded LV output at baseline ( P = 0.03) and l-NNA10 ( P < 0.02) but not at l-NNA25. Fetal body blood flow fell by 95 ± 25 ml · min−1 · kg−1 atl-NNA10 ( P < 0.01), but because placental blood flow decreased by 70 ± 22 ml · min−1 · kg−1 atl-NNA10 ( P < 0.01) and a further 71 ± 21 ml · min−1 · kg−1 atl-NNA25 ( P < 0.01), the fetal body-to-placental blood flow ratio was near unity at baseline andl-NNA10 but rose to 1.5 ± 0.3 atl-NNA25 ( P < 0.05). In association with these flow changes, fetal O2 consumption declined by 1.4 ± 0.3 ml · min−1 · kg−1 atl-NNA10 ( P < 0.05) and by a further 1.5 ± 0.6 ml · min−1 · kg−1 atl-NNA25 ( P < 0.02). These findings suggest that, in midgestation fetal lambs, NO supports an RV flow dominance, whole body O2 utilization, and the maintenance of a near-equal fetoplacental blood flow distribution.


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