Kohei Sato

The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans

Non‐technical summary  The mechanism underlying the plateau or relative decrease in cerebral blood flow during maximal incremental dynamic exercise remains unclear. We show that during graded dynamic exercise, the regulation of internal carotid artery blood flow was limited by a large increase in external carotid artery blood flow, one function of which is thermoregulation during heavy exercise. The mechanism of the plateau or decrease in internal carotid artery blood flow appears to be partly due to exercise‐induced redistribution of arterial blood flow to the head and brain.

Differential blood flow responses to CO2 in human internal and external carotid and vertebral arteries

•  Arterial CO2 serves as a mediator of cerebral blood flow, and its relative influence on the regulation of cerebral blood flow is defined as cerebral CO2 reactivity. •  Because of methodological limitations, almost all previous studies have evaluated the response of blood flow velocity in the middle cerebral artery to changes in CO2 as a measure of CO2 reactivity across the whole brain. •  We found that the vertebral artery has lower CO2 reactivity than the internal carotid artery. Moreover, CO2 reactivity in the external carotid artery was markedly lower than in the cerebral circulation. •  These results demonstrate regional differences in CO2 regulation of blood flow between the internal carotid, external carotid, and vertebro‐basilar circulation.

Blood flow in internal carotid and vertebral arteries during orthostatic stress

It remains unclear whether orthostatic stress evokes regional differences in cerebral blood flow. The present study compared blood flow in the internal carotid (ICA) and vertebral arteries (VA) during orthostatic stress (60 deg head‐up tilt; HUT) in six healthy young men. The ICA and VA blood flow were measured using Doppler ultrasonography. Dynamic cerebral autoregulation was also determined during supine (Supine) and HUT conditions, from the rate of regulation (RoR) in cerebrovascular conductance of the ICA and VA during acute hypotension induced by the release of bilateral thigh‐cuffs. The HUT decreased ICA blood flow by −9.4 ± 1.7% (P < 0.01 versus Supine), leaving ICA conductance unchanged. In contrast, there was no significant difference in VA blood flow between Supine and HUT, and VA conductance increased (+12.9 ± 0.8%, P < 0.01). In addition, dynamic cerebral autoregulation in both the ICA and VA was attenuated during HUT, and the magnitude of the attenuation in RoR was greater in the VA [0.25 ± 0.03 s−1 Supine versus 0.16 ± 0.02 s−1 HUT (−33.9 ± 5.8%); P < 0.05] compared with the ICA [0.23 ± 0.02 s−1 Supine versus 0.20 ± 0.03 s−1 HUT (−10.6 ± 13.4%); P > 0.05]. These data indicate that orthostatic stress evokes regional differences in cerebral blood flow and possible differences in dynamic cerebral autoregulation between two main brain vascular areas in response to an acute change in blood pressure during orthostatic stress.

The effect of phenylephrine on arterial and venous cerebral blood flow in healthy subjects

Aim:  Sympathetic regulation of the cerebral circulation remains controversial. Although intravenous phenylephrine (PE) infusion reduces the near‐infrared spectroscopy (NIRS)‐determined measure of frontal lobe oxygenation (ScO2) and increases middle cerebral artery mean blood velocity (MCA Vmean), suggesting α‐adrenergic‐mediated cerebral vasoconstriction, this remains unconfirmed by evaluation of arterial and venous cerebral blood flow.

Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

•  What is the central question of this study? Does hypoxia enhance blood flow to all parts of the brain uniformly? •  What is the main finding and its importance? During hypoxia, internal carotid artery flow is maintained despite a reduction in (end‐tidal) carbon dioxide tension, while vertebral artery blood flow increases. Only with maintained end‐tidal carbon dioxide tension is there an increase in both vertebral and internal carotid blood flow during hypoxia.

Different blood flow responses to dynamic exercise between internal carotid and vertebral arteries in women

The blood flow regulation in vertebral system during dynamic exercise in humans remains unclear. We examined the blood flow responses in both the internal carotid artery (QICA) and vertebral artery (QVA) simultaneously during graded dynamic exercise by Doppler ultrasound to evaluate whether cerebrovascular responses to exercise were similar. In the semisupine position, 10 young women performed a graded cycling exercise at three loads of 30, 50, and 70% of peak oxygen uptake (VO2peak) for 5 min for each workload. Mean arterial pressure, heart rate, and cardiac output increased progressively with three workloads (P<0.01). The end-tidal partial pressure of CO2 (PetCO2) in the expired gas increased from the resting level (P<0.01) at 30 and 50% VO2peak. The PetCO2 at 70% VO2peak (43.2±1.6 Torr) was significantly lower than that at 50% VO2peak (45.3±1.4 Torr). In parallel with the changes in PetCO2, QICA increased from resting level by 11.6±1.5 and 18.4±2.7% at 30 and 50% VO2peak (P<0.01), respectively, and leveled off at 70% VO2peak. In contrast, QVA did not show a leveling off and increased proportionally with workload: 16.8±3.1, 32.8±3.6, and 39.5±3.4% elevations at the three exercise loads, respectively (P<0.01). With increasing exercise load, the cerebrovascular resistance in internal carotid artery increased (P<0.01), while cerebrovascular resistance in vertebral artery remained stable during exercise. The different responses between QICA and QVA in the present study indicate a heterogenous blood flow and cerebrovascular control in the internal carotid and vertebral systems during dynamic exercise in humans.

Blood flow distribution during heat stress: cerebral and systemic blood flow.

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.

A Decrease in Spatially Resolved Near-infrared Spectroscopy-determined Frontal Lobe Tissue Oxygenation by Phenylephrine Reflects Reduced Skin Blood Flow

BACKGROUND:Spatially resolved near-infrared spectroscopy-determined frontal lobe tissue oxygenation (ScO2) is reduced with administration of phenylephrine, while cerebral blood flow may remain unaffected. We hypothesized that extracranial vasoconstriction explains the effect of phenylephrine on ScO2. METHODS:We measured ScO2 and internal and external carotid as well as vertebral artery blood flow in 7 volunteers (25 [SD 4] years) by duplex ultrasonography during IV infusion of phenylephrine, together with middle cerebral artery mean blood velocity, forehead skin blood flow, and mean arterial blood pressure. RESULTS:During phenylephrine infusion, mean arterial blood pressure increased, while ScO2 decreased by −19% ± 3% (mean ± SE; P = 0.0005). External carotid artery (−27.5% ± 3.0%) and skin blood flow (−25.4% ± 7.8%) decreased in response to phenylephrine administration, and there was a relationship between ScO2 and forehead skin blood flow (Pearson r = 0.55, P = 0.042, 95% confidence interval [CI], = 0.025–0.84; Spearman r = 0.81, P < 0.001, 95% CI, 0.49–0.94) and external carotid artery conductance (Pearson r = 0.62, P = 0.019, 95% CI, 0.13 to 0.86; Spearman r = 0.64, P = 0.012, 95% CI, 0.17–0.88). CONCLUSIONS:These findings suggest that a phenylephrine-induced decrease in ScO2, as determined by INVOS-4100 near-infrared spectroscopy, reflects vasoconstriction in the extracranial vasculature rather than a decrease in cerebral oxygenation.

Quantification of delayed oxygenation in ipsilateral primary motor cortex compared with contralateral side during a unimanual dominant-hand motor task using near-infrared spectroscopy

Using near-infrared spectroscopy (NIRS) techniques, it is possible to examine bilateral motor cortex oxygenation during a static motor task. Cortical activation was assumed to be reflected by increased oxygenation. The purpose of the present study was to examine the time course of oxygenation in the bilateral motor cortex during a low-intensity handgrip task. Six healthy, right-handed subjects participated in the study. The near-infrared spectroscopy probes positioned over the bilateral motor cortex were used to measure the cortical activation throughout a handgrip task carried out. The subjects performed a 3-min handgrip task with increasing intensity in a ramp-like manner [10-30% of the maximal voluntary contraction (MVC) at 6.67% MVC.min(-1)]. Contralateral motor cortex oxygenation increased significantly from 100 to 180 s after the start of the motor task compared with the baseline value (p<0.05). Ipsilateral motor cortex oxygenation also increased significantly from 130 to 180 s after the start of the motor task (p<0.05). The onset of increase in oxyhemoglobin ([HbO2]) and decrease in deoxyhemoglobin ([Hb]) in contralateral motor cortex area (M1) were significantly earlier than in ipsilateral M1 (respectively, p<0.05). These results show that there is a delayed oxygenation in ipsilateral primary motor cortex area compared with contralateral side during a unimanual dominant-hand motor task.

Dynamic cerebral autoregulation during and after handgrip exercise in humans

The purpose of the present study was to examine the effect of static exercise on dynamic cerebral autoregulation (CA). In nine healthy subjects at rest before, during, and after static handgrip exercise at 30% maximum voluntary contraction, the response to an acute drop in mean arterial blood pressure and middle cerebral artery mean blood velocity was examined. Acute hypotension was induced nonpharmacologically via rapid release of bilateral thigh occlusion cuffs. Subjects were instructed to avoid executing a Valsalva maneuver during handgrip. To quantify dynamic CA, the rate of regulation (RoR) was calculated from the change in cerebral vascular conductance index during the transient fall in blood pressure. There was no significant difference in RoR between rest (mean+/-SE; 0.278+/-0.052/s), exercise (0.333+/-0.053/s), and recovery (0.305+/-0.059/s) conditions (P=0.747). In addition, there was no significant difference in the rate of absolute cerebral vasodilatory response to acute hypotension between three conditions (P=0.737). This finding indicates that static exercise and related elevations in blood pressure do not alter dynamic CA.