External Carotid Blood Flow Research Articles

Revascularisation patterns and characteristics after erythropoietin pretreatment and multiple burr holes in patients who had acute stroke with perfusion impairment

BackgroundTransdural collaterals, originating mainly from the extracalvarial superficial temporal artery and intracalvarial middle meningeal artery via the external carotid artery (ECA), have been observed after revascularisation surgery. However, the origin...

Hemodynamic Responses in Carotid Bifurcation Induced by Enhanced External Counterpulsation Stimulation in Healthy Controls and Patients With Neurological Disorders.

Enhanced external counterpulsation is a Food and Drug Administration–approved, non-invasive, assisted circulation therapy for ischemic cardiovascular and cerebrovascular diseases. Previous studies have confirmed that EECP stimulation induces largely different cerebral hemodynamic responses in patients with ischemic stroke and healthy controls. However, the underlying mechanisms remain uncertain. We hypothesize that different blood redistributions at the carotid bifurcation may play a key role. Ten subjects were enrolled in this study, namely, five patients with neurological disorders and five young healthy volunteers as controls. Magnetic resonance angiography (MRA) was performed on the carotid artery. All the subjects received a single session of EECP treatment, with external cuff pressures ranging from 20 to 40 kPa. Vascular ultrasound measurements were taken in the common carotid artery (CCA), external carotid artery (ECA) and internal carotid artery (ICA). Three-dimensional patient-specific numerical models were developed to calculate the WSS-derived hemodynamic factors. The results indicated that EECP increased CCA and ECA blood flow in both groups. The ICA blood flow in the patient group exhibited a mean increase of 6.67% during EECP treatment compared with the pre-EECP condition; a mean decrease of 9.2% was observed in the healthy control group. EECP increased the averaged wall shear stress (AWSS) throughout the carotid bifurcation in the patient group; the ICA AWSS of the healthy group decreased during EECP. In both groups, the oscillatory shear index (OSI) in the ICA increased proportionally with external cuff pressure. In addition, the relative resident time (RRT) was constant or slightly decreased in the CCA and ECA in both groups but increased in the ICA. We suggest that the benefits of EECP to patients with neurological disorders may partly result from blood flow promotion in the ICA and increase in WSS at the carotid bifurcation. In the healthy subjects, the ICA blood flow remained constant during EECP, although the CCA blood flow increased significantly. A relatively low external cuff pressure (20 kPa) is recommended as the optimal treatment pressure for better hemodynamic effects. This study may play an important role in the translation of physiological benefits of EECP treatment in populations with or without neurological disorders.

Integrated respiratory chemoreflex-mediated regulation of cerebral blood flow in hypoxia: Implications for oxygen delivery and acute mountain sickness.

What is the central question of this study? To what extent do hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral oxygen delivery, with corresponding implications for susceptibility to acute mountain sickness? What is the main finding and its importance? We provide evidence for site-specific regulation of cerebral blood flow in hypoxia that preserves oxygen delivery in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. External carotid artery vasodilatation might prove to be an alternative haemodynamic risk factor that predisposes to acute mountain sickness. The aim of the present study was to determine the extent to which hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral blood flow (CBF) and oxygen delivery (CDO2 ), with corresponding implications for the pathophysiology of the neurological syndrome, acute mountain sickness (AMS). Eight healthy men were randomly assigned single blind to 7h of passive exposure to both normoxia (21% O2 ) and hypoxia (12% O2 ). The peripheral and central respiratory chemoreflex, internal carotid artery, external carotid artery (ECA) and vertebral artery blood flow (duplex ultrasound) and AMS scores (questionnaires) were measured throughout. A reduction in internal carotid artery CDO2 was observed during hypoxia despite a compensatory elevation in perfusion. In contrast, vertebral artery and ECA CDO2 were preserved, and the former was attributable to a more marked increase in perfusion. Hypoxia was associated with progressive activation of the peripheral respiratory chemoreflex (P<0.001), whereas the central respiratory chemoreflex remained unchanged (P>0.05). Symptom severity in participants who developed clinical AMS was positively related to ECA blood flow (Lake Louise score, r=0.546-0.709, P=0.004-0.043; Environmental Symptoms Questionnaires-Cerebral symptoms score, r=0.587-0.771, P=0.001-0.027, n=4). Collectively, these findings highlight the site-specific regulation of CBF in hypoxia that maintains CDO2 selectively in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. Furthermore, ECA vasodilatation might represent a hitherto unexplored haemodynamic risk factor implicated in the pathophysiology of AMS.

Four collateral circulation pathways were observed after common carotid artery occlusion

BackgroundCommon carotid artery (CCA) occlusion (CCAO) is a rare condition. Owing to collateral circulation, ipsilateral internal carotid artery (ICA) and external carotid artery (ECA) are often patent.MethodsThis study included 16 patients with unilateral CCAO and patent ipsilateral ICA and ECA. The pathways which supplied ICA were investigated by digital subtraction angiography (DSA), transcranial Doppler (TCD), magnetic resonance angiography (MRA) and computed tomography angiography (CTA).ResultsIn all 16 patients, TCD found antegrade blood flow in ipsilateral ICA, which was supplied by retrograde blood flow in ipsilateral ECA through carotid bifurcation. We call this phenomenon “ICA steal”. DSA and CTA discovered four pathways of ICA steal, including 1) ipsilateral vertebral artery – occipital artery – ECA – ICA, 2) ipsilateral thyrocervical trunk or costocervical trunk – ascending cervical artery or deep cervical artery – occipital artery – ECA – ICA, 3) contralateral ECA – contralateral superior thyroid artery – ipsilateral superior thyroid artery – ipsilateral ECA – ICA, and 4) ipsilateral thyrocervical trunk – inferior thyroid artery – superior thyroid artery – ECA – ICA.ConclusionsICA is possible to be patent and supplied by several collateral circulation pathways after CCAO.

Associations between changes in precerebral blood flow and cerebral oximetry in the lower body negative pressure model of hypovolemia in healthy volunteers.

Reductions in cerebral oxygen saturation (ScO2) measured by near infra-red spectroscopy have been found during compensated hypovolemia in the lower body negative pressure (LBNP)-model, which may reflect reduced cerebral blood flow. However, ScO2 may also be contaminated from extracranial (scalp) tissues, mainly supplied by the external carotid artery (ECA), and it is possible that a ScO2 reduction during hypovolemia is caused by reduced scalp, and not cerebral, blood flow. The aim of the present study was to explore the associations between blood flow in precerebral arteries and ScO2 during LBNP-induced hypovolemia. Twenty healthy volunteers were exposed to LBNP 20, 40, 60 and 80 mmHg. Blood flow in the internal carotid artery (ICA), ECA and vertebral artery (VA) was measured by Doppler ultrasound. Stroke volume for calculating cardiac output was measured by suprasternal Doppler. Associations of changes within subjects were examined using linear mixed-effects regression models. LBNP reduced cardiac output, ScO2 and ICA and ECA blood flow. Changes in flow in both ICA and ECA were associated with changes in ScO2 and cardiac output. Flow in the VA did not change during LBNP and changes in VA flow were not associated with changes in ScO2 or cardiac output. During experimental compensated hypovolemia in healthy, conscious subjects, a reduced ScO2 may thus reflect a reduction in both cerebral and extracranial blood flow.

The effects of aging on the distribution of cerebral blood flow with postural changes and mild hyperthermia.

Cerebral blood flow (CBF) would be impaired with dual stresses of heat and orthostatic changes, even if those stresses are mild, in the elderly with declined cardio- and cerebrovascular functions with aging. To test the hypothesis, we compared the response of blood flow in the internal carotid artery (ICA) and vertebral artery (VA) to dual stresses of heat and orthostatic changes between the elderly and young individuals. Nine elderly and eight young healthy men (71.3 ± 3.0 and 23.3 ± 3.1 years, mean ± SD, respectively) underwent measurements of blood flow in the ICA, VA and external carotid artery (ECA) via ultrasonography. The measurements were obtained in sitting and supine positions under normothermic (NT) and mildly hyperthermic (HT) conditions (ambient temperature 28°C). Esophageal temperatures increased from NT (36.4 ± 0.2°C, mean ± SE) to HT (37.4 ± 0.2°C) with lower legs immersion in 42°C water. With heat stress, ECA blood flow increased in both postures in both age groups (effect of heat, p < 0.001), whereas ICA blood flow remained unchanged. With postural changes from supine to sitting, ECA blood flow remained unchanged whereas ICA blood flow decreased (effect of posture, p = 0.027) by 18% in NT in the young and by 20% in HT in the elderly. VA blood flow remained unchanged under both heat stress and postural changes. The CBF is impaired under dual stresses of heat and orthostatic changes in healthy aged individuals, even if the levels of the stresses are mild.

Remifentanil decreases oral tissue blood flow while maintaining internal carotid artery blood flow during sevoflurane anesthesia in rabbits.

The aim of this study was to investigate the effect of remifentanil infusion on oral tissue blood flow including submandibular gland tissue blood flow (SBF) and internal carotid artery blood flow (ICBF) in rabbits during sevoflurane anesthesia. Twelve male Japan White rabbits were anesthetized with sevoflurane and remifentanil. Remifentanil was infused at 0.2 and 0.4 µg/kg/min. Measurements included circulatory variables, common and external carotid artery blood flow (CCBF, ECBF), ICBF, tongue mucosal blood flow (TMBF), masseter muscle tissue blood flow (MBF), mandibular bone marrow tissue blood flow (BBF), tongue muscle tissue blood flow (TBF) and SBF. Vascular resistances for each tissue, including the tongue mucosa, masseter muscle, mandibular bone marrow, tongue muscle and submandibular gland, were calculated by dividing the mean arterial pressure by the respective tissue blood flow. Remifentanil infusion decreased oral tissue blood flow and circulatory variables. CCBF, ECBF and ICBF did not change. The calculated vascular resistance in each oral tissue, except for the tongue mucosa, increased in an infusion-rate-dependent manner. These results showed that remifentanil infusion reduced TMBF, MBF, BBF, TBF and SBF in an infusion-rate-dependent manner without affecting ICBF under sevoflurane anesthesia.

Effect of increases in cardiac contractility on cerebral blood flow in humans.

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.

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

What is the central question of this study? The extent to which weightlessness associated with a fluid shift from the peripheral to the central circulation influences the blood flow in each cerebral artery remains unknown. The present study was designed to explore the effect of short-term weightlessness conditions on both anterior and posterior cerebral blood flow. What is the main finding and its importance? Short-term weightlessness affects both anterior and posterior cerebral vasculature. However, a heterogeneous cerebral blood flow response in each cerebral artery did not occur during 3days of dry immersion. We have recently demonstrated that a heterogeneous cerebral blood flow (CBF) response in each cerebral artery might contribute to the maintenance of circulatory homeostasis in the brain. However, the extent to which weightlessness associated with a fluid shift from the peripheral to the central circulation influences the distribution of CBF in each cerebral artery remains unknown. We hypothesized that a dry immersion-induced fluid shift (weightlessness conditions) would cause a heterogeneous CBF response in each cerebral artery. During and after 3days of dry immersion, the blood flows in the internal carotid (ICA), external carotid (ECA) and vertebral arteries (VA) were measured by Doppler ultrasonography using an 8MHz linear transducer. Although the 3days of dry immersion and the 2days recovery period did not change the blood flow in each cerebral artery, the conductance in both ICA and VA decreased during dry immersion on days 2 and 3 (ICA, 2.95 and 3.23mlmin-1 mmHg-1 ; VA, 1.10 and 1.05mlmin-1 mmHg-1 , respectively) from the baseline (ICA, 3.47mlmin-1 mmHg-1 , P=0.027; VA, 1.23mlmin-1 mmHg-1 , P=0.004). In addition, Pearson correlation analysis demonstrated that the 3days of dry immersion induced a decrease in cardiac output (P=0.004) that was associated with changes in ICA (P=0.046) and VA blood flow (P=0.021), but not ECA blood flow (P=0.466). These findings suggest that short exposures to weightlessness, acting via a cephalad redistribution of fluid volume and blood flow in the human body, influenced the cerebral vasculature in each cerebral artery but did not cause a heterogeneous CBF response in each cerebral artery.

Dynamic cerebral autoregulation is unrelated to decrease in external carotid artery blood flow during acute hypotension in healthy young men.

What is the central question of this study? Dynamic cerebral autoregulation (CA) is impaired by sympathetic blockade, and the external carotid artery (ECA) vascular bed may prevent adequate internal carotid artery blood flow. We examined whether α1 -receptor blockade-induced attenuation of dynamic CA is related to reduced ECA vasoconstriction. What is the main finding and its importance? α1 -Receptor blockade attenuated dynamic CA, but in contrast to our hypothesis did not affect the ECA blood flow response to acute hypotension. These findings suggest that the recovery of cerebral blood flow during acute hypotension is unrelated to vasoconstriction within the ECA territory. External carotid artery (ECA) vasoconstriction may defend internal carotid artery (ICA) blood flow during acute hypotension. We hypothesized that the α1 -receptor blockade-induced delay in ICA recovery to the baseline level from acute hypoperfusion is related to attenuated ECA vasoconstriction. The ICA and ECA blood flow were determined by duplex ultrasound during thigh-cuff release-induced acute hypotension while the α1 -receptor blocker prazosin [1mg(20kg)(-1) ] was administered to nine seated young healthy men. Both ICA (mean±SD; by 17±8%, P=0.005) and ECA (by 37±15%, P<0.001) blood flow decreased immediately after occluded thigh-cuff release, with a more rapid ICA blood flow recovery to the baseline level (9±5s) than for the ECA blood flow (17±5s; P=0.019). The ICA blood flow recovery from hypoperfusion was delayed with prazosin (17±4s versus control 9±5s, P=0.006), whereas ECA recovery remained unchanged (P=0.313) despite a similar reduction in mean arterial pressure (-20±4mmHg versus control -23±7mmHg, P=0.148). These findings suggest that α1 -receptor blockade-induced attenuation of the ICA blood flow response to acute hypotension is unrelated to the reduction in ECA blood flow. The sympathetic nervous system via the ECA vascular bed does not contribute to dynamic CA during acute hypotension.

Heat stress redistributes blood flow in arteries of the brain during dynamic exercise.

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.

Dehydration accelerates reductions in cerebral blood flow during prolonged exercise in the heat without compromising brain metabolism.

Dehydration hastens the decline in cerebral blood flow (CBF) during incremental exercise, whereas the cerebral metabolic rate for O2 (CMRO2 ) is preserved. It remains unknown whether CMRO2 is also maintained during prolonged exercise in the heat and whether an eventual decline in CBF is coupled to fatigue. Two studies were undertaken. In study 1, 10 male cyclists cycled in the heat for ∼2 h with (control) and without fluid replacement (dehydration) while internal and external carotid artery blood flow and core and blood temperature were obtained. Arterial and internal jugular venous blood samples were assessed with dehydration to evaluate CMRO2 . In study 2, in 8 male subjects, middle cerebral artery blood velocity was measured during prolonged exercise to exhaustion in both dehydrated and euhydrated states. After a rise at the onset of exercise, internal carotid artery flow declined to baseline with progressive dehydration (P < 0.05). However, cerebral metabolism remained stable through enhanced O2 and glucose extraction (P < 0.05). External carotid artery flow increased for 1 h but declined before exhaustion. Fluid ingestion maintained cerebral and extracranial perfusion throughout nonfatiguing exercise. During exhaustive exercise, however, euhydration delayed but did not prevent the decline in cerebral perfusion. In conclusion, during prolonged exercise in the heat, dehydration accelerates the decline in CBF without affecting CMRO2 and also restricts extracranial perfusion. Thus, fatigue is related to a reduction in CBF and extracranial perfusion rather than CMRO2 .

Correlation Between Pulpal and Carotid Arteries Blood Flow in Two Age Groups

Abstract Introduction Vascular network of dental pulp is supplied through common and external carotid artery and terminal dental branches that supply each pulp tissue. Age related changes of pulp tissue influence pulpal vascularization as well. The aim of this study was to compare and correlate pulpal and common and external carotid artery blood flow in young and middle age individuals of general population. Material and Methods Two groups of 10 participants were included in the study, young (20-25 years) and middle age (50-55 years) group. Pulpal blood flow (PBF) measurements on intact right and left upper central incisors were performed using laser Doppler flowmetry (LDF) method. Carotid arteries blood flow was assessed using carotid ultrasonography. Results PBF levels were significantly higher in young (3.11±0.67 and 3.46±1.11, right and left upper central incisors, respectively) compared to middle age (1.93±0.47 and 2.30±0.64, right and left upper central incisors, respectively) participants (independent sample t test; p&lt;0.05). There was no correlation between common and external carotid artery blood flow and upper central incisors PBF in young as well as middle age participants, for right or left side. Conclusion Absence of correlation between carotid arteries blood flow and PBF suggests that reduced PBF in middle age participants was probably not due to reduced blood supply from carotid arteries but it was result of age related changes at the level of pulpal blood vessels.

Increased carotid artery flow rate in a patient with Parry-Romberg syndrome

Parry-Romberg syndrome (PRS) is a rarely seen connective tissue disorder and is characterized by chronic inflammation of the face. Anti-nuclear antibodies, anti-extractable nuclear antigens and skin biopsy are helpful for diagnosis. In this study, we determined that the external carotid artery blood flow rate was faster on the affected side than on the unaffected side. We believe that patients suffering from PRS who also have central nervous system symptoms must be examined for vascular structure by Doppler ultrasonography, magnetic resonance imaging or conventional angiography.

Inhibitory effect of chronic oral treatment with fluoxetine on capsaicin-induced external carotid vasodilatation in anaesthetised dogs.

During migraine, capsaicin-sensitive trigeminal sensory nerves release calcitonin gene-related peptide (CGRP), resulting in cranial vasodilatation and central nociception. Moreover, 5-HT is involved in the pathophysiology of migraine and depression. Interestingly, some limited lines of evidence suggest that fluoxetine may be effective in migraine prophylaxis, but the underlying mechanisms are uncertain. Hence, this study investigated the canine external carotid vasodilator responses to capsaicin, α-CGRP and acetylcholine before and after acute and chronic oral treatment with fluoxetine. Forty-eight vagosympathectomised male mongrel dogs were prepared to measure blood pressure, heart rate and external carotid blood flow. The thyroid artery was cannulated for infusions of agonists. In 16 of these dogs, a spinal cannula was inserted (C1-C3) for infusions of 5-HT. The external carotid vasodilator responses to capsaicin, α-CGRP and acetylcholine remained unaffected after intracarotid or i.v. fluoxetine. In contrast, the vasodilator responses to capsaicin, but not those to α-CGRP or acetylcholine, were inhibited after chronic oral treatment with fluoxetine (300 µg/kg; for 90 days) or intrathecal 5-HT. Chronic oral fluoxetine inhibited capsaicin-induced external carotid vasodilatation, and this inhibition could partly explain its potential prophylactic antimigraine action.

Experimental and computational study on the effects of wearing neck collar on the carotid blood flow

Article history: Received September 6, 2014 Accepted 22 November 2014 Available online 23 December 2014 The effect of football neck collar on the right external carotid blood flow was investigated for ten healthy subjects using Echo-Doppler technique and computational fluid dynamics (CFD) approach. Carotid is in charge of blooding head’s parts including the brain and eyes. Hence, the evaluation of affected carotid flow by using neck collars is crucial for an improved ergonomic design. The testings were divided into three main categories; participants without wearing neck collar (Category 1), wearing neck collar (Category 2), and finally wearing neck collar with an embedded gap adjacent to the carotid artery position (Category 3). The experimental and numerical results revealed that wearing the neck collar (Category 2) reduced the average blood carotid flow by 28% compared to the case with no neck collar (Category 1). This average blood carotid flow reduction was improved by 15% when a gap separates the collar from the carotid artery position (Category 3). The results of this paper suggest a new design for the next generation of the neck collar by devising an appropriate gap near to carotid artery. The numerical results were validated and were in a reasonable agreement with the experimental data. © 2015 Growing Science Ltd. All rights reserved.

External carotid artery flow maintains near infrared spectroscopy-determined frontal lobe oxygenation during ephedrine administration

Phenylephrine and ephedrine affect frontal lobe oxygenation ([Formula: see text]) differently when assessed by spatially resolved near infrared spectroscopy. We evaluated the effect of phenylephrine and ephedrine on extra- vs intra-cerebral blood flow and on [Formula: see text]. In 10 healthy males (age 20-54 yr), phenylephrine or ephedrine was infused for an ∼20 mm Hg increase in mean arterial pressure. Cerebral oxygenation (SavO₂) was calculated from the arterial and jugular bulb oxygen saturations. Blood flow in the internal carotid artery (ICAf) and blood flow in the external carotid artery (ECAf) were assessed by duplex ultrasonography. Invos-5100c (SinvosO₂) and Foresight (SforeO₂) determined [Formula: see text] while forehead skin oxygenation (SskinO₂) was assessed. Phenylephrine reduced SforeO₂ by 6.9% (95% confidence interval: 4.8-9.0%; P<0.0001), SinvosO₂ by 10.5 (8.2-12.9%; P<0.0001), and ECAf (6-28%; P=0.0001), but increased ICAf (5-21%; P=0.003) albeit with no consequence for SskinO₂ or SavO₂. In contrast, SforeO₂ was maintained with administration of ephedrine while SinvosO₂ and SavO₂ decreased [by 3.1 (0.7-4.5%; P=0.017) and 2.1 (0.5-3.3%; P=0.012)] as arterial carbon dioxide pressure decreased (P=0.003). ICAf was stable and ECAf increased by 11 (4-18%; P=0.005) with administration of ephedrine while SskinO₂ did not change. The effect of phenylephrine on ScO₂ is governed by a decrease in external carotid blood flow since it increases cerebral blood flow as determined by flow in the internal carotid artery. In contrast, ScO₂ is largely maintained with administration of ephedrine because blood flow to extracerebral tissue increases.

English

&nbsp; High-volume intra- and extra cranial artery bypass surgery has been widely used, but it remains a difficult technique for most of surgeons. The objective of this study is to explore a training mode and platform. Six healthy dogs were divided into three groups at random. Twelve high-volume common carotid-external carotid bypasses were operated on both sides of six dogs (n=12). Digital subtraction angiography (DSA) and color Doppler sonography were taken to measure the hemodynamic parameters of grafts one week (n=4), four weeks (n=4) and 24 weeks (n=4) after the operations. The grafts were taken out for histopathological examination 24 weeks after the operations. The high-volume common carotid-external carotid bypass model (n=12) was successfully established in six dogs under microscope. Post-operative DSA in Week 1 (n=4), Week 4 (n=4) and Week 24 (n=4) showed bilateral external carotid blood flow was supplied by contralateral common carotid grafts. Both ends and the whole grafts were patent. Color Doppler sonography showed clearly that the blood flow volume of grafts was higher than 90 ml/min. Histopathological examination taken 24 weeks after the operations showed intimal hyperplasia of grafts. Dog model of high-volume common carotid-external carotid bypass has the advantages of similar material, high volume, similar blood pressure, feasible operation and high patent rate compared to the traditional microsurgery model, making it a better simulation training platform which is closer to the real surgical procedure for surgeons willing to master the technique of high-volume bypass operation. &nbsp; Key words: Dog, animal model, bypass, high-volume, vascular anastomosis.

Hyperthermia modulates regional differences in cerebral blood flow to changes in CO2.

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.

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