The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Anders Gould - One of the best experts on this subject based on the ideXlab platform.
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vessel length on snap mra and tof mra is a potential imaging biomarker for Brain Blood Flow
Magnetic Resonance Imaging, 2021Co-Authors: Anders Gould, Zhensen Chen, Duygu Baylam Geleri, Niranjan Balu, Zechen Zhou, Li Chen, Baocheng Chu, Kristi Pimentel, Gador CantonAbstract:Abstract Purpose To explore feasibility of using the vessel length on time-of-flight (TOF) or simultaneous non-contrast angiography and intraplaque hemorrhage (SNAP) MRA as an imaging biomarker for Brain Blood Flow, by using arterial spin labeling (ASL) perfusion imaging and 3D phase contrast (PC) quantitative Flow imaging as references. Methods In a population of thirty subjects with carotid atherosclerotic disease, the visible intracranial arteries on TOF and SNAP were semi-automatically traced and the total length of the distal segments was calculated with a dedicated software named iCafe. ASL Blood Flow was calculated automatically using the recommended hemodynamic model. PC Blood Flow was obtained by generating cross-sectional arterial images and semi-automatically drawing the lumen contours. Pearson correlation coefficients were used to assess the associations between the different whole-Brain or hemispheric Blood Flow measurements. Results Under the imaging protocol used in this study, TOF vessel length was larger than SNAP vessel length (P Conclusion The results suggest that length of the visible intracranial arteries on TOF or SNAP MRA can serve as a potential imaging marker for Brain Blood Flow.
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vessel length on snap mra and tof mra is a potential imaging biomarker for Brain Blood Flow
Magnetic Resonance Imaging, 2021Co-Authors: Anders Gould, Zhensen Chen, Duygu Baylam Geleri, Niranjan Balu, Zechen Zhou, Li Chen, Baocheng Chu, Kristi Pimentel, Gador Canton, Thomas S HatsukamiAbstract:PURPOSE To explore feasibility of using the vessel length on time-of-flight (TOF) or simultaneous non-contrast angiography and intraplaque hemorrhage (SNAP) MRA as an imaging biomarker for Brain Blood Flow, by using arterial spin labeling (ASL) perfusion imaging and 3D phase contrast (PC) quantitative Flow imaging as references. METHODS In a population of thirty subjects with carotid atherosclerotic disease, the visible intracranial arteries on TOF and SNAP were semi-automatically traced and the total length of the distal segments was calculated with a dedicated software named iCafe. ASL Blood Flow was calculated automatically using the recommended hemodynamic model. PC Blood Flow was obtained by generating cross-sectional arterial images and semi-automatically drawing the lumen contours. Pearson correlation coefficients were used to assess the associations between the different whole-Brain or hemispheric Blood Flow measurements. RESULTS Under the imaging protocol used in this study, TOF vessel length was larger than SNAP vessel length (P < 0.001). Both whole-Brain TOF and SNAP vessel length showed a correlation with whole Brain ASL and 3D PC Blood Flow measurements, and the correlation coefficients were higher for SNAP vessel length (TOF vs ASL: R = 0.554, P = 0.002; SNAP vs ASL: R = 0.711, P < 0.001; TOF vs 3D PC: R = 0.358, P = 0.052; SNAP vs 3D PC: R = 0.425, P = 0.019). Similar correlation results were observed for the hemispheric measurements. Hemispheric asymmetry index of SNAP vessel length also showed a significant correlation with hemispheric asymmetry index of ASL cerebral Blood Flow (R = 0.770, P < 0.001). CONCLUSION The results suggest that length of the visible intracranial arteries on TOF or SNAP MRA can serve as a potential imaging marker for Brain Blood Flow.
Hale Z Toklu - One of the best experts on this subject based on the ideXlab platform.
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the functional and structural changes in the basilar artery due to overpressure blast injury
Journal of Cerebral Blood Flow and Metabolism, 2015Co-Authors: Hale Z Toklu, Judy M Mullerdelp, Zhihui Yang, Payal Ghosh, Kevin H Strang, şehkar Oktay, Yasemin Sakarya, Michael D Delp, Philip J ScarpaceAbstract:Overpressure blast-wave induced Brain injury (OBI) leads to progressive pathophysiologic changes resulting in a reduction in Brain Blood Flow, Blood Brain barrier breakdown, edema, and cerebral ischemia. The aim of this study was to evaluate cerebral vascular function after single and repeated OBI. Male Sprague-Dawley rats were divided into three groups: Control (Naive), single OBI (30 psi peak pressure, 1 to 2 msec duration), and repeated (days 1, 4, and 7) OBI (r-OBI). Rats were killed 24 hours after injury and the basilar artery was isolated, cannulated, and pressurized (90 cm H2O). Vascular responses to potassium chloride (KCl) (30 to 100 mmol/L), endothelin-1 (10−12 to 10−7 mol/L), acetylcholine (ACh) (10−10 to 10−4 mol/L) and diethylamine-NONO-ate (DEA-NONO-ate) (10−10 to 10−4 mol/L) were evaluated. The OBI resulted in an increase in the contractile responses to endothelin and a decrease in the relaxant responses to ACh in both single and r-OBI groups. However, impaired DEA-NONO-ate-induced vasodilation and increased wall thickness to lumen ratio were observed only in the r-OBI group. The endothelin-1 type A (ETA) receptor and endothelial nitric oxide synthase (eNOS) immunoreactivity were significantly enhanced by OBI. These findings indicate that both single and r-OBI impairs cerebral vascular endothelium-dependent dilation, potentially a consequence of endothelial dysfunction and/or vascular remodelling in basilar arteries after OBI.
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the functional changes in the basilar artery due to overpressure blast injury 685 1
The FASEB Journal, 2014Co-Authors: Hale Z Toklu, Judy M Mullerdelp, Zhihui Yang, Payal Ghosh, Kevin H Strang, Philip J Scarpace, Kevin K W Wang, Nihal TumerAbstract:Overpressure blast-wave induced Brain injury (OBI) leads to progressive pathophysiological changes resulting in a reduction in Brain Blood Flow, Blood Brain barrier breakdown, edema and ischemia. The aim was to evaluate cerebral vascular function after single and repeated OBI. Male Sprague Dawley rats (250-300 g) were divided into 3 groups: Control (Naive), single OBI [30 psi peak pressure, 1-2 msec duration], and repeated (every three days) OBI (r-OBI). Rats were sacrificed 24 h post injury (8th day) and the basilar artery was cannulised in the pressurized system (90cm H2O). Vascular responses to KCl (30-50-100 mM) endothelin (10-11-10-7 M), acetylcholine (ACh) (10-9-10-4 M) and diethylamine (DEA)-NONO-ate (10-9-10-4 M) were evaluated. OBI resulted in an increase in the contractile responses to endothelin and a decrease in the relaxant responses to ACh in both single and repeated injury groups. However, impaired DEA-induced dilation and increased wall thickness to lumen ratio were observed only in the r-...
Gador Canton - One of the best experts on this subject based on the ideXlab platform.
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vessel length on snap mra and tof mra is a potential imaging biomarker for Brain Blood Flow
Magnetic Resonance Imaging, 2021Co-Authors: Anders Gould, Zhensen Chen, Duygu Baylam Geleri, Niranjan Balu, Zechen Zhou, Li Chen, Baocheng Chu, Kristi Pimentel, Gador CantonAbstract:Abstract Purpose To explore feasibility of using the vessel length on time-of-flight (TOF) or simultaneous non-contrast angiography and intraplaque hemorrhage (SNAP) MRA as an imaging biomarker for Brain Blood Flow, by using arterial spin labeling (ASL) perfusion imaging and 3D phase contrast (PC) quantitative Flow imaging as references. Methods In a population of thirty subjects with carotid atherosclerotic disease, the visible intracranial arteries on TOF and SNAP were semi-automatically traced and the total length of the distal segments was calculated with a dedicated software named iCafe. ASL Blood Flow was calculated automatically using the recommended hemodynamic model. PC Blood Flow was obtained by generating cross-sectional arterial images and semi-automatically drawing the lumen contours. Pearson correlation coefficients were used to assess the associations between the different whole-Brain or hemispheric Blood Flow measurements. Results Under the imaging protocol used in this study, TOF vessel length was larger than SNAP vessel length (P Conclusion The results suggest that length of the visible intracranial arteries on TOF or SNAP MRA can serve as a potential imaging marker for Brain Blood Flow.
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vessel length on snap mra and tof mra is a potential imaging biomarker for Brain Blood Flow
Magnetic Resonance Imaging, 2021Co-Authors: Anders Gould, Zhensen Chen, Duygu Baylam Geleri, Niranjan Balu, Zechen Zhou, Li Chen, Baocheng Chu, Kristi Pimentel, Gador Canton, Thomas S HatsukamiAbstract:PURPOSE To explore feasibility of using the vessel length on time-of-flight (TOF) or simultaneous non-contrast angiography and intraplaque hemorrhage (SNAP) MRA as an imaging biomarker for Brain Blood Flow, by using arterial spin labeling (ASL) perfusion imaging and 3D phase contrast (PC) quantitative Flow imaging as references. METHODS In a population of thirty subjects with carotid atherosclerotic disease, the visible intracranial arteries on TOF and SNAP were semi-automatically traced and the total length of the distal segments was calculated with a dedicated software named iCafe. ASL Blood Flow was calculated automatically using the recommended hemodynamic model. PC Blood Flow was obtained by generating cross-sectional arterial images and semi-automatically drawing the lumen contours. Pearson correlation coefficients were used to assess the associations between the different whole-Brain or hemispheric Blood Flow measurements. RESULTS Under the imaging protocol used in this study, TOF vessel length was larger than SNAP vessel length (P < 0.001). Both whole-Brain TOF and SNAP vessel length showed a correlation with whole Brain ASL and 3D PC Blood Flow measurements, and the correlation coefficients were higher for SNAP vessel length (TOF vs ASL: R = 0.554, P = 0.002; SNAP vs ASL: R = 0.711, P < 0.001; TOF vs 3D PC: R = 0.358, P = 0.052; SNAP vs 3D PC: R = 0.425, P = 0.019). Similar correlation results were observed for the hemispheric measurements. Hemispheric asymmetry index of SNAP vessel length also showed a significant correlation with hemispheric asymmetry index of ASL cerebral Blood Flow (R = 0.770, P < 0.001). CONCLUSION The results suggest that length of the visible intracranial arteries on TOF or SNAP MRA can serve as a potential imaging marker for Brain Blood Flow.
Ibrahim Humoud - One of the best experts on this subject based on the ideXlab platform.
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astrocytes monitor cerebral perfusion and control systemic circulation to maintain Brain Blood Flow
Nature Communications, 2020Co-Authors: Nephtali Marina, Isabel N Christie, Alla Korsak, Maxim Doronin, A R Brazhe, Patrick S Hosford, Jack A Wells, Shahriar Sheikhbahaei, Ibrahim HumoudAbstract:Astrocytes provide neurons with essential metabolic and structural support, modulate neuronal circuit activity and may also function as versatile surveyors of Brain milieu, tuned to sense conditions of potential metabolic insufficiency. Here we show that astrocytes detect falling cerebral perfusion pressure and activate CNS autonomic sympathetic control circuits to increase systemic arterial Blood pressure and heart rate with the purpose of maintaining Brain Blood Flow and oxygen delivery. Studies conducted in experimental animals (laboratory rats) show that astrocytes respond to acute decreases in Brain perfusion with elevations in intracellular [Ca2+]. Blockade of Ca2+-dependent signaling mechanisms in populations of astrocytes that reside alongside CNS sympathetic control circuits prevents compensatory increases in sympathetic nerve activity, heart rate and arterial Blood pressure induced by reductions in cerebral perfusion. These data suggest that astrocytes function as intracranial baroreceptors and play an important role in homeostatic control of arterial Blood pressure and Brain Blood Flow. The Brain receives 20% of cardiac output, but in accord with the current knowledge lacks a specialized sensor of its own Blood Flow. Here, the authors show that Brain astrocytes detect drops in perfusion and trigger compensatory increases in arterial pressure and heart rate to preserve Brain Blood Flow and oxygen delivery.
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astrocytes monitor cerebral perfusion and control systemic circulation to maintain Brain Blood Flow
Nature Communications, 2020Co-Authors: Nephtali Marina, Isabel N Christie, Alla Korsak, Maxim Doronin, A R Brazhe, Patrick S Hosford, Jack A Wells, Shahriar Sheikhbahaei, Ibrahim HumoudAbstract:Astrocytes provide neurons with essential metabolic and structural support, modulate neuronal circuit activity and may also function as versatile surveyors of Brain milieu, tuned to sense conditions of potential metabolic insufficiency. Here we show that astrocytes detect falling cerebral perfusion pressure and activate CNS autonomic sympathetic control circuits to increase systemic arterial Blood pressure and heart rate with the purpose of maintaining Brain Blood Flow and oxygen delivery. Studies conducted in experimental animals (laboratory rats) show that astrocytes respond to acute decreases in Brain perfusion with elevations in intracellular [Ca2+]. Blockade of Ca2+-dependent signaling mechanisms in populations of astrocytes that reside alongside CNS sympathetic control circuits prevents compensatory increases in sympathetic nerve activity, heart rate and arterial Blood pressure induced by reductions in cerebral perfusion. These data suggest that astrocytes function as intracranial baroreceptors and play an important role in homeostatic control of arterial Blood pressure and Brain Blood Flow.
Christopher K Willie - One of the best experts on this subject based on the ideXlab platform.
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regulation of Brain Blood Flow and oxygen delivery in elite breath hold divers
Journal of Cerebral Blood Flow and Metabolism, 2015Co-Authors: Christopher K Willie, David B Macleod, Philip N Ainslie, Ivan Drvis, Anthony R Bain, Dennis Madden, Petra Zubin Maslov, Zeljko DujicAbstract:The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral Blood Flow (CBF), arterial Blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers (n=17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing ('clamp') was then used to replicate an identical temporal pattern of decreasing arterial PO2 (PaO2) and increasing arterial PCO2 (PaCO2) while breathing. End-apnea PaO2 ranged from 23 to 37 mm Hg (30 ± 7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54 ± 24% versus 34 ± 26%, respectively; however, CBF increased similarly between apnea and clamp (93.6 ± 28% and 83.4 ± 38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the Brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.
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integrative regulation of human Brain Blood Flow
The Journal of Physiology, 2014Co-Authors: Christopher K Willie, Yuchieh Tzeng, Joseph A Fisher, Philip N AinslieAbstract:Herein, we review mechanisms regulating cerebral Blood Flow (CBF), with specific focus on humans. We revisit important concepts from the older literature and describe the interaction of various mechanisms of cerebrovascular control. We amalgamate this broad scope of information into a brief review, rather than detailing any one mechanism or area of research. The relationship between regulatory mechanisms is emphasized, but the following three broad categories of control are explicated: (1) the effect of Blood gases and neuronal metabolism on CBF; (2) buffering of CBF with changes in Blood pressure, termed cerebral autoregulation; and (3) the role of the autonomic nervous system in CBF regulation. With respect to these control mechanisms, we provide evidence against several canonized paradigms of CBF control. Specifically, we corroborate the following four key theses: (1) that cerebral autoregulation does not maintain constant perfusion through a mean arterial pressure range of 60–150 mmHg; (2) that there is important stimulatory synergism and regulatory interdependence of arterial Blood gases and Blood pressure on CBF regulation; (3) that cerebral autoregulation and cerebrovascular sensitivity to changes in arterial Blood gases are not modulated solely at the pial arterioles; and (4) that neurogenic control of the cerebral vasculature is an important player in autoregulatory function and, crucially, acts to buffer surges in perfusion pressure. Finally, we summarize the state of our knowledge with respect to these areas, outline important gaps in the literature and suggest avenues for future research.
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regional Brain Blood Flow in man during acute changes in arterial Blood gases
The Journal of Physiology, 2012Co-Authors: Christopher K Willie, David B Macleod, Kurt J Smith, Keita Ikeda, Andrew D Shaw, Yuchieh Tzeng, Neil D Eves, J Graham, Nia C S LewisAbstract:Despite the importance of Blood Flow on Brainstem control of respiratory and autonomic function, little is known about regional cerebral Blood Flow (CBF) during changes in arterial Blood gases.We quantified: (1) anterior and posterior CBF and reactivity through a wide range of steady-state changes in the partial pressures of CO2 (PaCO2) and O2 (PaO2) in arterial Blood, and (2) determined if the internal carotid artery (ICA) and vertebral artery (VA) change diameter through the same range.We used near-concurrent vascular ultrasound measures of Flow through the ICA and VA, and Blood velocity in their downstream arteries (the middle (MCA) and posterior (PCA) cerebral arteries). Part A (n =16) examined iso-oxic changes in PaCO2, consisting of three hypocapnic stages (PaCO2 =∼15, ∼20 and ∼30 mmHg) and four hypercapnic stages (PaCO2 =∼50, ∼55, ∼60 and ∼65 mmHg). In Part B (n =10), during isocapnia, PaO2 was decreased to ∼60, ∼44, and ∼35 mmHg and increased to ∼320 mmHg and ∼430 mmHg. Stages lasted ∼15 min. Intra-arterial pressure was measured continuously; arterial Blood gases were sampled at the end of each stage. There were three principal findings. (1) Regional reactivity: the VA reactivity to hypocapnia was larger than the ICA, MCA and PCA; hypercapnic reactivity was similar.With profound hypoxia (35 mmHg) the relative increase in VA Flow was 50% greater than the other vessels. (2) Neck vessel diameters: changes in diameter (∼25%) of the ICA was positively related to changes in PaCO2 (R2, 0.63±0.26; P<0.05); VA diameter was unaltered in response to changed PaCO2 but yielded a diameter increase of +9% with severe hypoxia. (3) Intra- vs. extra-cerebral measures: MCA and PCA Blood velocities yielded smaller reactivities and estimates of Flow than VA and ICA Flow. The findings respectively indicate: (1) disparate Blood Flow regulation to the Brainstem and cortex; (2) cerebrovascular resistance is not solely modulated at the level of the arteriolar pial vessels; and (3) transcranial Doppler ultrasound may underestimate measurements of CBF during extreme hypoxia and/or hypercapnia.
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reductions in cerebral Blood Flow during passive heat stress in humans partitioning the mechanisms
The Journal of Physiology, 2011Co-Authors: Michael D Nelson, Christopher K Willie, Kurt J Smith, Mark J Haykowsky, Michael K Stickland, Luis Altamiranodiaz, Stewart R Petersen, Philip N AinslieAbstract:Non-technical summary Heat stress reduces Brain Blood Flow and impairs orthostatic tolerance. Brain Blood Flow is largely controlled by the partial pressure of arterial . Indeed, hyperthermia-induced over-breathing and related reductions in arterial account for ∼50% of the reduction in Brain Blood Flow. This investigation tested the unique hypothesis that the distribution of cardiac output during heat stress (challenged by thermoregulatory increases in skin Blood Flow and sweat loss) contributes to the remaining 50%. We show that cardiac output is not related to Brain Blood Flow, but rather arterial plays a much larger role than previously suggested. These findings help us understand the mechanisms relating heat stress with an increased likelihood of fainting, and are also relevant to pathological conditions that are accompanied by elevations in body temperature.