The Experts below are selected from a list of 6117 Experts worldwide ranked by ideXlab platform
Andreas A Linninger - One of the best experts on this subject based on the ideXlab platform.
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mathematical synthesis of the cortical circulation for the whole mouse brain part ii microcirculatory closure
Microcirculation, 2021Co-Authors: Grant Hartung, David Kleinfeld, Shoale Badr, Samuel A Mihelic, Andrew K Dunn, Xiaojun Cheng, Sreekanth Kura, David A Boas, Ali Alaraj, Andreas A LinningerAbstract:Recent advancements in multiphoton imaging and vascular reconstruction algorithms have increased the amount of data on cerebrovascular circulation for statistical analysis and hemodynamic simulations. Experimental observations offer fundamental insights into Capillary network topology but mainly within a narrow field of view typically spanning a small fraction of the cortical surface (less than 2%). In contrast, larger-resolution imaging modalities, such as computed tomography (CT) or magnetic resonance imaging (MRI), have whole-brain coverage but capture only larger blood vessels, overlooking the microscopic Capillary Bed. To integrate data acquired at multiple length scales with different neuroimaging modalities and to reconcile brain-wide macroscale information with microscale multiphoton data, we developed a method for synthesizing hemodynamically equivalent vascular networks for the entire cerebral circulation. This computational approach is intended to aid in the quantification of patterns of cerebral blood flow and metabolism for the entire brain. In part I, we descriBed the mathematical framework for image-guided generation of synthetic vascular networks covering the large cerebral arteries from the circle of Willis through the pial surface network leading back to the venous sinuses. Here in part II, we introduce novel procedures for creating microcirculatory closure that mimics a realistic Capillary Bed. We demonstrate our capability to synthesize synthetic vascular networks whose morphometrics match empirical network graphs from three independent state-of-the-art imaging laboratories using different image acquisition and reconstruction protocols. We also successfully synthesized twelve vascular networks of a complete mouse brain hemisphere suitable for performing whole-brain blood flow simulations. Synthetic arterial and venous networks with microvascular closure allow whole-brain hemodynamic predictions. Simulations across all length scales will potentially illuminate organ-wide supply and metabolic functions that are inaccessible to models reconstructed from image data with limited spatial coverage.
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the Capillary Bed offers the largest hemodynamic resistance to the cortical blood supply
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Ian Gopal Gould, Philbert S Tsai, David Kleinfeld, Andreas A LinningerAbstract:The cortical angioarchitecture is a key factor in controlling cerebral blood flow and oxygen metabolism. Difficulties in imaging the complex microanatomy of the cortex have so far restricted insigh...
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the Capillary Bed offers the largest hemodynamic resistance to the cortical blood supply
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Ian Gopal Gould, Philbert S Tsai, David Kleinfeld, Andreas A LinningerAbstract:The cortical angioarchitecture is a key factor in controlling cerebral blood flow and oxygen metabolism. Difficulties in imaging the complex microanatomy of the cortex have so far restricted insight about blood flow distribution in the microcirculation. A new methodology combining advanced microscopy data with large scale hemodynamic simulations enabled us to quantify the effect of the angioarchitecture on the cerebral microcirculation. High-resolution images of the mouse primary somatosensory cortex were input into with a comprehensive computational model of cerebral perfusion and oxygen supply ranging from the pial vessels to individual brain cells. Simulations of blood flow, hematocrit and oxygen tension show that the wide variation of hemodynamic states in the tortuous, randomly organized Capillary Bed is responsible for relatively uniform cortical tissue perfusion and oxygenation. Computational analysis of microcirculatory blood flow and pressure drops further indicates that the Capillary Bed, including capillaries adjacent to feeding arterioles (d < 10 µm), are the largest contributors to hydraulic resistance.
David Kleinfeld - One of the best experts on this subject based on the ideXlab platform.
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mathematical synthesis of the cortical circulation for the whole mouse brain part ii microcirculatory closure
Microcirculation, 2021Co-Authors: Grant Hartung, David Kleinfeld, Shoale Badr, Samuel A Mihelic, Andrew K Dunn, Xiaojun Cheng, Sreekanth Kura, David A Boas, Ali Alaraj, Andreas A LinningerAbstract:Recent advancements in multiphoton imaging and vascular reconstruction algorithms have increased the amount of data on cerebrovascular circulation for statistical analysis and hemodynamic simulations. Experimental observations offer fundamental insights into Capillary network topology but mainly within a narrow field of view typically spanning a small fraction of the cortical surface (less than 2%). In contrast, larger-resolution imaging modalities, such as computed tomography (CT) or magnetic resonance imaging (MRI), have whole-brain coverage but capture only larger blood vessels, overlooking the microscopic Capillary Bed. To integrate data acquired at multiple length scales with different neuroimaging modalities and to reconcile brain-wide macroscale information with microscale multiphoton data, we developed a method for synthesizing hemodynamically equivalent vascular networks for the entire cerebral circulation. This computational approach is intended to aid in the quantification of patterns of cerebral blood flow and metabolism for the entire brain. In part I, we descriBed the mathematical framework for image-guided generation of synthetic vascular networks covering the large cerebral arteries from the circle of Willis through the pial surface network leading back to the venous sinuses. Here in part II, we introduce novel procedures for creating microcirculatory closure that mimics a realistic Capillary Bed. We demonstrate our capability to synthesize synthetic vascular networks whose morphometrics match empirical network graphs from three independent state-of-the-art imaging laboratories using different image acquisition and reconstruction protocols. We also successfully synthesized twelve vascular networks of a complete mouse brain hemisphere suitable for performing whole-brain blood flow simulations. Synthetic arterial and venous networks with microvascular closure allow whole-brain hemodynamic predictions. Simulations across all length scales will potentially illuminate organ-wide supply and metabolic functions that are inaccessible to models reconstructed from image data with limited spatial coverage.
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the Capillary Bed offers the largest hemodynamic resistance to the cortical blood supply
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Ian Gopal Gould, Philbert S Tsai, David Kleinfeld, Andreas A LinningerAbstract:The cortical angioarchitecture is a key factor in controlling cerebral blood flow and oxygen metabolism. Difficulties in imaging the complex microanatomy of the cortex have so far restricted insigh...
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the Capillary Bed offers the largest hemodynamic resistance to the cortical blood supply
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Ian Gopal Gould, Philbert S Tsai, David Kleinfeld, Andreas A LinningerAbstract:The cortical angioarchitecture is a key factor in controlling cerebral blood flow and oxygen metabolism. Difficulties in imaging the complex microanatomy of the cortex have so far restricted insight about blood flow distribution in the microcirculation. A new methodology combining advanced microscopy data with large scale hemodynamic simulations enabled us to quantify the effect of the angioarchitecture on the cerebral microcirculation. High-resolution images of the mouse primary somatosensory cortex were input into with a comprehensive computational model of cerebral perfusion and oxygen supply ranging from the pial vessels to individual brain cells. Simulations of blood flow, hematocrit and oxygen tension show that the wide variation of hemodynamic states in the tortuous, randomly organized Capillary Bed is responsible for relatively uniform cortical tissue perfusion and oxygenation. Computational analysis of microcirculatory blood flow and pressure drops further indicates that the Capillary Bed, including capillaries adjacent to feeding arterioles (d < 10 µm), are the largest contributors to hydraulic resistance.
Ian Gopal Gould - One of the best experts on this subject based on the ideXlab platform.
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the Capillary Bed offers the largest hemodynamic resistance to the cortical blood supply
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Ian Gopal Gould, Philbert S Tsai, David Kleinfeld, Andreas A LinningerAbstract:The cortical angioarchitecture is a key factor in controlling cerebral blood flow and oxygen metabolism. Difficulties in imaging the complex microanatomy of the cortex have so far restricted insigh...
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the Capillary Bed offers the largest hemodynamic resistance to the cortical blood supply
Journal of Cerebral Blood Flow and Metabolism, 2017Co-Authors: Ian Gopal Gould, Philbert S Tsai, David Kleinfeld, Andreas A LinningerAbstract:The cortical angioarchitecture is a key factor in controlling cerebral blood flow and oxygen metabolism. Difficulties in imaging the complex microanatomy of the cortex have so far restricted insight about blood flow distribution in the microcirculation. A new methodology combining advanced microscopy data with large scale hemodynamic simulations enabled us to quantify the effect of the angioarchitecture on the cerebral microcirculation. High-resolution images of the mouse primary somatosensory cortex were input into with a comprehensive computational model of cerebral perfusion and oxygen supply ranging from the pial vessels to individual brain cells. Simulations of blood flow, hematocrit and oxygen tension show that the wide variation of hemodynamic states in the tortuous, randomly organized Capillary Bed is responsible for relatively uniform cortical tissue perfusion and oxygenation. Computational analysis of microcirculatory blood flow and pressure drops further indicates that the Capillary Bed, including capillaries adjacent to feeding arterioles (d < 10 µm), are the largest contributors to hydraulic resistance.
Ying Zheng - One of the best experts on this subject based on the ideXlab platform.
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increased oxygen consumption following activation of brain theoretical footnotes using spectroscopic data from barrel cortex
NeuroImage, 2001Co-Authors: John E W Mayhew, David Johnston, John Martindale, Myles Jones, Jason Berwick, Ying ZhengAbstract:Optical imaging spectroscopy (OIS) and laser Doppler flowmetry (LDF) data sequences from anesthetized rats were used to determine the relationship between changes in oxy-and deoxygenated hemoglobin concentration and changes in blood volume and flow in the presence and absence of stimulation. The data from Jones et al. (accompanying paper) were used to explore the differences between two theoretical models of flow activation coupling. The essential difference between the two models is the extension of the model of Buxton and Frank by Hyder et al. (1998, J. Appl. Physiol. 85: 554–564) to incorporate change in Capillary diffusivity coupled to flow. In both models activation-increased flow changes increase oxygen transport from the Capillary; however, in Hyder et al.'s model the diffusivity of the Capillary itself is increased. Hyder et al. proposed a parameter (Ω), a scaling “constant” linking increased blood flow and oxygen “diffusivity” in the Capillary Bed. Thus, in Buxton and Frank's theory, Ω = 0; i.e., there are no changes in diffusivity. In Hyder et al.'s theory, 0 < Ω < 1, and changes in diffusivity are assumed to be linearly related to flow changes. We elaborate the theoretical position of both models to show that, in principle, the different predictions from the two theories can be evaluated using optical imaging spectroscopy data. We find that both theoretical positions have limitations when applied to data from brief stimulation and when applied to data from mild hypercapnia. In summary, the analysis showed that although Hyder et al.'s proposal that diffusivity increased during activation did occur; it was shown to arise from an implementation of Buxton and Frank's theory under episodes of brief stimulation. The results also showed that the scaling parameter Ω is not a constant as the Hyder et al. model entails but in fact varies over the time course of the flow changes. Data from experiments in which mild hypercapnia was administered also indicated changes in the diffusivity of the Capillary Bed, but in this case the changes were negative; i.e., oxygen transport from the Capillary decreased relative to baseline under hypercapnia. Neither of the models could account for the differences between the hypercapnia and activation data when matched for equivalent flow changes. A modification to the models to allow non-null tissue oxygen concentrations that can be moderated by changes due to increased metabolic demand following increased neural activity is proposed. This modification would allow modulation of oxygen transport from the Capillary Bed (e.g., changes in diffusivity) by tissue oxygen tension and would allow a degree of decoupling of flow and oxygen delivery, which can encompass both the data from stimulation and from hypercapnia.
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increased oxygen consumption following activation of brain theoretical footnotes using spectroscopic data from barrel cortex
NeuroImage, 2001Co-Authors: John E W Mayhew, David Johnston, John Martindale, Myles Jones, Jason Berwick, Ying ZhengAbstract:Optical imaging spectroscopy (OIS) and laser Doppler flowmetry (LDF) data sequences from anesthetized rats were used to determine the relationship between changes in oxy-and deoxygenated hemoglobin concentration and changes in blood volume and flow in the presence and absence of stimulation. The data from Jones et al. (accompanying paper) were used to explore the differences between two theoretical models of flow activation coupling. The essential difference between the two models is the extension of the model of Buxton and Frank by Hyder et al. (1998, J. Appl. Physiol. 85: 554--564) to incorporate change in Capillary diffusivity coupled to flow. In both models activation-increased flow changes increase oxygen transport from the Capillary; however, in Hyder et al.'s model the diffusivity of the Capillary itself is increased. Hyder et al. proposed a parameter (Omega), a scaling "constant" linking increased blood flow and oxygen "diffusivity" in the Capillary Bed. Thus, in Buxton and Frank's theory, Omega = 0; i.e., there are no changes in diffusivity. In Hyder et al.'s theory, 0 < Omega < 1, and changes in diffusivity are assumed to be linearly related to flow changes. We elaborate the theoretical position of both models to show that, in principle, the different predictions from the two theories can be evaluated using optical imaging spectroscopy data. We find that both theoretical positions have limitations when applied to data from brief stimulation and when applied to data from mild hypercapnia. In summary, the analysis showed that although Hyder et al.'s proposal that diffusivity increased during activation did occur; it was shown to arise from an implementation of Buxton and Frank's theory under episodes of brief stimulation. The results also showed that the scaling parameter Omega is not a constant as the Hyder et al. model entails but in fact varies over the time course of the flow changes. Data from experiments in which mild hypercapnia was administered also indicated changes in the diffusivity of the Capillary Bed, but in this case the changes were negative; i.e., oxygen transport from the Capillary decreased relative to baseline under hypercapnia. Neither of the models could account for the differences between the hypercapnia and activation data when matched for equivalent flow changes. A modification to the models to allow non-null tissue oxygen concentrations that can be moderated by changes due to increased metabolic demand following increased neural activity is proposed. This modification would allow modulation of oxygen transport from the Capillary Bed (e.g., changes in diffusivity) by tissue oxygen tension and would allow a degree of decoupling of flow and oxygen delivery, which can encompass both the data from stimulation and from hypercapnia.
Klaus Addicks - One of the best experts on this subject based on the ideXlab platform.
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anabolic steroids impair the exercise induced growth of the cardiac Capillary Bed
International Journal of Sports Medicine, 2000Co-Authors: Christos V M Tagarakis, G. Hartmann, Wildor Hollmann, Wilhelm Bloch, Klaus AddicksAbstract:BACKGROUND Concomitant application of anabolic-androgenic steroids and physical exercise can induce cardiac hypertrophy. These experiments investigate the still unknown response of the cardiac myocytes and capillaries to the combined influence of various anabolic steroids and muscular exercise. METHODS Female SPF-NMRI mice were divided into the following groups: a) sedentary control, b) exercise (treadmill running); c) sedentary receiving Dianabol; d) exercise + Dianabol; e) exercise + Oral-Turinabol. After 3 and 6 weeks the left ventricular papillary muscles were studied morphometrically. Evaluated variables: minimal myocyte diameter, number of capillaries around a single myocyte, Capillary density and interCapillary distance. RESULTS Only the anabolic steroids + exercise groups showed a mild myocyte hypertrophy. In contrast, only exercise alone caused a significant increase of the Capillary density after both experimental periods; e.g. Capillary density after 6 weeks (capillaries/mm2, mean values +/- standard deviation, p < 0.05): control (4,272 +/- 287), exercise (5411 +/- 755), dianabol (4,004 +/- 333), dianabol + exercise (4,076 +/- 403), oral-turinabol + exercise (4,053 +/- 306). Moreover, unlike all other regimens, only exercise alone shortened the interCapillary distance. Finally, exercise without drugs induced the greatest increase in the number of capillaries around a single myocyte. CONCLUSIONS Anabolic steroids combined with exercise: 1) induce mild hypertrophy of the cardiac myocytes, 2) impair the cardiac microvascular adaptation to physical conditioning. The microvascular impairment may cause a detrimental alteration of the myocardial oxygen supply, especially during muscular exercise.
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testosterone propionate impairs the response of the cardiac Capillary Bed to exercise
Medicine and Science in Sports and Exercise, 2000Co-Authors: Christos V M Tagarakis, G. Hartmann, Wildor Hollmann, Wilhelm Bloch, Klaus AddicksAbstract:OBJECTIVE: Experimental application of anabolic-androgenic steroids and exercise training induce cardiac hypertrophy. This study quantifies for the first time, on microscopical level, the adaptation of the cardiac capillaries and myocytes to the concomitant application of testosterone-propionate and exercise training. METHODS: Female SPF-NMRI mice were studied over 3 and 6 wk. Experimental groups: (i) sedentary control (C); (ii) exercise (treadmill running, E); (iii) testosterone-propionate (TP); and (iv) testosterone-propionate+exercise (TPE). Morphometric parameters: 1) papillary muscles: Capillary density, interCapillary distance, number of capillaries around a myocyte, and minimal myocyte diameter; and 2) left ventricular wall: Capillary density and interCapillary distance. RESULTS: Papillary muscle: A striking suppression of the exercise-induced improvement in Capillary supply occurs in the testosterone-propionate+exercise groups over 3 and 6 wk. Exercise without drugs increases significantly (P < 0.05) the Capillary density, shortens significantly (P < 0.05) the interCapillary distance, whereas it increases the number of capillaries around a myocyte. These alterations are not observed in the testosterone-propionate treated sedentary animals; e.g., Capillary density after 6 wk (mean values +/- standard deviation, capillaries x mm(-2)): C: 4272 +/- 287, E: 5411 +/- 758, TP: 4221 +/- 364, and TPE: 3997 +/- 397. Moreover, only in the testosterone-propionate+exercise groups occurs a mild myocyte hypertrophy after both time periods: there is a trend toward hypertrophy (P < 0.1) in comparison with the C groups and a significant hypertrophy (P < 0.05) in comparison with the E groups. CONCLUSIONS: Testosterone-propionate profoundly inhibits the exercise-induced augmented capillarization, whereas (under training conditions) it leads to a mild myocyte hypertrophy. The microvascular impairment could trigger an imbalance between the myocardial oxygen supply and demand, especially during physical exercise.
