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Автор: Grafiati
Опубліковано: 7 липня 2024

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1

Wang, Xin, Caio Seguin, Andrew Zalesky, Wan-wa Wong, Winnie Chiu-wing Chu, and Raymond Kai-yu Tong. "Synchronization lag in post stroke: relation to motor function and structural connectivity." Network Neuroscience 3, no. 4 (January 2019): 1121–40. http://dx.doi.org/10.1162/netn_a_00105.

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Stroke is characterized by delays in the resting-state hemodynamic response, resulting in synchronization lag in neural activity between brain regions. However, the structural basis of this lag remains unclear. In this study, we used resting-state functional MRI (rs-fMRI) to characterize synchronization lag profiles between homotopic regions in 15 individuals (14 males, 1 female) with brain lesions consequent to stroke as well as a group of healthy comparison individuals. We tested whether the network communication efficiency of each individual’s structural brain network (connectome) could explain interindividual and interregional variation in synchronization lag profiles. To this end, connectomes were mapped using diffusion MRI data, and communication measures were evaluated under two schemes: shortest paths and navigation. We found that interindividual variation in synchronization lags was inversely associated with communication efficiency under both schemes. Interregional variation in lag was related to navigation efficiency and navigation distance, reflecting its dependence on both distance and structural constraints. Moreover, severity of motor deficits significantly correlated with average synchronization lag in stroke. Our results provide a structural basis for the delay of information transfer between homotopic regions inferred from rs-fMRI and provide insight into the clinical significance of structural-functional relationships in stroke individuals.
2

Braban, Andra, Robert Leech, Kevin Murphy, and Fatemeh Geranmayeh. "Cerebrovascular Reactivity Has Negligible Contribution to Hemodynamic Lag After Stroke: Implications for Functional Magnetic Resonance Imaging Studies." Stroke 54, no. 4 (April 2023): 1066–77. http://dx.doi.org/10.1161/strokeaha.122.041880.

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Background: Functional magnetic resonance imaging (fMRI) is ubiquitously used to study poststroke recovery. However, the fMRI–derived hemodynamic responses are vulnerable to vascular insult which can result in reduced magnitude and temporal delays (lag) in the hemodynamic response function (HRF). The cause of HRF lag remains controversial, and a better understanding of it is required to ensure accurate interpretation of poststroke fMRI studies. In this longitudinal study, we investigate the relationship between hemodynamic lag and cerebrovascular reactivity (CVR) following stroke. Methods: Voxel-wise lag maps were calculated relative to a mean gray matter reference signal for 27 healthy controls and 59 patients with stroke across 2 time points (≈2 weeks and ≈4 months poststroke) and 2 conditions: resting-state and breath-holding. The breath-holding condition was additionally used to calculate CVR in response to hypercapnia. HRF lag was computed for both conditions across tissue compartments: lesion, perilesional tissue, unaffected tissue of the lesioned hemisphere, and their homolog regions in the unaffected hemisphere. CVR and lag maps were correlated. Group, condition, and time effects were assessed using ANOVA analyses. Results: Compared with the average gray matter signal, a relative hemodynamic lead was observed in the primary sensorimotor cortices in resting-state and bilateral inferior parietal cortices in the breath-holding condition. Whole-brain hemodynamic lag was significantly correlated across conditions irrespective of group, with regional differences across conditions suggestive of a neural network pattern. Patients showed relative lag in the lesioned hemisphere which significantly reduced over time. Breath-hold derived lag and CVR had no significant voxel-wise correlation in controls, or patients within the lesioned hemisphere or the homologous regions of the lesion and perilesional tissue in the right hemisphere (mean r <0.1). Conclusions: The contribution of altered CVR to HRF lag was negligible. We suggest that HRF lag is largely independent of CVR, and could partly reflect intrinsic neural network dynamics among other factors.
3

Rindler, Tara N., Valerie M. Lasko, Michelle L. Nieman, Motoi Okada, John N. Lorenz та Jerry B. Lingrel. "Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction". American Journal of Physiology-Heart and Circulatory Physiology 304, № 8 (15 квітня 2013): H1147—H1158. http://dx.doi.org/10.1152/ajpheart.00594.2012.

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The α2-isoform of the Na,K-ATPase (α2) is the minor isoform of the Na,K-ATPase expressed in the cardiovascular system and is thought to play a critical role in the regulation of cardiovascular hemodynamics. However, the organ system/cell type expressing α2 that is required for this regulation has not been fully defined. The present study uses a heart-specific knockout of α2 to further define the tissue-specific role of α2 in the regulation of cardiovascular hemodynamics. To accomplish this, we developed a mouse model using the Cre/loxP system to generate a tissue-specific knockout of α2 in the heart using β-myosin heavy chain Cre. We have achieved a 90% knockout of α2 expression in the heart of the knockout mice. Interestingly, the heart-specific knockout mice exhibit normal basal cardiac function and systolic blood pressure, and in addition, these mice develop ACTH-induced hypertension in response to ACTH treatment similar to control mice. Surprisingly, the heart-specific knockout mice display delayed onset of cardiac dysfunction compared with control mice in response to pressure overload induced by transverse aortic constriction; however, the heart-specific knockout mice deteriorated to control levels by 9 wk post-transverse aortic constriction. These results suggest that heart expression of α2 does not play a role in the regulation of basal cardiovascular function or blood pressure; however, heart expression of α2 plays a role in the hypertrophic response to pressure overload. This study further emphasizes that the tissue localization of α2 determines its unique roles in the regulation of cardiovascular function.
4

van Meer, Maurits PA, Kajo van der Marel, Jan Willem Berkelbach van der Sprenkel, and Rick M. Dijkhuizen. "MRI of bilateral sensorimotor network activation in response to direct intracortical stimulation in rats after unilateral stroke." Journal of Cerebral Blood Flow & Metabolism 31, no. 7 (April 27, 2011): 1583–87. http://dx.doi.org/10.1038/jcbfm.2011.61.

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Reinstatement of perilesional activation and connectivity may underlie functional recovery after stroke. To measure activation responsiveness in perilesional cortex in relation to white matter integrity, we performed functional functional magnetic resonance imaging during stimulation of the contralesional cortex, together with diffusion tensor imaging, 3 and 28 days after stroke in rats. Despite disturbed sensorimotor function and abnormal callosal appearance at day 3, activation amplitudes were preserved in the perilesional sensorimotor cortex, although time-to-peak was significantly delayed. This indicates that in spite of dysfunction, perilesional cortical tissue can be activated subacutely after stroke, while delay of the hemodynamic activation response suggests impaired neurovascular coupling.
5

Medeiros, Júlio, Marco Simões, João Castelhano, Rodolfo Abreu, Ricardo Couceiro, Jorge Henriques, Miguel Castelo-Branco, Henrique Madeira, César Teixeira, and Paulo de Carvalho. "EEG as a potential ground truth for the assessment of cognitive state in software development activities: A multimodal imaging study." PLOS ONE 19, no. 3 (March 7, 2024): e0299108. http://dx.doi.org/10.1371/journal.pone.0299108.

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Cognitive human error and recent cognitive taxonomy on human error causes of software defects support the intuitive idea that, for instance, mental overload, attention slips, and working memory overload are important human causes for software bugs. In this paper, we approach the EEG as a reliable surrogate to MRI-based reference of the programmer’s cognitive state to be used in situations where heavy imaging techniques are infeasible. The idea is to use EEG biomarkers to validate other less intrusive physiological measures, that can be easily recorded by wearable devices and useful in the assessment of the developer’s cognitive state during software development tasks. Herein, our EEG study, with the support of fMRI, presents an extensive and systematic analysis by inspecting metrics and extracting relevant information about the most robust features, best EEG channels and the best hemodynamic time delay in the context of software development tasks. From the EEG-fMRI similarity analysis performed, we found significant correlations between a subset of EEG features and the Insula region of the brain, which has been reported as a region highly related to high cognitive tasks, such as software development tasks. We concluded that despite a clear inter-subject variability of the best EEG features and hemodynamic time delay used, the most robust and predominant EEG features, across all the subjects, are related to the Hjorth parameter Activity and Total Power features, from the EEG channels F4, FC4 and C4, and considering in most of the cases a hemodynamic time delay of 4 seconds used on the hemodynamic response function. These findings should be taken into account in future EEG-fMRI studies in the context of software debugging.
6

Yoshie, Koji, Pradeep S. Rajendran, Louis Massoud, OhJin Kwon, Vasudev Tadimeti, Siamak Salavatian, Jeffrey L. Ardell, Kalyanam Shivkumar, and Olujimi A. Ajijola. "Cardiac vanilloid receptor-1 afferent depletion enhances stellate ganglion neuronal activity and efferent sympathetic response to cardiac stress." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 5 (May 1, 2018): H954—H966. http://dx.doi.org/10.1152/ajpheart.00593.2017.

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Afferent fibers expressing the vanilloid receptor 1 (VR1) channel have been implicated in cardiac nociception; however, their role in modulating reflex responses to cardiac stress is not well understood. We evaluated this role in Yorkshire pigs by percutaneous epicardial application of resiniferatoxin (RTX), a toxic activator of the VR1 channel, resulting in the depletion of cardiac VR1-expressing afferents. Hemodynamics, epicardial activation recovery intervals, and in vivo activity of stellate ganglion neurons (SGNs) were recorded in control and RTX-treated animals. Stressors included inferior vena cava or aortic occlusion and rapid right ventricular pacing (RVP) to induce dyssynchrony and ischemia. In the epicardium, stellate ganglia, and dorsal root ganglia, immunostaining for the VR1 channel, calcitonin gene-related peptide, and substance P was significantly diminished by RTX. RTX-treated animals exhibited higher basal systolic blood pressures and contractility than control animals. Reflex responses to epicardial bradykinin and capsaicin were mitigated by RTX. Cardiovascular reflex function, as assessed by inferior vena cava or aortic occlusion, was similar in RTX-treated versus control animals. RTX-treated animals exhibited resistance to hemodynamic collapse induced by RVP. Activation recovery interval shortening during RVP, a marker of cardiac sympathetic outflow, was greater in RTX-treated animals and exhibited significant delay in returning to baseline values after cessation of RVP. The basal firing rate of SGNs and firing rates in response to RVP were also greater in RTX-treated animals, as was the SGN network activity in response to cardiac stressors. These data suggest that elimination of cardiac nociceptive afferents reorganizes the central-peripheral nervous system interaction to enhance cardiac sympathetic outflow. NEW & NOTEWORTHY Our work demonstrates a role for cardiac vanilloid receptor-1-expressing afferents in reflex processing of cardiovascular stress. Current understanding suggests that elimination of vanilloid receptor-1 afferents would decrease reflex cardiac sympathetic outflow. We found, paradoxically, that sympathetic outflow to the heart is instead enhanced at baseline and during cardiac stress.
7

Chen, Xiaoxiao, Javier A. Sala-Mercado, Robert L. Hammond, Masashi Ichinose, Soroor Soltani, Ramakrishna Mukkamala, and Donal S. O'Leary. "Dynamic control of maximal ventricular elastance via the baroreflex and force-frequency relation in awake dogs before and after pacing-induced heart failure." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 1 (July 2010): H62—H69. http://dx.doi.org/10.1152/ajpheart.00922.2009.

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We investigated to what extent maximal ventricular elastance ( Emax) is dynamically controlled by the arterial baroreflex and force-frequency relation in conscious dogs and to what extent these mechanisms are attenuated after the induction of heart failure (HF). We mathematically analyzed spontaneous beat-to-beat hemodynamic variability. First, we estimated Emax for each beat during a baseline period using the ventricular unstressed volume determined with the traditional multiple beat method during vena cava occlusion. We then jointly identified the transfer functions (system gain value and time delay per frequency) relating beat-to-beat fluctuations in arterial blood pressure (ABP) to Emax (ABP→ Emax) and beat-to-beat fluctuations in heart rate (HR) to Emax (HR→ Emax) to characterize the dynamic properties of the arterial baroreflex and force-frequency relation, respectively. During the control condition, the ABP→ Emax transfer function revealed that ABP perturbations caused opposite direction Emax changes with a gain value of −0.023 ± 0.012 ml−1, whereas the HR→ Emax transfer function indicated that HR alterations caused same direction Emax changes with a gain value of 0.013 ± 0.005 mmHg·ml−1·(beats/min)−1. Both transfer functions behaved as low-pass filters. However, the ABP→ Emax transfer function was more sluggish than the HR→ Emax transfer function with overall time constants (indicator of full system response time to a sudden input change) of 11.2 ± 2.8 and 1.7 ± 0.5 s ( P < 0.05), respectively. During the HF condition, the ABP→ Emax and HR→ Emax transfer functions were markedly depressed with gain values reduced to −0.0002 ± 0.007 ml−1 and −0.001 ± 0.004 mmHg·ml−1·(beats/min)−1 ( P < 0.1). Emax is rapidly and significantly controlled at rest, but this modulation is virtually abolished in HF.
8

Feige, Bernd, Klaus Scheffler, Fabrizio Esposito, Francesco Di Salle, Jürgen Hennig, and Erich Seifritz. "Cortical and Subcortical Correlates of Electroencephalographic Alpha Rhythm Modulation." Journal of Neurophysiology 93, no. 5 (May 2005): 2864–72. http://dx.doi.org/10.1152/jn.00721.2004.

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Neural correlates of electroencephalographic (EEG) alpha rhythm are poorly understood. Here, we related EEG alpha rhythm in awake humans to blood-oxygen-level-dependent (BOLD) signal change determined by functional magnetic resonance imaging (fMRI). Topographical EEG was recorded simultaneously with fMRI during an open versus closed eyes and an auditory stimulation versus silence condition. EEG was separated into spatial components of maximal temporal independence using independent component analysis. Alpha component amplitudes and stimulus conditions served as general linear model regressors of the fMRI signal time course. In both paradigms, EEG alpha component amplitudes were associated with BOLD signal decreases in occipital areas, but not in thalamus, when a standard BOLD response curve (maximum effect at ∼6 s) was assumed. The part of the alpha regressor independent of the protocol condition, however, revealed significant positive thalamic and mesencephalic correlations with a mean time delay of ∼2.5 s between EEG and BOLD signals. The inverse relationship between EEG alpha amplitude and BOLD signals in primary and secondary visual areas suggests that widespread thalamocortical synchronization is associated with decreased brain metabolism. While the temporal relationship of this association is consistent with metabolic changes occurring simultaneously with changes in the alpha rhythm, sites in the medial thalamus and in the anterior midbrain were found to correlate with short time lag. Assuming a canonical hemodynamic response function, this finding is indicative of activity preceding the actual EEG change by some seconds.
9

Storti, S. F., E. Formaggio, A. Bertoldo, P. Manganotti, A. Fiaschi, and G. M. Toffolo. "Modelling hemodynamic response function in epilepsy." Clinical Neurophysiology 124, no. 11 (November 2013): 2108–18. http://dx.doi.org/10.1016/j.clinph.2013.05.024.

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10

Lesser, Ronald P. "Functional MRI of Interictal EEG Activity." Epilepsy Currents 2, no. 1 (January 2002): 17. http://dx.doi.org/10.1111/j.1535-7597.2002.00006.x.

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Simultaneous EEG and Functional MRI of Epileptic Activity: A Case Report Baudewig J, Bittermann HJ, Paulus W, Frahm J Clin Neurophysiol 2001;112:1196–1200 Objectives Attempts to localize the source of epileptic activity by linking electroencephalographic (EEG) abnormalities to blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) signal alterations are hampered mainly by EEG distortions during MRI, subject motion, and unknown hemodynamic response characteristics. Methods Using T2*-weighted echo-planar imaging at 2.0 T (2 s temporal resolution, 2 × 2 × 4 mm(3) spatial resolution), this work demonstrates strategies to alleviate some of these problems while studying a patient who had idiopathic generalized epilepsy with poly-spike and slow-wave complexes. Results Continuous EEG recordings during dynamic MRI (500 ms scanning, 1500 ms delay) and post-examination derivation of an EEG reference function for MRI analysis revealed positive BOLD MRI responses with temporal characteristics similar to those obtained for functional challenges. Conclusions The ability to map focal epileptic activity and/or associated cognitive processing provides new potential for both epilepsy research and clinical patient management. Spatio-Temporal Imaging of Focal Interictal Epileptiform Activity Using EEG-Triggered Functional MRI Krakow K, Lemieux L, Messina D, Scott CA, Symms MR, Duncan JS, Fish DR Epileptic Disord 2001;3:67–74 EEG-triggered, blood oxygen level-dependent functional MRI (BOLD-fMRI) was used in 24 patients with localization-related epilepsy and frequent interictal epileptiform discharges (spikes) to identify those brain areas involved in generating the spikes, and to study the evolution of the BOLD signal change over time. The location of the fMRI activation was compared with the scalp EEG spike focus and the structural MR abnormality. Twelve patients (50%) had an fMRI activation concordant with the EEG focus and structural brain abnormalities where present (n = 7). In 2 other patients, the fMRI activation was non-concordant with electroclinical findings. The remaining 10 patients (41.7%) showed no significant fMRI activation. These patients had significantly lower mean spike amplitudes compared to those with positive fMRI results (p = 0.03). The time course of the BOLD response was studied in 3 patients and this revealed a maximum signal change 1.5 to 7.5 sec after the spike. In conclusion, EEG-triggered fMRI can directly identify the generators of interictal epileptiform activity, with high spatial resolution, in selected patients with frequent spikes. The superior spatial resolution obtainable through EEG-triggered fMRI may provide an additional non-invasive tool in the presurgical evaluation of patients with intractable focal seizures.
11

Seghouane, Abd-Krim, and Davide Ferrari. "Robust Hemodynamic Response Function Estimation From fNIRS Signals." IEEE Transactions on Signal Processing 67, no. 7 (April 1, 2019): 1838–48. http://dx.doi.org/10.1109/tsp.2019.2899289.

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12

Beckwith, Christina, and Mark A. Munger. "Effect of Angiotensin-Converting Enzyme Inhibitors on Ventricular Remodeling and Survival following Myocardial Infarction." Annals of Pharmacotherapy 27, no. 6 (June 1993): 755–66. http://dx.doi.org/10.1177/106002809302700617.

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OBJECTIVE: To discuss the effects of angiotensin-converting enzyme (ACE) inhibitors on ventricular remodeling and survival after acute myocardial infarction (AMI). An overview is provided of the pathophysiologic changes produced by AMI and the ventricular remodeling process. ACE inhibitors have been studied for their use in the prevention of ventricular remodeling and reduction in postinfarction mortality. Trials in humans and animals are reviewed, including study methods, results, and limitations. DATA SOURCES: MEDLINE searches identified applicable literature, including experimental trials and review articles. STUDY SELECTION: All clinical trials of ACE inhibitors following AMI were reviewed. DATA EXTRACTION: Morbidity and mortality data evaluating the effect of postinfarction ventricular remodeling are rare. At the time of publication, all available clinical trials studying the effects of ACE inhibitors on postinfarction ventricular remodeling were included, regardless of whether morbidity and mortality were assessed. Data from the Survival and Ventricular Enlargement (SAVE) and Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II) trials include almost 10000 patients. Data were extracted by two independent observers. Data quality and validity were assessed based on sample size, stratification of study population, and statistical power of the studies. DATA SYNTHESIS: ACE inhibitors may prevent the deleterious consequences of AMI, including ventricular remodeling and neurohumoral activation. Ventricular hypertrophy begins acutely following infarction, an early physiologic response to myocardial injury. Hemodynamic benefits from the initial phase of left ventricular hypertrophy include increased ventricular working capacity, normalized systolic wall stress, and maintenance of stroke volume. Although acute dilatation may delay hemodynamic deterioration for six to eight months, it also results in reduced coronary reserve, decreased ventricular compliance, and altered myocardial contractility. With chronic dilatation, the beneficial effects reach a plateau, stroke volume decreases, contractility is reduced, and cardiac failure may ensue. Ventricular hypertrophy is associated with worsened prognosis following infarction and may be the most important single determinant of late prognosis. Ventricular hypertrophy contributes to postinfarction heart failure, angina, and sudden death. Clinical trials show a beneficial effect of the ACE inhibitor captopril on the prevention of left ventricular dysfunction. Although captopril therapy significantly improved survival and myocardial function following AMI in the SAVE trial, these results cannot be generalized to all patient subpopulations. The CONSENSUS II trial demonstrated a decreased survival rate when enalapril was administered within 24 hours of AMI, indicating that timing of therapy may be an important consideration. Captopril therapy may positively affect outcome when initiated 3–16 days following infarction in patients with ejection fractions below 40 percent and who have no signs of ischemia or heart failure. Based on the CONSENSUS II results, enalapril therapy immediately following AMI cannot be recommended. CONCLUSIONS: Clinical trials have demonstrated that ACE inhibitors can limit ventricular hypertrophy following AMI, resulting in clinical benefit and improved survival. These effects may be secondary to modulation of neurohumoral activation or the antiischemic effect of ACE inhibitors, which may also reduce the incidence of reinfarction. Early intervention with ACE inhibitors (within 3–16 days of infarction) can slow the progression of cardiovascular disease and improve the survival rate.
13

Martin, Chris, John Martindale, Jason Berwick, and John Mayhew. "Investigating neural–hemodynamic coupling and the hemodynamic response function in the awake rat." NeuroImage 32, no. 1 (August 2006): 33–48. http://dx.doi.org/10.1016/j.neuroimage.2006.02.021.

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14

Turcott, Robert G., and Todd J. Pavek. "Hemodynamic sensing using subcutaneous photoplethysmography." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 6 (December 2008): H2560—H2572. http://dx.doi.org/10.1152/ajpheart.00574.2008.

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Pacemakers and implantable defibrillators presently operate without access to hemodynamic information. If available, such data would allow tailoring of delivered therapy according to perfusion status, optimization of device function, and enhancement of disease monitoring and management. A candidate method for hemodynamic sensing in these devices is photoplethysmography (PPG), which uses light to noninvasively detect changes in blood volume. The present study tested the hypotheses that PPG can function in a subcutaneous location, that the acute changes in blood volume it detects are directly proportional to changes in arterial pressure, and that optimum pacing intervals identified by it are concordant with those determined by arterial pressure. Aortic pressure and PPG were simultaneously recorded in 10 dogs under general anesthesia during changes in atrioventricular (AV) delay and bursts of rapid pacing to simulate tachyarrhythmias. Direct proportionality between transient changes in pressure and PPG waveforms was tested using regression analysis. Scatter plots had a linear appearance, with correlation coefficients of 0.95 (SD 0.03) and 0.72 (SD 0.24) for rapid-pacing and AV delay protocols, respectively. The data were well described by a directly proportional relationship. Optimum AV delays estimated from the induced changes in aortic pressure and PPG waveforms were concordant. This preliminary canine study demonstrates that PPG can function subcutaneously and that it may serve as a surrogate for acute changes in arterial pressure.
15

Seyed Abbasi, Mahboobe, Salman Zakariaee, and Abbas Rahimiforoushani. "Estimation of Hemodynamic Response Function in the Brain and Brain Tumors: Comparison of Inverse Logistic and Canonical Hemodynamic Response Function Models." Neuroscience Journal of Shefaye Khatam 6, no. 3 (July 1, 2018): 1–9. http://dx.doi.org/10.29252/shefa.6.3.1.

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16

Zhang, Chunming, and Zhengjun Zhang. "Regularized estimation of hemodynamic response function for fMRI data." Statistics and Its Interface 3, no. 1 (2010): 15–31. http://dx.doi.org/10.4310/sii.2010.v3.n1.a2.

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17

Xia, Jing, Feng Liang, and Y. M. Wang. "Learning Hemodynamic Response Function with Neighborhood Cooperation in fMRI." NeuroImage 47 (July 2009): S167. http://dx.doi.org/10.1016/s1053-8119(09)71785-9.

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18

West, Kathryn L., Mark D. Zuppichini, Monroe P. Turner, Dinesh K. Sivakolundu, Yuguang Zhao, Dema Abdelkarim, Jeffrey S. Spence, and Bart Rypma. "BOLD hemodynamic response function changes significantly with healthy aging." NeuroImage 188 (March 2019): 198–207. http://dx.doi.org/10.1016/j.neuroimage.2018.12.012.

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19

Hailemeskel, Bisrat, and Vlncent F. Mauro. "Use of Angiotensin-Converting Enzyme Inhibitors in Heart Failure." Journal of Pharmacy Technology 10, no. 4 (July 1994): 156–63. http://dx.doi.org/10.1177/875512259401000406.

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Objective: To review the literature discussing the use of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure. Data Sources: English-language journal articles. Study Selection: Representative articles discussing the effects of ACE inhibitors on hemodynamics, symptoms, and survival. Data Extraction: Studies selected for review in the text were based on study design and clinical endpoints. Data Synthesis: Heart failure results in a series of compensatory responses that, although effective acutely, are ultimately maladaptive. A major mediator in this process is angiotensin II. The production of angiotensin II is dependent on the ACE. Inhibition of this enzyme by ACE inhibitors results in fewer symptoms, improved hemodynamic function, and prolonged survival in patients with heart failure. Conclusions: ACE inhibitors are beneficial in improving the survival of patients with symptomatic heart failure and of patients who have recently had an acute myocardial infarction (MI) and subsequently have a reduced ejection fraction. There appears to be no advantage for immediately initiating ACE-inhibitor therapy within the first few hours of an MI episode. With respect to patients with a reduced ejection fraction without symptoms of heart failure, current data suggest that ACE inhibitors delay the onset of symptoms of heart failure, reduce the need for hospitalization, and may possibly improve survival.
20

Quiroga, Andrés, Sergio Novi, Giovani Martins, Luis Felipe Bortoletto, Wagner Avelar, Ana Terezinha Guillaumon, Li Min Li, Fernando Cendes, and Rickson C. Mesquita. "Quantification of the Tissue Oxygenation Delay Induced by Breath-Holding in Patients with Carotid Atherosclerosis." Metabolites 12, no. 11 (November 21, 2022): 1156. http://dx.doi.org/10.3390/metabo12111156.

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Carotid artery stenosis (CAS) is a common vascular disease with long-term consequences for the brain. Although CAS is strongly associated with impaired cerebral hemodynamics and neurodegeneration, the mechanisms underlying hemodynamic impairment in the microvasculature remain unknown. In this work, we employed functional near-infrared spectroscopy (fNIRS) to introduce a methodological approach for quantifying the temporal delay of the evoked hemodynamic response. The method was validated during a vasodilatory task (breath-holding) in 50 CAS patients and 20 controls. Our results suggest that the hemodynamic response to breath-holding can be delayed by up to 6 s in the most severe patients, a significant increase from the median 4 s measured for the control group (p = 0.01). In addition, the fraction of brain regions that responded to the task decreased as the CAS severity increased, from a median of 90% in controls to 73% in the most severe CAS group (p = 0.04). The presence of collateral circulation increases the response to breath-holding and decreases the average time delays across the brain, although the number of communicating arteries alone cannot predict these fNIRS-based hemodynamic variables (p > 0.09). Overall, this work proposes a method to quantitatively assess impaired cerebral hemodynamics in CAS patients.
21

Martindale, John, John Mayhew, Jason Berwick, Myles Jones, Chris Martin, Dave Johnston, Peter Redgrave, and Ying Zheng. "The Hemodynamic Impulse Response to a Single Neural Event." Journal of Cerebral Blood Flow & Metabolism 23, no. 5 (May 2003): 546–55. http://dx.doi.org/10.1097/01.wcb.0000058871.46954.2b.

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This article investigates the relation between stimulus-evoked neural activity and cerebral hemodynamics. Specifically, the hypothesis is tested that hemodynamic responses can be modeled as a linear convolution of experimentally obtained measures of neural activity with a suitable hemodynamic impulse response function. To obtain a range of neural and hemodynamic responses, rat whisker pad was stimulated using brief (≤2 seconds) electrical stimuli consisting of single pulses (0.3 millisecond, 1.2 mA) combined both at different frequencies and in a paired-pulse design. Hemodynamic responses were measured using concurrent optical imaging spectroscopy and laser Doppler flowmetry, whereas neural responses were assessed through current source density analysis of multielectrode recordings from a single barrel. General linear modeling was used to deconvolve the hemodynamic impulse response to a single “neural event” from the hemodynamic and neural responses to stimulation. The model provided an excellent fit to the empirical data. The implications of these results for modeling schemes and for physiologic systems coupling neural and hemodynamic activity are discussed.
22

Desmond, John E., Laura C. Rice, Dominic T. Cheng, Jun Hua, Qin Qin, Jessica J. Rilee, Monica L. Faulkner, et al. "Changes in Hemodynamic Response Function Resulting From Chronic Alcohol Consumption." Alcoholism: Clinical and Experimental Research 44, no. 5 (April 27, 2020): 1099–111. http://dx.doi.org/10.1111/acer.14327.

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23

SRIKANTH, R., and A. G. RAMAKRISHNAN. "WAVELET-BASED ESTIMATION OF HEMODYNAMIC RESPONSE FUNCTION FROM fMRI DATA." International Journal of Neural Systems 16, no. 02 (April 2006): 125–38. http://dx.doi.org/10.1142/s012906570600055x.

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We present a new algorithm to estimate hemodynamic response function (HRF) and drift components of fMRI data in wavelet domain. The HRF is modeled by both parametric and nonparametric models. The functional Magnetic resonance Image (fMRI) noise is modeled as a fractional brownian motion (fBm). The HRF parameters are estimated in wavelet domain by exploiting the property that wavelet transforms with a sufficient number of vanishing moments decorrelates a fBm process. Using this property, the noise covariance matrix in wavelet domain can be assumed to be diagonal whose entries are estimated using the sample variance estimator at each scale. We study the influence of the sampling rate of fMRI time series and shape assumption of HRF on the estimation performance. Results are presented by adding synthetic HRFs on simulated and null fMRI data. We also compare these methods with an existing method,1 where correlated fMRI noise is modeled by a second order polynomial functions.
24

Maus, Bärbel, Gerard J. P. van Breukelen, Rainer Goebel, and Martijn P. F. Berger. "Optimal design for nonlinear estimation of the hemodynamic response function." Human Brain Mapping 33, no. 6 (May 12, 2011): 1253–67. http://dx.doi.org/10.1002/hbm.21289.

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25

Gössl, C., L. Fahrmeir, and D. P. Auer. "Bayesian Modeling of the Hemodynamic Response Function in BOLD fMRI." NeuroImage 14, no. 1 (July 2001): 140–48. http://dx.doi.org/10.1006/nimg.2001.0795.

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26

Jalali, A., P. Ghorbanian, A. Ghaffari, and C. Nataraj. "A Novel Technique for Identifying Patients with ICU Needs Using Hemodynamic Features." Advances in Fuzzy Systems 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/696194.

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Identification of patients requiring intensive care is a critical issue in clinical treatment. The objective of this study is to develop a novel methodology using hemodynamic features for distinguishing such patients requiring intensive care from a group of healthy subjects. In this study, based on the hemodynamic features, subjects are divided into three groups: healthy, risky and patient. For each of the healthy and patient subjects, the evaluated features are based on the analysis of existing differences between hemodynamic variables: Blood Pressure and Heart Rate. Further, four criteria from the hemodynamic variables are introduced: circle criterion, estimation error criterion, Poincare plot deviation, and autonomic response delay criterion. For each of these criteria, three fuzzy membership functions are defined to distinguish patients from healthy subjects. Furthermore, based on the evaluated criteria, a scoring method is developed. In this scoring method membership degree of each subject is evaluated for the three classifying groups. Then, for each subject, the cumulative sum of membership degree of all four criteria is calculated. Finally, a given subject is classified with the group which has the largest cumulative sum. In summary, the scoring method results in 86% sensitivity, 94.8% positive predictive accuracy and 82.2% total accuracy.
27

Lewis, Laura D., Kawin Setsompop, Bruce R. Rosen, and Jonathan R. Polimeni. "Fast fMRI can detect oscillatory neural activity in humans." Proceedings of the National Academy of Sciences 113, no. 43 (October 11, 2016): E6679—E6685. http://dx.doi.org/10.1073/pnas.1608117113.

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Oscillatory neural dynamics play an important role in the coordination of large-scale brain networks. High-level cognitive processes depend on dynamics evolving over hundreds of milliseconds, so measuring neural activity in this frequency range is important for cognitive neuroscience. However, current noninvasive neuroimaging methods are not able to precisely localize oscillatory neural activity above 0.2 Hz. Electroencephalography and magnetoencephalography have limited spatial resolution, whereas fMRI has limited temporal resolution because it measures vascular responses rather than directly recording neural activity. We hypothesized that the recent development of fast fMRI techniques, combined with the extra sensitivity afforded by ultra-high-field systems, could enable precise localization of neural oscillations. We tested whether fMRI can detect neural oscillations using human visual cortex as a model system. We detected small oscillatory fMRI signals in response to stimuli oscillating at up to 0.75 Hz within single scan sessions, and these responses were an order of magnitude larger than predicted by canonical linear models. Simultaneous EEG–fMRI and simulations based on a biophysical model of the hemodynamic response to neuronal activity suggested that the blood oxygen level-dependent response becomes faster for rapidly varying stimuli, enabling the detection of higher frequencies than expected. Accounting for phase delays across voxels further improved detection, demonstrating that identifying vascular delays will be of increasing importance with higher-frequency activity. These results challenge the assumption that the hemodynamic response is slow, and demonstrate that fMRI has the potential to map neural oscillations directly throughout the brain.
28

Frazier, Susan K., Kathleen S. Stone, Eric R. Schertel, Debra K. Moser, and Jerry W. Pratt. "A Comparison of Hemodynamic Changes during the Transition from Mechanical Ventilation to T-Piece, Pressure Support, and Continuous Positive Airway Pressure in Canines." Biological Research For Nursing 1, no. 4 (April 2000): 253–64. http://dx.doi.org/10.1177/109980040000100402.

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The immediate transition from positive pressure mechanical ventilation to spontaneous ventilation may generate significant cardiopulmonary hemodynamic alterations based on the mode of weaning selected, particularly in individuals with preexisting cardiac dysfunction. The purpose of this study was to compare hemodynamic responses associated with the initial transition to 3 modes of ventilator weaning (spontaneous ventilation/T-piece, pressure support [PS], and continuous positive airway pressure [CPAP]). Right ventricular hemodynamic responses were evaluated with a thermodilution pulmonary artery catheter; while left ventricular hemodynamic responses were measured by a transducer-tipped Millar catheter and conductance catheter. Two groups of canines were studied. Group 1: normal biventricular function (n = 10) and group 2: propranolol-induced biventricular failure (n = 10). Dependent variables were measured at baseline on controlled mechanical ventilation (MV) and following the initial transition to each of 3 randomized spontaneous ventilatory conditions: T-piece, PS 5 cmH2O, and CPAP 5 cmH2O. Both groups significantly increased cardiac output in response to T-piece. Right ventricular stroke work was also significantly increased with T-piece and CPAP in both groups of subjects. Left ventricular response depended on baseline ventricular function. Baseline ventricular function influenced hemodynamic response to the immediate transition from mechanical to spontaneous ventilation. There were also differential hemodynamic responses based on the ventilatory mode. Consideration of baseline cardiac function may be an important factor in the selection of an appropriate mode of spontaneous ventilation following controlled MV.
29

Munger, K. A., and R. C. Blantz. "Cyclooxygenase-dependent mediators of renal hemodynamic function in female rats." American Journal of Physiology-Renal Physiology 258, no. 5 (May 1, 1990): F1211—F1217. http://dx.doi.org/10.1152/ajprenal.1990.258.5.f1211.

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Previous studies have revealed a sex-dependent difference in response to cyclooxygenase inhibition in anesthetized male and female rats. Female rats have shown an unexpected vasodilation in response to prostaglandin (PG) inhibition. The present studies were designed to further investigate the sex-dependent role of the PG system in the control of normal renal hemodynamics in female Munich-Wistar rats. Renal hemodynamic studies were performed on anesthetized female rats before and during acute cyclooxygenase inhibition using a variety of protocols. One group underwent subacute unilateral renal denervation. A separate group was chronically catheterized and plasma catecholamines were measured during the awake state and then after anesthesia under the euvolemic protocol. Another group was administered the angiotensin II blocker, saralasin, before and during cyclooxygenase inhibition. In a final group, flow to the distal nephron was interrupted via placement of a wax block into the late proximal tubule to determine the role of distal nephron flow and tubuloglomerular feedback in the glomerular response to cyclooxygenase inhibition. It was determined that neither the wax block nor saralasin administration attenuated the vasodilatory response observed in normal female rats due to cyclooxygenase inhibition; however, subacute unilateral renal denervation completely blocked the vasodilatory response to PG inhibition in these female Munich-Wistar rats. Plasma catecholamines were found to be similar whether awake or under anesthesia. These studies indicate the importance of the adrenergic system in modulating PG production in the acutely anesthetized intact female rat.
30

Turner, Jacob E., Daniel R. Stinebring, Maura A. McLaughlin, Anne M. Archibald, Timothy Dolch, and Ryan S. Lynch. "Scattering Delay Mitigation in High-accuracy Pulsar Timing: Cyclic Spectroscopy Techniques." Astrophysical Journal 944, no. 2 (February 1, 2023): 191. http://dx.doi.org/10.3847/1538-4357/acb6fd.

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Abstract We simulate scattering delays from the interstellar medium to examine the effectiveness of three estimators in recovering these delays in pulsar timing data. Two of these estimators use the more traditional process of fitting autocorrelation functions to pulsar dynamic spectra to extract scintillation bandwidths, while the third estimator uses the newer technique of cyclic spectroscopy on baseband pulsar data to recover the interstellar medium’s impulse response function. We find that either fitting a Lorentzian or Gaussian distribution to an autocorrelation function or recovering the impulse response function from the cyclic spectrum are, on average, accurate in recovering scattering delays, although autocorrelation function estimators have a large variance, even at high signal-to-noise ratio (S/N). We find that, given sufficient S/N, cyclic spectroscopy is more accurate than both Gaussian and Lorentzian fitting for recovering scattering delays at specific epochs, suggesting that cyclic spectroscopy is a superior method for scattering estimation in high-quality data.
31

Lu, Yingli, Andrew P. Bagshaw, Christophe Grova, Eliane Kobayashi, François Dubeau, and Jean Gotman. "Using voxel-specific hemodynamic response function in EEG-fMRI data analysis." NeuroImage 32, no. 1 (August 2006): 238–47. http://dx.doi.org/10.1016/j.neuroimage.2005.11.040.

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32

Wu, Guo-Rong, Carol Di Perri, Vanessa Charland-Verville, Charlotte Martial, Manon Carrière, Audrey Vanhaudenhuyse, Steven Laureys, and Daniele Marinazzo. "Modulation of the spontaneous hemodynamic response function across levels of consciousness." NeuroImage 200 (October 2019): 450–59. http://dx.doi.org/10.1016/j.neuroimage.2019.07.011.

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33

Wang, Jiaping, Hongtu Zhu, Jianqing Fan, Kelly Giovanello, and Weili Lin. "Multiscale adaptive smoothing models for the hemodynamic response function in fMRI." Annals of Applied Statistics 7, no. 2 (June 2013): 904–35. http://dx.doi.org/10.1214/12-aoas609.

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34

Rangaprakash, D., Guo-Rong Wu, Daniele Marinazzo, Xiaoping Hu, and Gopikrishna Deshpande. "Hemodynamic response function (HRF) variability confounds resting-state fMRI functional connectivity." Magnetic Resonance in Medicine 80, no. 4 (April 15, 2018): 1697–713. http://dx.doi.org/10.1002/mrm.27146.

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35

Çiftçi, Koray, Bülent Sankur, Yasemin P. Kahya, and Ata Akın. "Constraining the general linear model for sensible hemodynamic response function waveforms." Medical & Biological Engineering & Computing 46, no. 8 (April 22, 2008): 779–87. http://dx.doi.org/10.1007/s11517-008-0347-6.

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36

Hanlon, Faith M., Nicholas A. Shaff, Andrew B. Dodd, Josef M. Ling, Juan R. Bustillo, Christopher C. Abbott, Shannon F. Stromberg, Swala Abrams, Denise S. Lin, and Andrew R. Mayer. "Hemodynamic response function abnormalities in schizophrenia during a multisensory detection task." Human Brain Mapping 37, no. 2 (November 24, 2015): 745–55. http://dx.doi.org/10.1002/hbm.23063.

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37

Roberto, Silvana, Gabriele Mulliri, Raffaele Milia, Roberto Solinas, Virginia Pinna, Gianmarco Sainas, Massimo F. Piepoli, and Antonio Crisafulli. "Hemodynamic response to muscle reflex is abnormal in patients with heart failure with preserved ejection fraction." Journal of Applied Physiology 122, no. 2 (February 1, 2017): 376–85. http://dx.doi.org/10.1152/japplphysiol.00645.2016.

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The aim of the present investigation was to assess the role of cardiac diastole on the hemodynamic response to metaboreflex activation. We wanted to determine whether patients with diastolic function impairment showed a different hemodynamic response compared with normal subjects during this reflex. Hemodynamics during activation of the metaboreflex obtained by postexercise muscle ischemia (PEMI) was assessed in 10 patients with diagnosed heart failure with preserved ejection fraction (HFpEF) and in 12 age-matched healthy controls (CTL). Subjects also performed a control exercise-recovery test to compare data from the PEMI test. The main results were that patients with HFpEF achieved a similar mean arterial blood pressure (MAP) response as the CTL group during the PEMI test. However, the mechanism by which this response was achieved was markedly different between the two groups. Patients with HFpEF achieved the target MAP via an increase in systemic vascular resistance (+389.5 ± 402.9 vs. +80 ± 201.9 dynes·s−1·cm−5 for HFpEF and CTL groups respectively), whereas MAP response in the CTL group was the result of an increase in cardiac preload (−1.3 ± 5.2 vs. 6.1 ± 10 ml in end-diastolic volume for HFpEF and CTL groups, respectively), which led to a rise in stroke volume and cardiac output. Moreover, early filling peak velocities showed a higher response in the CTL group than in the HFpEF group. This study demonstrates that diastolic function is important for normal hemodynamic adjustment to the metaboreflex. Moreover, it provides evidence that HFpEF causes hemodynamic impairment similar to that observed in systolic heart failure. NEW & NOTEWORTHY This study provides evidence that diastolic function is important for normal hemodynamic responses during the activation of the muscle metaboreflex in humans. Moreover, it demonstrates that diastolic impairment leads to hemodynamic consequences similar to those provoked by systolic heart failure. In both cases the target blood pressure is obtained mainly by means of exaggerated vasoconstriction than by a flow-mediated mechanism.
38

Cai, Yuting, Chuncheng Wang, and Dejun Fan. "Stability and bifurcation in a delayed predator-prey model with Holling-type IV response function and age structure." Electronic Journal of Differential Equations 2021, no. 01-104 (May 14, 2021): 42. http://dx.doi.org/10.58997/ejde.2021.42.

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In this article, we study a predator-prey model with age structure, Holling-type IV response, and two time delays. By an algebraic method, we determine all the critical values for these two delays, such that the characteristic equation has purely imaginary roots. This provides a sharp stability region on the parameter plane of the positive equilibrium. Applying integrated semigroup theory and Hopf bifurcation theorem for abstract Cauchy problems with non-dense domain, we can show the occurrence of Hopf bifurcation as the time delays pass through these critical values. In particular, the phenomenon of stability switches can also be observed as the time delays vary. Numerical simulations are carried out to illustrate the theoretical results. For more information see https://ejde.math.txstate.edu/Volumes/2021/42/abstr.html
39

Verbeek, Xander A. A. M., Angelo Auricchio, Yinghong Yu, Jiang Ding, Thierry Pochet, Kevin Vernooy, Andrew Kramer, Julio Spinelli, and Frits W. Prinzen. "Tailoring cardiac resynchronization therapy using interventricular asynchrony. Validation of a simple model." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (March 2006): H968—H977. http://dx.doi.org/10.1152/ajpheart.00641.2005.

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This study explores the use of interventricular asynchrony (interVA) for optimizing cardiac resynchronization therapy (CRT), an idea emerging from a simple pathway model of conduction in the ventricles. Measurements were performed in six dogs with chronic left bundle branch block (LBBB) and in 29 patients of the Pacing Therapies for Congestive Heart Failure (PATH-CHF)-I study. In the dogs, intraventricular asynchrony (intraVA) was determined using left ventricular (LV) endocardial activation maps. In dogs and patients, the maximum rate of rise of LV pressure (LV dP/d tmax) and the pulse pressure (PP) and interVA [time delay between upslope of LV and right ventricular (RV) pressure curves] were measured during LV, RV, and biventricular (BiV) pacing with various atrioventricular (AV) delays. Measurements in the canine hearts supported the pathway model in that optimal resynchronization occurred at ∼50% reduction of intraVA and at an interVA value halfway that during LBBB and LV pacing. In patients with significant hemodynamic response during pacing ( n = 22), intrinsic interVA and interVA at peak improvement (interVAp) varied widely between patients (from −83 to −15 ms and from −42 to +31 ms, respectively). However, the model predicted individual interVAp accurately (SD of ±6 ms and ±12 ms for LV dP/d tmax and PP, respectively). At equal interVA, LV and BiV pacing produced equal hemodynamic response, but in 11 of 22 responders, BiV pacing reduced interVA insufficiently to reach the maximum hemodynamic response. LV pacing at short AV delay proved to result in better hemodynamics than predicted by the model, indicating that additional factors determine hemodynamics during LV preexcitation. Guided by a simple pathway model, interVA measurements accurately predict optimal hemodynamic performance in individual CRT patients.
40

Llinás, María T., Francisca Rodríguez, Carol Moreno, and F. Javier Salazar. "Role of cyclooxygenase-2-derived metabolites and nitric oxide in regulating renal function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 5 (November 1, 2000): R1641—R1646. http://dx.doi.org/10.1152/ajpregu.2000.279.5.r1641.

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The aim of this study was to examine the relative contribution of both cyclooxygenase (COX) isoforms in producing the prostaglandins (PG) involved in the regulation of renal function, when nitric oxide (NO) synthesis is reduced. In anesthetized dogs with reduction of NO synthesis, the renal effects of a nonisozyme-specific COX inhibitor (meclofenamate) were compared with those elicited by a selective COX-2 inhibitor (nimesulide) before and during an extracellular volume expansion (ECVE). Intrarenal N G- nitro-l-arginine methyl ester (l-NAME) infusion (1 μg · kg−1 · min−1; n = 6) did not elicit renal hemodynamic changes and reduced ( P < 0.01) the renal excretory response to ECVE. Intravenous nimesulide (5 μg · kg−1 · min−1; n = 6) did not modify renal hemodynamic and reduced ( P < 0.05) sodium excretion before ECVE. Simultaneousl-NAME and nimesulide infusion ( n = 7) elicited an increment (37%) in renal vascular resistance (RVR; P < 0.05) before ECVE and no hemodynamic changes during ECVE. The reduced excretory response elicited byl-NAME and nimesulide was similar to that found duringl-NAME infusion. Finally, simultaneous l-NAME and meclofenamate infusion (10 μg · kg−1 · min−1; n = 7) induced an increase in RVR (91%, P < 0.05), a decrease in glomerular filtration rate (35%, P < 0.05), and a reduction of the renal excretory response to ECVE that was greater ( P < 0.05) than that elicited by l-NAME alone. The results obtained support the notion that PG involved in regulating renal hemodynamic and excretory function when NO synthesis is reduced are mainly dependent on COX-1 activity.
41

SM,, Abbas, Siddique M,, Abbas MQ, Farooq MF, Malik S,, and Khan HA. "Role of Dexmedetomidine in Attenuation of Hemodynamic Response to Laryngoscopy - A Dose-Finding Study." Pakistan Journal of Medical and Health Sciences 17, no. 6 (June 16, 2023): 96–99. http://dx.doi.org/10.53350/pjmhs202317696.

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Aim: Determining efficacy of pre-operative bolus dose of dexmedetomidine 0.75 and 0.5µg/kg as an infusion and compare it with placebo in attenuation of hemodynamic response to laryngoscopy and tracheal intubation (LTI). Design: Double-blind randomized control. Place & duration: Sindh Institute of Urology & Transplantation, Karachi, Pakistan, from August 2019 to August 2021. Methodology: Patients were stratified into three groups. Group A received normal saline (NS), Group B received dexmedetomidine 0.5 μ/kg and Group C received dexmedetomidine 0.75 μ/kg as an infusion over 10 minutes followed by standardized general anaesthesia. Primary outcome measures were hemodynamic variables at 1, 3, 5 and 10 minutes post LTI. Secondary outcome measures were adverse effects related to dexmedetomidine. Results: Both dexmedetomidine groups showed better attenuation of hemodynamic response to LTI thansaline group. Dexmedetomidine 0.75 µg/kg attenuated hemodynamic response to LTIsignificantly better thandexmedetomidine 0.5 μ/kgand placebo without causing any statistically significant adverse effects. Practical implication: The function of dexmedetomidine in attenuating hemodynamic response to laryngoscopy has several practical implications, including improved patient safety, optimal dosing, reduced anaesthetic requirements, cost-effective treatment, and enhanced patient comfort. Conclusion: Dexmedetomidine 0.75 µg/kg efficient than 0.5 µg/kg and placebo in attenuating hemodynamic response to LTI when given as a pre-induction bolus. Keywords: Anesthesia; Dexmedetomidine, Laryngoscopy, Intubation, Stress Response.
42

Covino, Gregorio, Mario Volpicelli, and Paolo Capogrosso. "Automatic Continuous CRT Optimization to Improve Hemodynamic Response: An Italian Single-Center Experience." International Journal of Vascular Medicine 2020 (February 7, 2020): 1–6. http://dx.doi.org/10.1155/2020/7942381.

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Background. Optimization of cardiac resynchronization therapy (CRT) settings after implant can improve response to therapy. In this Italian single-center experience, we investigated the rate of hemodynamic and clinical response in heart failure patients treated with continuously and automatically optimized CRT. Methods. Patients were selected from June 2015 to April 2017 according to the most recent CRT guidelines; all were in sinus rhythm at implant and received a CRT-defibrillator system equipped with SonR, which automatically optimizes AV and VV delays every week. SonR was activated just after implant and remained active during follow-up. The rate of hemodynamic response (R-HR) was defined as ΔLVEF>5%, super-response (R-HSR) as ΔLVEF>15%, and clinical response as a negative transition of NYHA class≥−1 at 6 months follow-up vs. baseline (preimplant). Results. Mean follow-up for the 31 patients (aged 69.9±9.4 years; 61% male; NYHA class II/III 19%/81%; ischemic etiology 65%) was 6±0.7 months. At baseline, LVEF was 29.1%±4.7% and QRS duration 146±13 ms. LBBB morphology was observed in 65%. At 6 months, R-HR was 74% (23/31), R-HSR 32% (10/31), and clinical response rate 77% (24/31). Hemodynamically, patients with ischemic etiology benefited more than those without ischemic etiology, both in terms of response (80% versus 64%) and super-response (35% versus 27%). Conclusions. Continuous automatic weekly optimization of CRT over 6 months consistently improved R-HR, R-HSR, and clinical response in NYHA class II/III heart failure patients versus baseline. Patients with ischemic etiology in particular may benefit hemodynamically from this type of CRT optimization.
43

Marrelec, Guillaume, and Habib Benali. "Non-parametric Bayesian deconvolution of fMRI hemodynamic response function using smoothing prior." NeuroImage 13, no. 6 (June 2001): 194. http://dx.doi.org/10.1016/s1053-8119(01)91537-x.

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44

Lindquist, Martin A., Ji Meng Loh, Lauren Y. Atlas, and Tor D. Wager. "Modeling the hemodynamic response function in fMRI: Efficiency, bias and mis-modeling." NeuroImage 45, no. 1 (March 2009): S187—S198. http://dx.doi.org/10.1016/j.neuroimage.2008.10.065.

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45

Bazargani, Negar, and Aria Nosratinia. "Joint maximum likelihood estimation of activation and Hemodynamic Response Function for fMRI." Medical Image Analysis 18, no. 5 (July 2014): 711–24. http://dx.doi.org/10.1016/j.media.2014.03.005.

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46

Juengst, Shannon B., Howard J. Aizenstein, Jennifer Figurski, Oscar L. Lopez, and James T. Becker. "Alterations in the hemodynamic response function in cognitively impaired HIV/AIDS subjects." Journal of Neuroscience Methods 163, no. 2 (July 2007): 208–12. http://dx.doi.org/10.1016/j.jneumeth.2007.03.004.

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47

Hossein-Zadeh, Gholam-Ali, Babak A. Ardekani, and Hamid Soltanian-Zadeh. "A signal subspace approach for modeling the hemodynamic response function in fMRI." Magnetic Resonance Imaging 21, no. 8 (October 2003): 835–43. http://dx.doi.org/10.1016/s0730-725x(03)00180-2.

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48

Olszowy, W., G. Williams, C. Rua, and J. Aston. "Validation of the canonical hemodynamic response function model used in fMRI studies." European Neuropsychopharmacology 28 (March 2018): S55—S56. http://dx.doi.org/10.1016/j.euroneuro.2017.12.086.

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49

Seghouane, Abd-Krim, Adnan Shah, and Chee-Ming Ting. "fMRI hemodynamic response function estimation in autoregressive noise by avoiding the drift." Digital Signal Processing 66 (July 2017): 29–41. http://dx.doi.org/10.1016/j.dsp.2017.04.006.

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50

Joshi, Shailendra, Rajinder Singh-Moon, Mei Wang, Jeffrey N. Bruce, Irving J. Bigio, and Avraham Mayevsky. "Real-time hemodynamic response and mitochondrial function changes with intracarotid mannitol injection." Brain Research 1549 (February 2014): 42–51. http://dx.doi.org/10.1016/j.brainres.2013.12.036.

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