Hippocampal Blood Flow Is Increased After 20 min of Moderate-Intensity Exercise.

Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels' ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10-12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.

Calibrated fMRI for mapping absolute CMRO2: Practicalities and prospects.

Functional magnetic resonance imaging (fMRI) is an essential workhorse of modern neuroscience, providing valuable insight into the functional organisation of the brain. The physiological mechanisms underlying the blood oxygenation level dependent (BOLD) effect are complex and preclude a straightforward interpretation of the signal. However, by employing appropriate calibration of the BOLD signal, quantitative measurements can be made of important physiological parameters including the absolute rate of cerebral metabolic oxygen consumption or oxygen metabolism (CMRO2) and oxygen extraction (OEF). The ability to map such fundamental parameters has the potential to greatly expand the utility of fMRI and to broaden its scope of application in clinical research and clinical practice. In this review article we discuss some of the practical issues related to the calibrated-fMRI approach to the measurement of CMRO2. We give an overview of the necessary precautions to ensure high quality data acquisition, and explore some of the pitfalls and challenges that must be considered as it is applied and interpreted in a widening array of diseases and research questions.

Dual-calibrated fMRI measurement of absolute cerebral metabolic rate of oxygen consumption and effective oxygen diffusivity.

Dual-calibrated fMRI is a multi-parametric technique that allows for the quantification of the resting oxygen extraction fraction (OEF), the absolute rate of cerebral metabolic oxygen consumption (CMRO2), cerebral vascular reactivity (CVR) and baseline perfusion (CBF). It combines measurements of arterial spin labelling (ASL) and blood oxygenation level dependent (BOLD) signal changes during hypercapnic and hyperoxic gas challenges. Here we propose an extension to this methodology that permits the simultaneous quantification of the effective oxygen diffusivity of the capillary network (DC). The effective oxygen diffusivity has the scope to be an informative biomarker and useful adjunct to CMRO2, potentially providing a non-invasive metric of microvascular health, which is known to be disturbed in a range of neurological diseases. We demonstrate the new method in a cohort of healthy volunteers (n = 19) both at rest and during visual stimulation. The effective oxygen diffusivity was found to be highly correlated with CMRO2 during rest and activation, consistent with previous PET observations of a strong correlation between metabolic oxygen demand and effective diffusivity. The increase in effective diffusivity during functional activation was found to be consistent with previously reported increases in capillary blood volume, supporting the notion that measured oxygen diffusivity is sensitive to microvascular physiology.

A forward modelling approach for the estimation of oxygen extraction fraction by calibrated fMRI.

The measurement of the absolute rate of cerebral metabolic oxygen consumption (CMRO2) is likely to offer a valuable biomarker in many brain diseases and could prove to be important in our understanding of neural function. As such there is significant interest in developing robust MRI techniques that can quantify CMRO2 non-invasively. One potential MRI method for the measurement of CMRO2 is via the combination of fMRI and cerebral blood flow (CBF) data acquired during periods of hypercapnic and hyperoxic challenges. This method is based on the combination of two, previously independent, signal calibration techniques. As such analysis of the data has been approached in a stepwise manner, feeding the results of one calibration experiment into the next. Analysing the data in this manner can result in unstable estimates of the output parameter (CMRO2), due to the propagation of errors along the analysis pipeline. Here we present a forward modelling approach that estimates all the model parameters in a one-step solution. The method is implemented using a regularized non-linear least squares approach to provide a robust and computationally efficient solution. The proposed framework is compared with previous analytical approaches using modelling studies and in vivo acquisitions in healthy volunteers (n=10). The stability of parameter estimates is demonstrated to be superior to previous methods (both in vivo and in simulation). In vivo estimates made with the proposed framework also show better agreement with expected physiological variation, demonstrating a strong negative correlation between baseline CBF and oxygen extraction fraction. It is anticipated that the proposed analysis framework will increase the reliability of absolute CMRO2 measurements made with calibrated BOLD.

Understanding the contribution of neural and physiological signal variation to the low repeatability of emotion-induced BOLD responses.

Previous studies have reported low repeatability of BOLD activation measures during emotion processing tasks. It is not clear, however, whether low repeatability is a result of changes in the underlying neural signal over time, or due to insufficient reliability of the acquired BOLD signal caused by noise contamination. The aim of this study was to investigate the influence of "cleaning" the BOLD signal, by correcting for physiological noise and for differences in BOLD responsiveness, on measures of repeatability. Fifteen healthy volunteers were scanned on two different occasions, performing an emotion provocation task with faces (neutral, 50% fearful, 100% fearful) followed by a breath-hold paradigm to provide a marker of BOLD responsiveness. Repeatability of signal distribution (spatial repeatability) and repeatability of signal amplitude within two regions of interest (amygdala and fusiform gyrus) were estimated by calculating the intraclass correlation coefficient (ICC). Significant repeatability of signal amplitude was only found within the right amygdala during the perception of 50% fearful faces, but disappeared when physiological noise correction was performed. Spatial repeatability was higher within the fusiform gyrus than within the amygdala, and better at the group level than at the participant level. Neither physiological noise correction, nor consideration of BOLD responsiveness, assessed through the breath-holding, increased repeatability. The findings lead to the conclusion that low repeatability of BOLD response amplitude to emotional faces is more likely to be explained by the lack of stability in the underlying neural signal than by physiological noise contamination. Furthermore, reported repeatability might be a result of repeatability of task-correlated physiological variation rather than neural activity. This means that the emotion paradigm used in this study might not be useful for studies that require the BOLD response to be a stable measure of emotional processing, for example in the context of biomarkers.

Implications for psychedelic-assisted psychotherapy: functional magnetic resonance imaging study with psilocybin.

BACKGROUND: Psilocybin is a classic psychedelic drug that has a history of use in psychotherapy. One of the rationales for its use was that it aids emotional insight by lowering psychological defences. AIMS: To test the hypothesis that psilocybin facilitates access to personal memories and emotions by comparing subjective and neural responses to positive autobiographical memories under psilocybin and placebo. METHOD: Ten healthy participants received two functional magnetic resonance imaging scans (2 mg intravenous psilocybin v. intravenous saline), separated by approximately 7 days, during which they viewed two different sets of 15 positive autobiographical memory cues. Participants viewed each cue for 6 s and then closed their eyes for 16 s and imagined re-experiencing the event. Activations during this recollection period were compared with an equivalent period of eyes-closed rest. We split the recollection period into an early phase (first 8 s) and a late phase (last 8 s) for analysis. RESULTS: Robust activations to the memories were seen in limbic and striatal regions in the early phase and the medial prefrontal cortex in the late phase in both conditions (P<0.001, whole brain cluster correction), but there were additional visual and other sensory cortical activations in the late phase under psilocybin that were absent under placebo. Ratings of memory vividness and visual imagery were significantly higher after psilocybin (P<0.05) and there was a significant positive correlation between vividness and subjective well-being at follow-up (P<0.01). CONCLUSIONS: Evidence that psilocybin enhances autobiographical recollection implies that it may be useful in psychotherapy either as a tool to facilitate the recall of salient memories or to reverse negative cognitive biases.

Taking into account latency, amplitude, and morphology: improved estimation of single-trial ERPs by wavelet filtering and multiple linear regression.

Across-trial averaging is a widely used approach to enhance the signal-to-noise ratio (SNR) of event-related potentials (ERPs). However, across-trial variability of ERP latency and amplitude may contain physiologically relevant information that is lost by across-trial averaging. Hence, we aimed to develop a novel method that uses 1) wavelet filtering (WF) to enhance the SNR of ERPs and 2) a multiple linear regression with a dispersion term (MLR(d)) that takes into account shape distortions to estimate the single-trial latency and amplitude of ERP peaks. Using simulated ERP data sets containing different levels of noise, we provide evidence that, compared with other approaches, the proposed WF+MLR(d) method yields the most accurate estimate of single-trial ERP features. When applied to a real laser-evoked potential data set, the WF+MLR(d) approach provides reliable estimation of single-trial latency, amplitude, and morphology of ERPs and thereby allows performing meaningful correlations at single-trial level. We obtained three main findings. First, WF significantly enhances the SNR of single-trial ERPs. Second, MLR(d) effectively captures and measures the variability in the morphology of single-trial ERPs, thus providing an accurate and unbiased estimate of their peak latency and amplitude. Third, intensity of pain perception significantly correlates with the single-trial estimates of N2 and P2 amplitude. These results indicate that WF+MLR(d) can be used to explore the dynamics between different ERP features, behavioral variables, and other neuroimaging measures of brain activity, thus providing new insights into the functional significance of the different brain processes underlying the brain responses to sensory stimuli.

Changes in white matter microstructure and MRI-derived cerebral blood flow after 1-week of exercise training.

Exercise is beneficial for brain health, inducing neuroplasticity and vascular plasticity in the hippocampus, which is possibly mediated by brain-derived neurotrophic factor (BDNF) levels. Here we investigated the short-term effects of exercise, to determine if a 1-week intervention is sufficient to induce brain changes. Fifteen healthy young males completed five supervised exercise training sessions over seven days. This was preceded and followed by a multi-modal magnetic resonance imaging (MRI) scan (diffusion-weighted MRI, perfusion-weighted MRI, dual-calibrated functional MRI) acquired 1 week apart, and blood sampling for BDNF. A diffusion tractography analysis showed, after exercise, a significant reduction relative to baseline in restricted fraction-an axon-specific metric-in the corpus callosum, uncinate fasciculus, and parahippocampal cingulum. A voxel-based approach found an increase in fractional anisotropy and reduction in radial diffusivity symmetrically, in voxels predominantly localised in the corpus callosum. A selective increase in hippocampal blood flow was found following exercise, with no change in vascular reactivity. BDNF levels were not altered. Thus, we demonstrate that 1 week of exercise is sufficient to induce microstructural and vascular brain changes on a group level, independent of BDNF, providing new insight into the temporal dynamics of plasticity, necessary to exploit the therapeutic potential of exercise.

Functional changes in CSF volume estimated using measurement of water T2 relaxation.

Cerebrospinal fluid (CSF) provides hydraulic suspension for the brain. The general concept of bulk CSF production, circulation, and reabsorption is well established, but the mechanisms of momentary CSF volume variation corresponding to vasoreactive changes are far less understood. Nine individuals were studied in a 3T MR scanner with a protocol that included visual stimulation using a 10-Hz reversing checkerboard and administration of a 5% CO(2) mix in air. We acquired PRESS-localized spin-echoes (TR = 12 sec, TE = 26 ms to 1.5 sec) from an 8-mL voxel located in the visual cortex. Echo amplitudes were fitted to a two-compartmental model of relaxation to estimate the partial volume of CSF and the T(2) relaxation times of the tissues. CSF signal contributed 10.7 +/- 3% of the total, with T(2,csf) = 503.0 +/- 64.3 [ms], T(2,brain) = 61.0 +/- 2 [ms]. The relaxation time of tissue increased during physiological stimulation, while the fraction of signal contributed by CSF decreased significantly by 5-6% with visual stimulation (P < 0.03) and by 3% under CO(2) inhalation (P < 0.08). The CSF signal fraction is shown to represent well the volume changes under viable physiological scenarios. In conclusion, CSF plays a significant role in buffering the changes in cerebral blood volume, especially during rapid functional stimuli.

Investigation Of Interaction Between Physiological Signals And fMRI Dynamic Functional Connectivity Using Independent Component Analysis.

The blood oxygen level dependent (BOLD) fMRI signal is influenced not only by neuronal activity but also by fluctuations in physiological signals, including respiration, arterial CO2 and heart rate/ heart rate variability (HR/HRV). Even spontaneous physiological signal fluctuations have been shown to influence the BOLD fMRI signal in a regionally specific manner. Consequently, estimates of functional connectivity between different brain regions, performed when the subject is at rest, may be confounded by the effects of physiological signal fluctuations. In addition, resting functional connectivity has been shown to vary with respect to time (dynamic functional connectivity - DFC), with the sources of this variation not fully elucidated. The effect of physiological factors on dynamic (time-varying) resting-state functional connectivity has not been studied extensively, to our knowledge. In our previous study, we investigated the effect of heart rate (HR) and end-tidal CO2 (PETCO2) on the time-varying network degree of three well-described RSNs (DMN, SMN and Visual Network) using mask-based and seed-based analysis, and we identified brain-heart interactions which were more pronounced in specific frequency bands. Here, we extend this work, by estimating DFC and its corresponding network degree for the RSNs, employing a data-driven approach to extract the RSNs (low-and high-dimensional Independent Component Analysis (ICA)), which we subsequently correlate with the characteristics of simultaneously collected physiological signals. The results confirm that physiological signals have a modulatory effect on resting-state, fMRI-based DFC.

Attentional modulation of visceral and somatic pain.

A better understanding of the cortical processes underlying attentional modulation of visceral and somatic pain in health are essential for interpretation of future imaging studies of hypervigilance towards bodily sensations which is considered to be an aetiologically important factor in the heightened pain reported by patients with irritable bowel syndrome and fibromyalgia. Twelve healthy subjects were recruited for this study. Simultaneous trains of electrical pulses (delivered to either the rectum or lower abdomen) and auditory tones lasting 6 s were delivered to the subjects during a whole-brain functional scan acquisition. Subjects were instructed to attend to the auditory tones (distracter task) or electrical pulses (pain task). Pain intensity ratings were significantly lower during the distraction task compared with the pain task (P < 0.01) in both sensory modalities. The left primary somatosensory cortex increased in activity with increasing pain report, during attention to visceral pain. Bilateral anterior insula (aIns) cortex activity increased with increasing somatic pain report independent of the direction of attention. Conversely, the primary and secondary auditory cortices significantly increased in activation with decreased pain report. These results suggest that pain intensity perception during attentional modulation is reflected in the primary somatosensory cortex (visceral pain) and aIns cortex activity (somatic pain).

Automated single-trial measurement of amplitude and latency of laser-evoked potentials (LEPs) using multiple linear regression.

OBJECTIVE: Laser stimulation of Adelta-fibre nociceptors in the skin evokes nociceptive-specific brain responses (laser-evoked potentials, LEPs). The largest vertex complex (N2-P2) is widely used to assess nociceptive pathways in physiological and clinical studies. The aim of this study was to develop an automated method to measure amplitudes and latencies of the N2 and P2 peaks on a single-trial basis. METHODS: LEPs were recorded after Nd:YAP laser stimulation of the left hand dorsum in 7 normal volunteers. For each subject, a basis set of 4 regressors (the N2 and P2 waveforms and their respective temporal derivatives) was derived from the time-averaged data and regressed against every single-trial LEP response. This provided a separate quantitative estimate of amplitude and latency for the N2 and P2 components of each trial. RESULTS: All estimates of LEP parameters correlated significantly with the corresponding measurements performed by a human expert (N2 amplitude: R2=0.70; P2 amplitude: R2=0.70; N2 latency: R2=0.81; P2 latency: R2=0.59. All P<0.0001). Furthermore, regression analysis was able to extract an LEP response from a subset of the trials that had been classified by the human expert as without response. CONCLUSIONS: This method provides a simple, fast and unbiased measurement of different components of single-trial LEP responses. SIGNIFICANCE: This method is particularly desirable in several experimental conditions (e.g. drug studies, correlations with experimental variables, simultaneous EEG/fMRI and low signal-to-noise ratio data) and in clinical practice. The described multiple linear regression approach can be easily implemented for measuring evoked potentials in other sensory modalities.

Spontaneous physiological variability modulates dynamic functional connectivity in resting-state functional magnetic resonance imaging.

It is well known that the blood oxygen level-dependent (BOLD) signal measured by functional magnetic resonance imaging (fMRI) is influenced-in addition to neuronal activity-by fluctuations in physiological signals, including arterial CO2, respiration and heart rate/heart rate variability (HR/HRV). Even spontaneous fluctuations of the aforementioned physiological signals have been shown to influence the BOLD fMRI signal in a regionally specific manner. Related to this, estimates of functional connectivity between different brain regions, performed when the subject is at rest, may be confounded by the effects of physiological signal fluctuations. Moreover, resting functional connectivity has been shown to vary with respect to time (dynamic functional connectivity), with the sources of this variation not fully elucidated. In this context, we examine the relation between dynamic functional connectivity patterns and the time-varying properties of simultaneously recorded physiological signals (end-tidal CO2 and HR/HRV) using resting-state fMRI measurements from 12 healthy subjects. The results reveal a modulatory effect of the aforementioned physiological signals on the dynamic resting functional connectivity patterns for a number of resting-state networks (default mode network, somatosensory, visual). By using discrete wavelet decomposition, we also show that these modulation effects are more pronounced in specific frequency bands.

A role for the brainstem in central sensitisation in humans. Evidence from functional magnetic resonance imaging.

Animal studies have established a role for the brainstem reticular formation, in particular the rostral ventromedial medulla (RVM), in the development and maintenance of central sensitisation and its clinical manifestation, secondary hyperalgesia. Similar evidence in humans is lacking, as neuroimaging studies have mainly focused on cortical changes. To fully characterise the supraspinal contributions to central sensitisation in humans, we used whole-brain functional magnetic resonance imaging at 3T, to record brain responses to punctate mechanical stimulation in an area of secondary hyperalgesia. We used the heat/capsaicin sensitisation model to induce secondary hyperalgesia on the right lower leg in 12 healthy volunteers. A paired t-test was used to compare activation maps obtained during punctate stimulation of the secondary hyperalgesia area and those recorded during control punctate stimulation (same body site, untreated skin, separate session). The following areas showed significantly increased activation (Z>2.3, corrected P<0.01) during hyperalgesia: contralateral brainstem, cerebellum, bilateral thalamus, contralateral primary and secondary somatosensory cortices, bilateral posterior insula, anterior and posterior cingulate cortices, right middle frontal gyrus and right parietal association cortex. Brainstem activation was localised to two distinct areas of the midbrain reticular formation, in regions consistent with the location of nucleus cuneiformis (NCF) and rostral superior colliculi/periaqueductal gray (SC/PAG). The PAG and the NCF are the major sources of input to the RVM, and therefore in an ideal position to modulate its output. These results suggest that structures in the mesencephalic reticular formation, possibly the NCF and PAG, are involved in central sensitisation in humans.

Cortical processing of visceral and somatic stimulation: differentiating pain intensity from unpleasantness.

Visceral and somatic pain perception differs in several aspects: poor localization of visceral pain and the ability of visceral pain to be referred to somatic structures. The perception of pain intensity and affect in visceral and somatic pain syndromes is often different, with visceral pain reported as more unpleasant. To determine whether these behavioral differences are due to differences in the central processing of visceral and somatic pain, non-invasive imaging tools are required to examine the neural correlates of visceral and somatic events when the behavior has been isolated and matched for either unpleasantness or pain intensity. In this study we matched the unpleasantness of somatic and visceral sensations and imaged the neural representation of this perception using functional magnetic resonance imaging in 10 healthy right-handed subjects. Each subject received noxious thermal stimuli to the left foot and midline lower back and balloon distension of the rectum while being scanned. Stimuli were matched to the same unpleasantness rating, producing mild-moderate pain intensity for somatic stimuli but an intensity below the pain threshold for the visceral stimuli. Visceral stimuli induced deactivation of the perigenual cingulate bilaterally with a relatively greater activation of the right anterior insula-i.e. regions encoding affect. Somatic pain induced left dorso-lateral pre-frontal cortex and bilateral inferior parietal cortex activation i.e. regions encoding spatial orientation and assessing perceptual valence of the stimulus. We believe that the observed patterns of activation represent the differences in cortical process of interoceptive (visceral) and exteroceptive (somatic) stimuli when matched for unpleasantness.

Arterial CO2 effects modulate dynamic functional connectivity in resting-state fMRI.

It is well known that the blood-oxygen level dependent (BOLD) signal measured by functional magnetic resonance imaging (fMRI) is influenced - in addition to neuronal activity - by fluctuations in physiological signals, including arterial CO2. For instance, even spontaneous CO2 fluctuations have been shown to influence the BOLD fMRI signal regionally. Related to this, studies of functional connectivity between different brain regions, performed when the subject is at rest, may be confounded by the effects of physiological noise. Moreover, resting functional connectivity has been shown to vary with respect to time (dynamic functional connectivity), with the sources of this variation not fully understood at present. In this context, in the present paper we examine the relation between dynamic functional connectivity patterns and the properties of the end-tidal CO2 signal (PETCO2) using resting-state fMRI measurements from 12 healthy subjects. The results demonstrate that there exists a modulatory effect of the correlation strength between PETCO2 and the BOLD signal on dynamic resting functional connectivity. The extent to which this effect was observed was found to be strongly dependent on the data analysis methodology.

Correlation between baseline blood pressure and the brainstem FMRI response to isometric forearm contraction in human volunteers: a pilot study.

It has been shown previously that changes in brainstem neural activity correlate with changes in both mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA) during static handgrip (SHG). However, the relationship between baseline MAP and brainstem neural activity is unclear. We investigated changes in blood oxygen level-dependent (BOLD) signal induced by SHG in 12 young adults using BOLD functional magnetic resonance imaging (FMRI). An estimation of the blood pressure response to SHG was obtained in seven subjects during a session outside the MRI scanner and was used to model the blood pressure response to SHG inside the scanner. SHG at 40% of maximum grip increased MAP (mean ± s.d.) at the end of the 180-s squeeze from 85 ± 6 mm Hg to 108 ± 15 mm Hg, P = 0.0001. The brainstem BOLD signal change associated with SHG was localised to the ventrolateral medulla. This regional BOLD signal change negatively correlated with baseline MAP, r = -0.61, P = 0.01. This relationship between baseline MAP and brainstem FMRI responses to forearm contraction is suggestive of a possible role for brainstem activity in the control of MAP and may provide mechanistic insights into neurogenic hypertension.

Geometrical models of left ventricular contraction from MRI of the normal and spontaneously hypertensive rat heart.

This study develops a quantitative analysis and model for the differences in left ventricular dynamics in normal and spontaneously hypertensive rats, as determined using non-invasive magnetic resonance imaging (MRI). We emerge with a characterization of the geometrical changes in the left ventricle resulting from hypertension. In addition, the techniques we have adopted are potentially applicable to the study of other disease models for important human cardiac pathologies. A gradient-echo multislice imaging sequence (echo time 4.3 ms) achieved complete image coverage of the heart at high time resolution (13 ms) through the cardiac cycle. Cardiac anatomy in two age-matched groups of young adult (8 and 12 weeks old) normal Wistar-Kyoto (WKY, n = 8) and spontaneously hypertensive rats (SHR, n = 8) was imaged in synchrony with the electrocardiographic R wave in defined planes both parallel and perpendicular to the principal cardiac axis. The transverse left ventricular image sections were circularly symmetrical; this permitted application of different analytical models for the three-dimensional geometry of the epi- and endocardial borders. An ellipsoidal figure of revolution offered an effective description of the three-dimensional left ventricular geometry throughout the cardiac cycle in both normal WKY and SHR animals. The model successfully characterized both the dynamic changes in the shape of the left ventricle through the cardiac cycle and the pathological alterations resulting from spontaneous hypertension. The elliptical model also formed the basis of a simple stress distribution analysis. Such parametric descriptions thus provided a useful alternative to more complex finite element analyses of cardiac function. The eccentricity of the ventricle was characterized by an ellipticity factor a, where a = 1 for a sphere and a < 1 for a prolate ellipsoid. At end systole, the endocardial surface of the left ventricle gave a = 0.43+/-0.02 and 0.49+/-0.02 for the WKY and SHR animals respectively (probability, P < 0.05). At end diastole, the endocardial surface of the left ventricle gave a = 0.58+/-0.02 and 0.63+/-0.02 for the WKY and SHR animals respectively (P < 0.05). Such a difference in ventricular shape was a potential adaptation to increased blood pressure. Hypertension thus altered the left ventricular ellipticity to give a more spherical geometry compared with the normal rats.

Measurement of pulsatile flow using MRI and a Bayesian technique of probability analysis.

This work shows that complete spatial information of periodic pulsatile fluid flows can be rapidly obtained by Bayesian probability analysis of flow encoded magnetic resonance imaging data. These data were acquired as a set of two-dimensional images (complete two-dimensional sampling of k-space or reciprocal position space) but with a sparse (six point) and nonuniform sampling of q-space or reciprocal displacement space. This approach enables more precise calculation of fluid velocity to be achieved than by conventional two q-sample phase encoding of velocities, without the significant time disadvantage associated with the complete flow measurement required for Fourier velocity imaging. For experimental comparison with the Bayesian analysis applied to nonuniformly sampled q-space data, a Fourier velocity imaging technique was used with one-dimensional spatial encoding within a selected slice and a uniform sampling of q-space using 64 values of the pulsed gradients to encode fluid flow. Because the pulsatile flows were axially symmetric within the resolution of the experiment, the radial variation of fluid velocity, in the direction of the pulsed gradients, was reconstructed from one-dimensional spatial projections of the velocity by exploiting the central slice theorem. Data were analysed for internal consistency using linearised flow theories. The results show that nonuniform q-space sampling followed by Bayesian probability analysis is at least as accurate as the combined uniform q-space sampling with Fourier velocity imaging and projection reconstruction method. Both techniques give smaller errors than a two-point sampling of q-space (the conventional flow encoding experiment).

MRI analysis of right ventricular function in normal and spontaneously hypertensive rats.

Right ventricular structure and function were characterized in spontaneously hypertensive rats (SHR) using non-invasive magnetic resonance imaging (MRI) techniques. These studies therefore complement previous reports preoccupied with left ventricular changes associated with this condition. Eight SHR and eight control normotensive Wistar-Kyoto (WKY) rats were each subdivided into equal age-matched groups of 8 and 12 weeks. The right ventricle was imaged through a series of twelve contiguous 1.37-1.75 mm transverse sections at twelve equally spaced time-points that covered both systole and most of diastole thereby completely reconstructing right ventricular anatomy. This gave measurements of right ventricular myocardial mass that were consistent through all twelve time-points in all four experimental groups throughout their cardiac cycles. However, spontaneous hypertension increased this right ventricular myocardial mass, as well as the end-diastolic (EDV) and end-systolic volumes (ESV). Although stroke volume (SV) was conserved, decreases in ejection fraction (EF), a positive shift in the relationship between SV and EDV, and reduced indices of systolic ejection rates in SHR rats compared with the age-matched normal WKY controls indicated significant systolic dysfunction. Additionally, reductions in the rates of diastolic relaxation suggested the onset of diastolic dysfunction. Thus, the non-invasive nature of MRI has made it possible for the first time to demonstrate alterations in structure of the right ventricle and in quantitative indicators of its systolic and diastolic function in the SHR model of hypertension.