Cerebral blood flow (CBF) measures are central to the investigation of ischemic strokes, spreading depressions, functional and neuronal activation. Laser Speckle Contrast Imaging (LSCI) is an optical imaging technique that has been used to obtain CBF measures in vivo at high spatial and temporal resolutions, by quantifying the localized spatial blurring of backscattered coherent light induced by blood flow. Despite being widely used for biomedical applications, LSCI's critical limitations such as its tendency to underestimate large flow changes and its inability to accurately estimate CBF through a thinned skull have not been overcome. This dissertation presents a new Multi Exposure Speckle Imaging (MESI) technique that combines a new instrument and mathematical model to overcome these limitations. Additionally, in a pilot clinical study, an adapted neurosurgical microscope was used to obtain intra-operative LSCI images of CBF in humans. The MESI instrument accurately estimates experimental constants by imaging backscattered speckles over a wide range of the camera's exposure durations. The MESI mathematical model helps account for light that has scattered from both static and moving particles. In controlled flow experiments using tissue simulating phantoms, the MESI technique was found to estimate large changes in flow accurately and the estimates of flow changes were found to be unaffected by the presence of static particles in these phantoms. In an in vivo experiment in which the middle cerebral artery in mice was occluded to induce ~100% reduction in CBF, not only was the reduction in CBF accurately estimated by the MESI technique but these estimates of CBF changes were found to be unaffected by the presence of a thinned skull. The validity of statistical models used to derive the MESI mathematical model was confirmed using in vivo dynamic light scattering (DLS) measurements of CBF in mice. The MESI technique's potential to estimate absolute values of CBF in vivo was demonstrated by comparing CBF estimates obtained using the MESI technique to DLS measurements. The MESI technique's ability to measure CBF changes quantitatively through a thinned skull makes it particularly useful in chronic and long term studies leading to the development of better, more accurate stroke models. / text

Die Grundlage der modernen funktionellen Bildgebung des Gehirns mit der BOLD-fMRT ist die neurovaskuläre Kopplung. Sie ist in ihren Mechanismen wenig verstanden und führt zu einem komplexen Zusammenspiel von Blutfluß, Blutvolumen und Oxygenierung. Die Aufklärung der Blutflußantwort mit ihren Auswirkungen auf die Meßsignale ist für eine genaue Interpretation des BOLD-Signals kritisch. Zudem stellt sich seit einigen Jahren die Frage, ob es bei funktioneller Aktivierung aufgrund eines vermehrten neuronalen Sauerstoffverbrauchs zu einer frühen Deoxygenierung kommt. Diese könnte sich als initialer BOLD-Abfall für eine hochauflösende Bildgebung eignen. Ein Vergleich von optischen Methoden und funktioneller Magnetresonanztomographie am gleichen Stimulationsmodell kann diesen Fragen nachgehen. Wir haben die kortikale Blutflußantwort auf somatosensorische Stimulation der Ratte mit den optischen Methoden Optical Imaging und Imaging Spectroscopy sowie mit BOLD-fMRT und blutvolumengewichteter MION-fMRT gemessen. Bei der Stimulation eines einzelnen Whisker-Haares grenzte sich die entsprechende kortikale Kolumne über eine optische Abschwächung ab. Spektroskopisch zeigte sich, daß diesem Signal eine initiale Blutvolumenzunahme zugrundeliegt. Eine Lambert-Beer-Analyse, die die differentiellen Pfadlängen des Lichtes im streuenden Gewebe vernachlässigt, konnte die gemessenen Spektren nicht linear anpassen. Mit einer Annäherung errechnete sie einen artifiziellen Anstieg des Deoxy-Hb in der frühen Antwort. Die quantifizierte Lambert-Beer-Analyse unter Einschluß der differentiellen Pfadlängen konnte die gemessenen Spektren linear anpassen. Im berechneten Konzentrationsverlauf stieg Oxy-Hb zum Stimulationsbeginn an, Deoxy-Hb blieb zunächst auf dem Ruhewert und fiel dann ab. Diese Verzögerung lag im Bereich der kapillären Transitzeit. Die spektroskopisch gemessene frühe Antwort fand sich auch in der Messung der Antwort auf Vorderpfotenstimulation. Zum Vergleich wurden fMRT-Messungen an diesem Stimulationsmodell herangezogen. Die MION-fMRT erfaßte einen initialen Anstieg des plasmatischen Blutvolumens (pCBV), das BOLD-Signal delta-R2* eine verzögerte Hyperoxygenierung. Die Hyperoxygenierung im weiteren Verlauf der Blutflußantwort zeigte in Imaging Spectroscopy und fMRT einen linearen Zusammenhang mit der Dauer der Stimulation. Dabei korrelierte die delta-R2* stark mit der spektroskopisch gemessenen Deoxy-Hb-Konzentration. Auch die Antwort auf das Stimulationsende stellte sich als von der Stimulationsdauer abhängig heraus und wurde als vaskuläres Speicherphänomen interpretiert. BOLD und Deoxy-Hb zeigten beide eine Hypooxygenierung nach dem Stimulationsende. pCBV und das spektroskopisch gemessene korpuskuläre Blutvolumen, cCBV, verhielten sich nach dem Stimulationsende spiegelbildlich. Die pCBV-Zunahme bildete sich nur allmählich zurück, während das cCBV steil unter seinen Ruhewert abfiel. Im Laufe der Messung nahm das cCBV wieder zu und erreichte seinen Ruhewert zeitgleich mit dem pCBV. Eine vermehrte Volumenspeicherung als Folge venöser Streßrelaxation und eine Verschiebung des Hämatokrits aufgrund des Fahraeus-Lindquist-Effekts werden als Grund für diese Veränderungen in Betracht gezogen. Die experimentellen Daten belegen, daß optische und magnetresonanztomographische Methoden korrespondierende Signale von Oxygenierung und Blutvolumen messen. Eine frühe Deoxygenierung wurde nicht gemessen. Allerdings zeigte sich die frühe Komponente der Blutvolumenzunahme an die initiale Kapillarnetzfüllung einer kortikalen Kolumne gebunden. Ihre Detektion mit der fMRT bietet eine Perspektive auf dem Weg zu einer hochauflösenden funktionellen Bildgebung des Gehirns. / Neurovascular coupling forms the basis of modern functional brain imaging with BOLD-fMRI. Its mechanisms are poorly understood as it leads to a complex interaction of blood flow, blood volume and oxygenation. The investigation of the blood flow response with its influences on measured signals is critical for the exact interpretation of the BOLD-Signal. In addition to that, the question on whether or not an increase in oxygen consumption during functional activation leads to an early deoxygenation is not resolved yet. This early deoxygenation could cause an initial BOLD decrease suitable for high resolution imaging. A comparison of optical methods and functional magnetic resonance imaging on the same stimulation model can help to answer these questions. We have measured the cortical blood flow response on somatosensory stimulation of the rat with the optical methods Optical Imaging and Imaging Spectroscopy and with BOLD-fMRI and blood volume weighted MION-fMRI. During stimulation of a single whisker vibrissa the corresponding cortical column delineated itself as an area of increased optical attenuation. A spectroscopical analysis showed an initial blood volume increase responsible for this signal. A Lambert-Beer-Analysis that ignored the differential pathlength of light in scattering tissue could not fit the measured spectra. The result of its closest approximation showed an artificial increase of deoxy-Hb during the early response. The quantified Lambert-Beer-Analysis with inclusion of differential pathlengths succeeded in fitting the measured spectra. The calculated concentration time course showed an increase of oxy-Hb at stimulus onset with deoxy-Hb staying at baseline values and then decreasing. This delay was as long as the capillary mean transit time. The spectroscopically measured early response was also found when measuring the response to forepaw stimulation. For comparison, fMRI measurements on this stimulation model were done. MION-fMRI detected an early increase of plasmatic blood volume (pCBV), the BOLD-Signal delta-R2* a delayed hyperoxygenation. The time course of the hyperoxygenation during the blood flow response showed a linear relationship with the stimulus duration in Imaging Spectroscopy and fMRI. The delta-R2* correlated strongly with spectroscopically measured concentration changes of deoxy-Hb. In addition to that, the response on the stimulus offset was dependent on the stimulus duration. It was interpreted as a vascular storage phenomenon. Both BOLD and deoxy-Hb showed a hypooxygenation after stimulus offset. pCBV and the spectroscopically measured corpuscular blood volume, cCBV, showed mirroring signals after stimulus offset. While pCBV returned to baseline values gradually, cCBV fell below baseline values immediately. During the further measurement cCBV increased and returned to baseline values at the same time as pCBV. To explain this, an increased volume storage due to venous stress relaxation and a hematocrit shift due to the Fahraeus-Lindquist effect are taken into consideration. The experimental data proves that optical and fMRI methods measure corresponding signals of oxygenation and blood volume. An early deoxygenation was not seen. However, the early component of the blood volume increase seems to be restricted to the initial filling of the capillary net supplying a cortical column. Its detection with fMRI offers a perspective on the way to high resolution functional imaging of the brain.

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第21669号 / 医博第4475号 / 新制||医||1035(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 村井 俊哉, 教授 古川 壽亮, 教授 宮本 享 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

It is currently a well-established fact that the dynamics of interacting fluid compartments of the central nervous system (CNS) may play a role in the CNS fluid physiology and pathology of a number of neurological disorders, including neurodegenerative diseases associated with accumulation of waste products in the brain. However, the mechanisms and routes of waste clearance from the brain are still unclear. One of the main components of this interacting cerebral fluids dynamics is blood flow. In the last decades, mathematical modeling and fluid dynamics simulations have become a valuable complementary tool to experimental approaches, contributing to a deeper understanding of the circulatory physiology and pathology. However, modeling blood flow in the brain remains a challenging and demanding task, due to the high complexity of cerebral vascular networks and the difficulties that consequently arise to describe and reproduce the blood flow dynamics in these vascular districts. The first part of this work is devoted to the development of efficient numerical strategies for blood flow simulations in complex vascular networks. In cardiovascular modeling, one-dimensional (1D) and lumped-parameter (0D) models of blood flow are nowadays well-established tools to predict flow patterns, pressure wave propagation and average velocities in vascular networks, with a good balance between accuracy and computational cost. Still, the purely 1D modeling of blood flow in complex and large networks can result in computationally expensive simulations, posing the need for extremely efficient numerical methods and solvers. To address these issues, we develop a novel modeling and computational framework to construct hybrid networks of coupled 1D and 0D vessels and to perform computationally efficient and accurate blood flow simulations in such networks. Starting from a 1D model and a family of nonlinear 0D models for blood flow, with either elastic or viscoelastic tube laws, this methodology is based on (i) suitable coupling equations ensuring conservation principles; (ii) efficient numerical methods and numerical coupling strategies to solve 1D, 0D and hybrid junctions of vessels; (iii) model selection criteria to construct hybrid networks, which provide a good trade-off between accuracy in the predicted results and computational cost of the simulations. By applying the proposed hybrid network solver to very complex and large vascular networks, we show how this methodology becomes crucial to gain computational efficiency when solving networks and models where the heterogeneity of spatial and/or temporal scales is relevant, still ensuring a good level of accuracy in the predicted results. Hence, the proposed hybrid network methodology represents a first step towards a high-performance modeling and computational framework to solve highly complex networks of 1D-0D vessels, where the complexity does not only depend on the anatomical detail by which a network is described, but also on the level at which physiological mechanisms and mechanical characteristics of the cardiovascular system are modeled. Then, in the second part of the thesis, we focus on the modeling and simulation of cerebral blood flow, with emphasis on the venous side. We develop a methodology that, departing from the high-resolution MRI data obtained from a novel in-vivo microvascular imaging technique of the human brain, allows to reconstruct detailed subject-specific cerebral networks of specific vascular districts which are suitable to perform blood flow simulations. First, we extract segmentations of cerebral districts of interest in a way that the arterio-venous separation is addressed and the continuity and connectivity of the vascular structures is ensured. Equipped with these segmentations, we propose an algorithm to extract a network of vessels suitable and good enough, i.e. with the necessary properties, to perform blood flow simulations. Here, we focus on the reconstruction of detailed venous vascular networks, given that the anatomy and patho-physiology of the venous circulation is of great interest from both clinical and modeling points of view. Then, after calibration and parametrization of the MRI-reconstructed venous networks, blood flow simulations are performed to validate the proposed methodology and assess the ability of such networks to predict physiologically reasonable results in the corresponding vascular territories. From the results obtained we conclude that this work represents a proof-of-concept study that demonstrates that it is possible to extract subject-specific cerebral networks from the novel high-resolution MRI data employed, setting the basis towards the definition of an effective processing pipeline for detailed blood flow simulations from subject-specific data, to explore and quantify cerebral blood flow dynamics, with focus on venous blood drainage.

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Master of Science / Department of Kinesiology / Timothy I. Musch / During exercise aged individuals exhibit endothelial dysfunction and decreased levels of whole-limb blood flow (BF), both of which may be linked mechanistically to age-related increases in reactive oxygen species (ROS). Ascorbic acid (AA) reduces levels of ROS and has been shown to alleviate vascular and hyperemic dysfunction at rest (Jablonski et al., 2007) and during small muscle mass exercise in humans (Kirby et al., 2009). However, the effect of AA on vascular function and BF to individual muscles during whole-body exercise is not known. PURPOSE: To test the hypothesis that a single high-dose infusion of AA would increase BF to the hindlimb musculature of old rats at rest and during treadmill running. METHODS: 18 old (~28 months) Fischer 344 x Brown Norway rats were randomized into rest (n=9) and exercise (n=9) groups. BF to the total hindlimb and individual muscles (28 individual muscles and muscle parts) was evaluated via radiolabeled microspheres before and after intra-arterial AA administration (76 mg/kg in 3 ml heparinized saline, 30 minute infusion) at rest and during submaximal treadmill running (20m/min, 5% grade). Total antioxidant capacity (TAC) and thiobarbituric acid reactive species (TBARS) were measured before and after AA to determine the ability of this specific dose of AA to increase levels of plasma antioxidants and decrease levels of ROS, respectively. RESULTS: At rest: AA increased TAC (~37%, P<0.05) but did not change TBARS (Pre: 6.8±0.7 vs Post: 7.0±1.0 µM, P>0.05). AA decreased total hindlimb BF (Pre: 25±3 vs Post: 16±2 ml/min/100g, P<0.05) and BF to 8 of the 28 muscles that were evaluated. During exercise: TAC was increased (~35%, P<0.05) and TBARS were decreased (Pre: 9.8±2.0 vs Post: 7.0±1.0 µM, P<0.05). However, there was no effect on either total hindlimb BF (Pre: 154±14 vs Post: 162±13, P>0.05) or BF to any of the individual muscles evaluated. CONCLUSIONS: Increased TAC via AA infusion reduces hindlimb muscle BF at rest but had no effect on BF during whole-body dynamic exercise. Thus, even though TBARS decreased, there was no evidence that AA supplementation increases blood flow to the locomotor muscles of old rats during whole-body exercise.

Limb haemodynamic responses during heat-stress and the importance of local vs. central temperature-sensitive mechanisms towards their regulation remain poorly understood, both at a whole-limb level and within individual tissues (i.e. skeletal muscle and skin). The aims of this thesis were to 1) investigate the haemodynamic responses at rest to direct thermal challenges both at a local level and during progressive elevations in systemic heat stress, 2) to ascertain the contribution of local vs. systemic mechanisms towards this regulation, and 3) to investigate the same responses during single-legged small-muscle mass exercise to near maximal levels. Results from Chapters 4 and 5 characterised the haemodynamic responses during isolated cooling and heating of the arm and leg, and provided evidence of alterations in both skin and skeletal muscle blood flow controlled solely through local temperature-sensitive mechanisms. While local cooling led to modest decreases in limb blood flow due to decreases in mean blood velocity alone, increases during heating occurred as a result of an increased antegrade flow, a diminished retrograde flow, and a reduction in the potentially pro-atherogenic oscillatory shear index. In Chapter 6, whole-body heating with isolated single leg cooling displayed the continued control of limb blood flow via local thermosensitive mechanisms alone, as cooled leg blood flow remained unchanged despite significant elevations in core temperature, cardiac output, and opposing heated leg blood flow. Furthermore, elevations in heated leg V̇O2 suggested a possible metabolic contribution to the observed skeletal muscle hyperaemic response. During incremental single-legged knee-extensor exercise to near maximal levels, blood flow was determined by a combination of metabolic workload and local tissue temperatures, regardless of whether systemic heat stress was present. Chapter 7 revealed that whilst skin and muscle blood flow in the leg continued to increase in line with local temperatures to levels of severe heat stress, rapid cooling of the leg when hyperthermic resulted in a similar reverse response in muscle tissues only, as skin blood flow remained elevated despite the abolition of high skin and subcutaneous temperatures. In addition, evidence was provided that moderate levels of whole-body heat stress provided little additional benefit to anti-atherogenic shear profiles than that experienced during isolated limb heating alone. Taken together, these findings suggest that local thermosensitive mechanisms dominate limb blood flow control during direct rapid heating in humans both at rest and during small muscle mass exercise, but that underlying central mechanisms may act to maintain flow when local temperatures are reduced in the face of high core temperatures.

Distortion to hemodynamic, ischemic and metabolic stimuli during low load resistance exercise with blood flow restriction (BFR) may influence regional vascular adaptation. This thesis investigated the acute response and chronic adaptations of the peripheral vasculature to low load resistance exercise with BFR. The methodology utilised Doppler ultrasound, strain gauge plethysmography and muscle biopsy for insightful measures of the vasculature at different regions of the arterial tree. Short term (4-6 weeks) localised low load (30-40% 1RM) resistance exercise with BFR increased brachial (3.1%) and popliteal (3.3%) artery maximal diameter (in response to ischemic exercise), forearm (29%) and calf (24%) post-occlusive blood flow, and calf filtration capacity (14%). These findings indicate potential vascular remodelling at the conduit (chapters 3, 4) resistance (chapter 4) and capillary (chapter 4) level of the vascular tree. Regional, rather than systemic, factors are responsible for these adaptations as evidenced by an absent response in the contralateral control limb. Transient improvements in popliteal artery FMD% occurred at week 2 before increased maximal diameter at week 6, suggesting functional changes precede structural remodelling (chapter 4). Maximal brachial artery diameter and forearm post-occlusive blood flow returned to baseline values after a 2 week detraining period, signifying rapid structural normalisation after stimulus removal (chapter 3). Enhanced capillarity, despite low training loads, could be explained by augmentation of VEGF (~7 fold), PGC-1α (~6 fold) and eNOS (~5 fold) mRNA, and upregulation VEGFR-2 (~5 fold) and HIF-1α (~2.5 fold) mRNA with BFR (chapter 5). This indicates a targeted angiogenic response potentially mediated through enhanced metabolic, ischemic and shear stress stimuli. Large between subject variability in the level of BFR was observed during upper and lower limb cuff inflation protocols. Adipose tissue thickness and mean arterial pressure were the largest independent determinants of upper and lower limb BFR, respectively (Chapter 6). In conclusion, this thesis demonstrates that low load resistance exercise with BFR induces adaptation in the conduit, resistance and capillary vessels. The mediators of this response are likely to be the hemodynamic and chemical signals elicited by repeated bouts of BFR resistance exercise, although confirmation of these mechanisms is required. The functional significance of these adaptations is unknown and warrants further investigation.

Assignment (MPhil)--University of Stellenbosch, 2003. / ENGLISH ABSTRACT: The mechanisms of blood flow (BF) control to skeletal muscle during dynamic exercise are still not clearly understood. The paraplegic subject (P) has reduced sympathetic innervation to the lower limbs. The current study was designed to focus on the contribution of neural control, specifically the sympathetic nervous system (SNS), as part of the central vascular mechanism to skeletal muscle BF during dynamic exercise. Aims: We studied BF parameters in P vs. able-bodied subjects (AB) to determine whether the paraplegic can serve as a model for assessing the contribution of the SNS to changes in active vs. inactive muscle BF during exercise. Further questions addressed include: the influence of level of fitness on resting and exercise BF, how lesion level affects BF control in the paraplegic, the 'muscle pump' theory and its hypothesized role in exercise hyperemia and whether blood pooling occurs in the legs of paraplegics. Method: Noninvasive duplex Doppler studies of the large conduit arteries (brachial and common femoral) were performed on 10 elite paraplegic athletes (EP), 10 sedentary paraplegics (SP) en 10 sedentary able-bodied subjects (AB). The paraplegic groups were further subdivided by lesion level with T6 being the critical level. Tests were carried out at rest and after 2 bouts of arm ergometer exercise: a maximal incremental test and 3 minutes at 75% of maximal. Diameter, mean velocity, pulsatile index and blood flow were measured/calculated. Results: Resting heart rate was significantly higher in the paraplegic groups (EP = 80 bpm ± 10, SP = 83 bpm ± 12) vs. the AB group (69 bpm ± 7), p < 0.05. Resting diameter in the common femoral artery (CFA) was similar in EP (5.93 mm ± 1.54) and SP (6.52 mm ± 0.95), but significantly lower than in AB (7.87 mm ± 1.38), p < 0.05. Similar resting pulsatile index (PI) in the CFA were contrary to that previously reported, casting doubt on venous blood pooling theories. Post-exercise values need to be interpreted with caution in view of the large resting differences in CFA diameter. Percentage change values are therefore more appropriate. These differences were not statistically significant, but may suggest interesting trends. Large variability existed for most resting and post-exercise values. Conclusion: The paraplegic subject is an ideal model for the study of the influence of the SNS on blood supply to exercising skeletal muscle. The difference in CFA diameter at rest in the paraplegic vs. the AB group confirms previous results and is probably due to structural/non-physiological changes. Our observation that the BA and CFA diameters in EP and SP subjects do not differ significantly at rest, suggests that training does not have a spillover vasomotor effect on lower limb conduit arteries in paraplegia. Similar BF and PI values post-exercise in the SP and AB groups challenge the muscle pump theory. The SNS has an important role in the control of skeletal muscle blood flow - both at rest (vascular tone) and during exercise (redistribution). Suggestions for future research are made. / AFRIKAANSE OPSOMMING: Die meganismes betrokke by die beheer van bloedvloei (BV) gedurende dinamiese oefening is nog onduidelik. Die parapleeg (P) het verminderde simpatiese innervasie na die onderste ledemate. Die huidige studie fokus op die bydrae van die simpatiese senuwee sisteem (SSS), as deel van die sentrale vaskulêre meganisme, tot skeletale spier BV tydens dinamiese oefening. Doelstellings: Ons het BV parameters in P vs. nie-gestremde proefpersone (kontrole) bestudeer om vas te stelof die parapleeg as model gebruik kan word om die bydrae van die SSS tot veranderings in die BV in aktiewe- en onaktiewe spiere gedurende oefening, te ondersoek. Verdere aspekte wat ondersoek is, sluit in: die invloed van tiksheidvlak ten opsigte van rustende en oefenings BV, of die verlammingsvlak by die parapleeg BV kontrole beïnvloed, die 'spierpomp-teorie' en sy hipotetiese rol in oefeninghiperremie, asook die vraag of bloedsaamstorting in die bene van parapleë plaasvind. Metode: Nie-indringende duplex Doppler studies van die groot geleidingsarteries (bragiaal [BA] en gemene femoral [CFA]) is by 10 elite paraplegiese atlete (EP), 10 sedentêre parapleë (SP) en 10 sedentêre nie-gestremde proefpersone (AB) uitgevoer. Die paraplegiese proefpersone is verder onderverdeel deur die vlak van T6 as kritiese verlammingsvlak te gebruik. Toetse is tydens rus en na 2 arm-ergometer oefeningsessies uitgevoer: een maksimale inkrementeie toets en een van 75% van maksimum intensiteit. Deursnit, gemiddelde vloeispoed, pulsatiewe indeks en bloedvloei is gemeet en/of bereken. Resultate: Rustende hartspoed was beduidend hoër in die paraplegiese groepe (EP = 80 slaelminuut ± 10 en SP = 83 slm ± 12) vs. die AB groep (69 slm ± 7), p < 0.05. Rustende deursnit in die gemene femorale arterie (CFA) was dieselfde in EP (5.93 mm ± 1.54) en SP (6.52 mm ± 0.95), maar beduidend laer as in AB (7.87 mm ± 1.38), p < 0.05. Die feit dat rustende pulsatiewe indeks (PI) in die CFA dieselfde in albei groepe was, laat twyfelontstaan oor die veneuse bloedopdammings teorieë soos weergegee in die literatuur. Na-oefeningswaardes moet omsigtig evalueer word met inagneming van die groot rustende verskille in CFA deursnit. Persentasieverskilwaardes is dus meer toepaslik. Hierdie veskille was nie statisties beduidend nie, maar suggereer interessante tendense. Groot variasie het voorgekom vir beide rustende en na-oefenings waardes. Gevolgtrekking: Die parapleeg is 'n ideale model vir studies om die invloed van die SSS op bloedvloei aan aktiewe skeletale spier te bestudeer. Die verskil in rustende CFA deursnit in die parapleeg vs. die AB groep bevestig vorige resultate en is waarskynlik te wyte aan strukturele, nie-funksionele veranderinge. Ons bevindinge dat die BA en CFA deursneë nie beduidend verskil in die SP en EP groep gedurende rus nie, dui daarop dat gereëlde oefening nie 'n oorloop vasomotor effek op die onderste ledemate in die parapleeg het nie. Die feit dat daar geen verskil aangetoon kon word tussen BV en PI waardes na-oefening in die SP en AB groepe, betwis die spierpomp teorie. Die studie toon dat die SSS 'n belangrike rol in die beheer van skeletale spier bloedvloei speel - beide met rus (vaskulêre tonus) en gedurende oefening (herdistribusie). Voorstelle vir toekomstige navorsing word gemaak.