Blood flow subject to a single cycle of body acceleration

The present study deals with the effect of a single cycle of body accelerations on blood flow in arteries. Such body accelerations are usually caused unintentionally, for example during travel in road vehicles, aircraft or spacecraft. A mathematical model of flow in single arteries subject to a pulsating pressure gradient due to the normal heart action as well as body acceleration expressible in terms of unit functions is presented. The body acceleration is such that it builds up from zero to a maximum value at a uniform rate, remains constant at the maximum value for some time, and thereafter reduces to zero at a uniform rate. The resulting equations are solved by using the technique of Laplace transforms. Computational results are presented for the effects of body accelerations on flow variables namely flow rate, velocity of flow, acceleration and shear stress corresponding to blood flow in the human aorta.     

Arterial flow under periodic body acceleration

The present study deals with the effect of externally-imposed body accelerations on blood flow in arteries. Body accelerations may be caused deliberately, for example making the subjecs lie down on vibrating tables: or unintentionally during travel in road vehicles, aircraft or spacecraft. A mathematical model of flow in single arteries subject to a pulsating pressure gradient as well as body acceleration is presented. The resulting equations are solved by using the technique of Laplace transforms. Computational results are presented for the effects of body accelerations on flow variables namely flow rate, velocity of flow, acceleration and shear stress corresponding to typical arteries of human subjects.     

Analysis of blood flow through a model of the human arterial system under periodic body acceleration

The human system may be subjected to a body acceleration deliberated for example by making subjects lie down on vibrating tables or more frequently unintentionally, for example during travel in water and land or in air and space. The present study is concerned with the effects of externally imposed body accelerations on blood flow in a branched system of arteries. A finite-element model of flow in the arterial system subject to periodic body accelerations is presented. Computational results on the flow rates through selected arteries and the corresponding inlet and outlet pressures under different conditions (magnitude, frequency and direction) of applied acceleration are presented.     

A preliminary theoretical study of arterial pressure perturbations under shock acceleration

The artero-venous system is often stressed by accelerative perturbation, not only during exceptional performances, but also in normal life. For example, when the body is subject to fast pressure changes, accelerative perturbations combined with a change in hydrostatic pressure could have severe effects on the circulation. In such cases a preliminary mathematical inquiry, whose results allow qualitative evaluation of the perturbation produced is useful. Pressure variations are studied in this work when the body is subjected both to rectilinear and rotational movements as well as posture change. The dominant modes of the hemodynamic oscillations are emphasized and the numerical simulation results presented. The artery model used for simulation is obviously simplified with respect to the anatomical structure of an artery. Nevertheless, behavior of the main arteries (like the common carotid and aorta) can be approximately described, choosing suitable model parameters. The frequency of blood oscillations strictly depends on the Young modulus of the arterial wall. This connection could be employed for new clinical tests on the state of the arteries.     

On the potential of lower limb muscles to accelerate the body's centre of mass during walking

Quantification of lower limb muscle function during gait or other common activities may be achieved using an induced acceleration analysis, which determines the contributions of individual muscles to the accelerations of the body's centre of mass. However, this analysis is reliant on a mathematical optimisation for the distribution of net joint moments among muscles. One approach that overcomes this limitation is the calculation of a muscle's potential to accelerate the centre of mass based on either a unit-force or maximum-activation assumption. Unit-force muscle potential accelerations are determined by calculating the accelerations induced by a 1 N muscle force, whereas maximum-activation muscle potential accelerations are determined by calculating the accelerations induced by a maximally activated muscle. The aim of this study was to describe the acceleration potentials of major lower limb muscles during normal walking obtained from these two techniques, and to evaluate the results relative to absolute (optimisation-based) muscle-induced accelerations. Dynamic simulations of walking were generated for 10 able-bodied children using musculoskeletal models, and potential- and absolute induced accelerations were calculated using a perturbation method. While the potential accelerations often correctly identified the major contributors to centre-of-mass acceleration, they were noticeably different in magnitude and timing from the absolute induced accelerations. Potential induced accelerations predicted by the maximum-activation technique, which accounts for the force-generating properties of muscle, were no more consistent with absolute induced accelerations than unit-force potential accelerations. The techniques described may assist treatment decisions through quantitative analyses of common gait abnormalities and/or clinical interventions.     

Multilevel Upper Body Movement Control during Gait in Children with Cerebral Palsy

Upper body movements during walking provide information about balance control and gait stability. Typically developing (TD) children normally present a progressive decrease of accelerations from the pelvis to the head, whereas children with cerebral palsy (CP) exhibit a general increase of upper body accelerations. However, the literature describing how they are transmitted from the pelvis to the head is lacking. This study proposes a multilevel motion sensor approach to characterize upper body accelerations and how they propagate from pelvis to head in children with CP, comparing with their TD peers. Two age- and gender-matched groups of 20 children performed a 10m walking test at self-selected speed while wearing three magneto-inertial sensors located at pelvis, sternum, and head levels. The root mean square value of the accelerations at each level was computed in a local anatomical frame and its variation from lower to upper levels was described using attenuation coefficients. Between-group differences were assessed performing an ANCOVA, while the mutual dependence between acceleration components and the relationship between biomechanical parameters and typical clinical scores were investigated using Regression Analysis and Spearman’s Correlation, respectively (α = 0.05). New insights were obtained on how the CP group managed the transmission of accelerations through the upper body. Despite a significant reduction of the acceleration from pelvis to sternum, children with CP do not compensate for large accelerations, which are greater than in TD children. Furthermore, those with CP showed negative sternum-to-head attenuations, in agreement with the documented rigidity of the head-trunk system observed in this population. In addition, the estimated parameters proved to correlate with the scores used in daily clinical practice. The proposed multilevel approach was fruitful in highlighting CP-TD gait differences, supported the in-field quantitative gait assessment in children with CP and might prove beneficial to designing innovative intervention protocols based on pelvis stabilization.     

Ventilation by high-frequency oscillation of thorax or at trachea in rats

The efficiency of ventilation by high-frequency oscillation (HFO) applied to the thorax (external HFO) has been compared with that of HFO applied through a tracheal cannula (internal HFO) in a group of normal rats. Anesthetized, paralyzed, tracheotomized rats were placed in a whole-body plethysmograph. External HFO was achieved by varying the pressure surrounding the animal by means of a piston pump connected to the body plethysmograph; internal HFO was obtained in the same animals by connecting the pump to the tracheal cannula. Arterial CO2 and O2 partial pressures were measured in blood sampled from a carotid artery and were compared for external and internal HFO applied at 20 Hz with matched tidal volumes of 0.8, 1.4, 1.9, and 2.4 ml/kg. With increasing tidal volume, the mean arterial CO2 partial pressure decreased progressively from 68 to 30 Torr and was identical in the two modes of HFO; no difference was noted for the CO2 elimination or for the arterial O2 partial pressure. These results indicate that, in terms of gas exchange, external and internal HFO are equally efficient in normal rats.     

A numerical and experimental analysis of the flow field in a two-dimensional model of the human carotid artery bifurcation

Axial velocities were measured in an enlarged, two-dimensional, rigid model of the carotid artery bifurcation by means of a laser-Doppler anemometer, under both steady and unsteady flow conditions. Also a numerical model was developed, based on the finite element approximation of the Navier-Stokes and continuity equations. From this study it appeared that the numerically predicted velocities agree well with the experimentally obtained values. Besides, the bifurcation hardly influenced the upstream flow in the main branch (common carotid artery), high velocity gradients were observed at the divider walls of the daughter branches (internal and external carotid arteries) and large zones with reversed flow were present near the nondivider walls of these branches. For steady flow the maximal diameter of this zone at the entrance of the internal carotid artery (carotid sinus) was about 25% of the local diameter of this branch. For unsteady flow this zone was absent during the initial phase of flow acceleration and maximal at the end of flow deceleration with a maximal diameter of about 50% of the local diameter of the carotid sinus.     

Modeling the Carotid Sinus Baroreceptor

A mathematical model that describes the relationship between sinus pressure and nerve discharge frequency of the carotid sinus baroreceptor is presented. It is partly based upon the single-fiber data obtained by Clarke from the sinus nerve of a dog. The model takes into account what is currently known about the physiology of the baroreceptor. It consists of two nonlinear ordinary differential equations and eight free parameters. With one set of values for these eight parameters, the model reproduces well the experimental results reported by Clarke for positive ramp pressure inputs. Only three parameters needed to be adjusted in order to fit the dynamic data. The remaining five were obtained from static and steady-state data.     

Posterior acceleration as a mechanism of blunt traumatic injury of the aorta

Rupture of the thoracic aorta is a leading cause of rapid fatality in automobile crashes, but the exact mechanisms of this injury remain unidentified. One commonly postulated mechanism is a differential motion of the aortic arch relative to the heart and its neighboring vessels caused by high-magnitude acceleration of the thorax. This paper investigates acceleration as an aortic injury mechanism using nine impact-sled tests with human cadaver thoraces. The test system utilized generates very high posteriorly directed thoracic accelerations with minimal compression of the chest. The sled tests resulted in peak mid-spine accelerations of 169+/-35.0 g (mean+/-standard deviation) with sustained mid-spine accelerations of up to 80 g for 20 ms in most cases. The tests resulted in maximum chest compressions of 7+/-3.1% of the total chest depth, and maximum recorded increases in intra-aortic, tracheal, and esophageal pressure of 177, 112, and 156 kPa, respectively. No macroscopic injuries to the thoracic aorta resulted from these tests, though other limited visceral injury was observed. The results suggest that posteriorly directed acceleration alone (up to the magnitudes studied here) is not sufficient to cause gross aortic injury. Furthermore, the observed transient increases in intra-aortic and extra-aortic pressure indicate that complex pressure distributions are present during dynamic thoracic deceleration events. This suggests that any attempt to model traumatic aortic injury should include consideration for both the intra-aortic fluid pressure and the extra-aortic, intra-thoracic pressure present during the event.     

Ventilatory responses to specific CNS hypoxia in sleeping dogs.

Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial PO(2) = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5-25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 +/- 7% at arterial PO(2) = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.     

内膜下血管成形术动物模型的构建

目的建立一种稳定可靠的内膜下血管成形术(subintimal angioplasty,SIA)的动物模型,进而探索术后血管壁有关组成成分的变化规律。方法以巴马猪为实验对象,一组(7只)先建立动脉硬化狭窄模型,另一组(9只)为正常动脉,在颈总动脉施行SIA,在术后不同时间观察造模段动脉的通畅率及病理变化等。结果手术操作成功率为93.8%(15/16)。SIA术后总的通畅率为53.3%(8/15)。病理组织学观察发现SIA术后动脉管壁有新内膜形成,中膜增厚,平滑肌细胞数量增多,较多泡沫细胞出现,胶原纤维及弹力纤维染色范围增大、染色密度增加。超微结构观察提示SIA术后中膜层平滑肌细胞的收缩型与合成型同时存在;细胞外基质中胶原纤维和弹力纤维含量异常丰富。结论①首次成功设计、构建内膜下血管成形术的动物模型。②内膜下血管成形术模型构建术后的病理组织学改变与腔内血管成形术后的变化基本一致。     

Interaction between acoustic startle and habituated neck postural responses in seated subjects.

Postural and startle responses rapidly habituate with repeated exposures to the same stimulus, and the first exposure to a seated forward acceleration elicits a startle response in the neck muscles. Our goal was to examine how the acoustic startle response is integrated with the habituated neck postural response elicited by forward accelerations of seated subjects. In experiment 1, 14 subjects underwent 11 sequential forward accelerations followed by 5 additional sled accelerations combined with a startling tone (124-dB sound pressure level) initiated 18 ms after sled acceleration onset. During the acceleration-only trials, changes consistent with habituation occurred in the root-mean-square amplitude of the neck muscles and in the peak amplitude of five head and torso kinematic variables. The subsequent addition of the startling tone restored the amplitude of the neck muscles and four of the five kinematic variables but shortened onset of muscle activity by 9-12 ms. These shortened onset times were further explored in experiment 2, wherein 16 subjects underwent 11 acceleration-only trials followed by 15 combined acceleration-tone trials with interstimulus delays of 0, 13, 18, 23, and 28 ms. Onset times shortened further for the 0- and 13-ms delays but did not lengthen for the 23- and 28-ms delays. These temporal and spatial changes in EMG can be explained by a summation of the excitatory drive converging at or before the neck muscle motoneurons. The present observations suggest that habituation to repeated sled accelerations involves extinguishing the startle response and tuning the postural response to the whole body disturbance.     

A high-frequency lung injury mechanism in blunt thoracic impact

When a mechanical load is applied very rapidly to the thoracic wall, part of the internal damage is suspected to be due to a "high-frequency" injury mechanism, that is, a phenomenon in which waves are involved. This paper addresses a specific high-frequency mechanism for lung injury in which a stress wave is generated through rapid acceleration of the body wall. Displacement-related injuries, which are rather "low-frequency" phenomena, are not considered. The present work was done in the context of assessing behind armor blunt trauma (injury to thoracic organs occurring when a bullet is stopped by a body armor) through mathematical modeling. One aspect of the thorax response to high-speed blunt impact and an associated injury mechanism are investigated based on an idealized model of thorax and a set of computations presented in previous papers. The injury mechanism considered elucidates a possible mathematical relationship between the acceleration at the surface of the thoracic wall and the occurrence of lung injury.     

Assessment of Model Based (Input) Impedance,Pulse Wave Velocity,and Wave Reflection in the Asklepios Cohort

Objectives

Arterial stiffness and wave reflection parameters assessed from both invasive and non-invasive pressure and flow readings are used as surrogates for ventricular and vascular load. They have been reported to predict adverse cardiovascular events, but clinical assessment is laborious and may limit widespread use. This study aims to investigate measures of arterial stiffness and central hemodynamics provided by arterial tonometry alone and in combination with aortic root flows derived by echocardiography against surrogates derived by a mathematical pressure and flow model in a healthy middle-aged cohort.

Methods

Measurements of carotid artery tonometry and echocardiography were performed on 2226 ASKLEPIOS study participants and parameters of systemic hemodynamics, arterial stiffness and wave reflection based on pressure and flow were measured. In a second step, the analysis was repeated but echocardiography derived flows were substituted by flows provided by a novel mathematical model. This was followed by a quantitative method comparison.

Results

All investigated parameters showed a significant association between the methods. Overall agreement was acceptable for all parameters (mean differences: -0.0102 (0.033 SD) mmHg*s/ml for characteristic impedance, 0.36 (4.21 SD) mmHg for forward pressure amplitude, 2.26 (3.51 SD) mmHg for backward pressure amplitude and 0.717 (1.25 SD) m/s for pulse wave velocity).

Conclusion

The results indicate that the use of model-based surrogates in a healthy middle aged cohort is feasible and deserves further attention.     

HUMAN GROWTH CURVE

The human growth curve shows two (and only two) outstanding periods of accelerated growth—the circumnatal and the adolescent. The circumnatal growth cycle attains great velocity, which reaches a maximum at the time of birth. The curve of this cycle is best fitted by a theoretical skew curve of Pearson''s Type I. It has a theoretical range of 44 months and a standard deviation of 5.17 months. The modal velocity is 10.2 kilos per year. The adolescent growth cycle has less maximum velocity and greater range in time than the circumnatal cycle. The best fitting theoretical curve is a normal frequency curve ranging over about 10 years with a standard deviation of about 21 months and a modal velocity of 4.5 kilos per year. The two great growth accelerations are superimposed on a residual curve of growth which measures a substratum of growth out of which the accelerations arise. This probably extends from conception to 55 years, on the average. It is characterized by low velocity, averaging about 2 kilos per year from 2 to 12 years. It is interpreted as due to many growth operations coincident or closely blending in time. Our curve shows no third marked period of acceleration at between the 3rd and 6th years. The total growth in weight of the body is the sum of the weight of its constituent organs. In some cases these keep pace with the growth of the body as a whole; great accelerations of body growth are due to great accelerations in growth of the constituent organs. In other cases one of the organs of the body (like the thymus gland) may undergo a change in weight that is not in harmony with that of the body as a whole. The development of the weight in man is the resultant of many more or less elementary growth processes. These result in two special episodes of growth and numerous smaller, blending, growth operations. Hypotheses are suggested as to the basis of the special growth accelerations.     

Measurement of hemodynamics in human carotid artery using ultrasound and computational fluid dynamics.

The objective of the study was to investigate the feasibility of using computational fluid dynamic modeling (CFD) with noninvasive ultrasound measurements to determine time-variant three-dimensional (3D) carotid arterial hemodynamics in humans in vivo. The effects of hyperoxia and hypoxic hypercapnia on carotid artery local hemodynamics were examined by use of this approach. Six normotensive volunteers followed a double-blind randomized crossover design. Blood pressure, heart rate, and carotid blood flow were measured while subjects breathed normal air, a mixture of 5% CO(2) and 15% O(2) (hypoxic hypercapnia), and 100% O(2) (hyperoxia). Carotid artery geometry was reconstructed on the basis of B-mode ultrasound images by using purpose-built image processing software. Time-variant 3D carotid hemodynamics were estimated by using finite volume-based CFD. Systemic blood pressure was not significantly affected by hyperoxia or hypoxic hypercapnia, but heart rate decreased significantly with hyperoxia. There was an increase in diastolic flow velocity in the external carotid artery after hypoxic hypercapnia, but otherwise carotid blood flow velocities did not change significantly. Compared with normal air, hyperoxic conditions were associated with a decrease in the width of the region of flow separation in the external carotid artery. During hyperoxia, there was also an increase in the minimum and a decrease in maximum shear stress in the bifurcation and hence a reduction in cyclic variation in shear stress. Hypoxic hypercapnia was associated with a reduced duration of flow separation in the external carotid artery and an increase in the minimum shear stress without affecting the cyclic variation in shear stress. This study demonstrates the feasibility of using noninvasive ultrasound techniques in conjunction with CFD to describe time-variant 3D hemodynamics in the human carotid arterial bifurcation in vivo.     

Hemodynamic role of the circle of Willis in stenoses of internal carotid arteries. An analytical solution of a linear model

A mathematical model of blood flow through the circle of Willis was developed, within a linear framework. Comprehensive analytical solutions, including a remarkably small number of parameters, were derived in the cases of obstructive lesions of extracranial carotid arteries. The influence of these lesions and the role of anterior and posterior communicating arteries on the blood pressure at the entry of the cerebral territories were quantified and analyzed emphasizing that the responses of the system of Willis to obstructive carotid lesions are extremely varied, depending on the communicating artery anatomy. Comparison with numerical results obtained by using a non-linear model showed no physiologically significant differences. Such a model might be an essential tool for an accurate assessment of the cerebral hemodynamics in carotid diseases.     

Kinematics and hydrodynamics of linear acceleration in eels, Anguilla rostrata

The kinematics and hydrodynamics of routine linear accelerations were studied in American eels, Anguilla rostrata, using high-speed video and particle image velocimetry. Eels were examined both during steady swimming at speeds from 0.6 to 1.9 body lengths (L) per second and during accelerations from -1.4 to 1.3 L s(-2). Multiple regression of the acceleration and steady swimming speed on the body kinematics suggests that eels primarily change their tail-tip velocity during acceleration. By contrast, the best predictor of steady swimming speed is body wave speed, keeping tail-tip velocity an approximately constant fraction of the swimming velocity. Thus, during steady swimming, Strouhal number does not vary with speed, remaining close to 0.32, but during acceleration, it deviates from the steady value. The kinematic changes during acceleration are indicated hydrodynamically by axial fluid momentum in the wake. During steady swimming, the wake consists of lateral jets of fluid and has minimal net axial momentum, which reflects a balance between thrust and drag. During acceleration, those jets rotate to point downstream, adding axial momentum to the fluid. The amount of added momentum correlates with the acceleration, but is greater than the necessary inertial force by 2.8+/-0.6 times, indicating a substantial acceleration reaction.