Local and Distant Intramedullary Pressure and Bone Strain by Dynamic Hydraulic Stimulation

2011 ◽  
Author(s):  
Y. X. Qin ◽  
M. Hu ◽  
F. Serra-Hsu ◽  
J. Cheng ◽  
S. Ferreri ◽  
...  
Keyword(s):  
Fluid Flow ◽  
Bone Adaptation ◽  
External Loading ◽  
Bone Strain ◽  
Dependent Manner ◽  
Frequency Dependent ◽  
Hydraulic Stimulation ◽  
Bone Fluid Flow ◽  
Intramedullary Pressure ◽  
Osteogenic Response

Osteoporosis gives rise to fragile bones that have higher fracture risks due to diminished bone mass and altered bone microarchitecture [1]. Mechanical loading mediated bone adaptation has demonstrated promising potentials as a non-pharmacological alteration for both osteogenic response and attenuation of osteopenia [2]. Intramedullary pressure (ImP) has been proposed as a key factor for fluid flow initiation and mechanotransductive signal inductions in bone. It is also suggested that integration of strain signals over time allows low-level mechanical strain in the skeleton to trigger osteogenic activities. The potential bone fluid flow induced by strain and ImP mediates adaptive responses in the skeleton [3]. Previous in vivo studies using oscillatory electrical stimulations showed that dynamic muscle contractions can generate ImP and bone strain to mitigate disuse osteopenia in a frequency-dependent manner. To apply ImP alteration as a means for bone fluid flow regulation, it may be necessary to develop a new method that could couple external loading with internal bone fluid flow. In order to further study the direct effect of ImP on bone adaptation, it was hypothesized that external dynamic hydraulic stimulation (DHS) can generate ImP with minimal strain in a frequency-dependent manner. The aim of this study was to evaluate the immediate effects on local and distant ImP and bone strain induced by a novel, non-invasive dynamic external pressure stimulus in response to a range of loading frequencies.

Induced Intramedullary Pressure by Dynamic Hydraulic Stimulation and Its Potential in Attenuation of Bone Loss

2011 ◽  
Author(s):  
M. Hu ◽  
J. Cheng ◽  
S. Ferreri ◽  
F. Serra-Hsu ◽  
W. Lin ◽  
...  
Keyword(s):  
Fluid Flow ◽  
Bone Loss ◽  
Bone Adaptation ◽  
Dependent Manner ◽  
Hydraulic Stimulation ◽  
Flow Coupling ◽  
Bone Fluid Flow ◽  
Intramedullary Pressure ◽  
New Treatments

Bone loss is a critical health problem of astronauts in long-term space missions. A growing number of evidence has pointed out bone fluid flow as a critical regulator in mechanotransductive signaling and bone adaptation. Intramedullary pressure (ImP) is a key mediator for bone fluid flow initiation and it influences the osteogenic signals within the skeleton. The potential ImP-induced bone fluid flow then triggers bone adaptation [1]. Previous in vivo study has demonstrated that ImP induced by oscillatory electrical stimulations can effectively mitigate disuse osteopenia in a frequency-dependent manner in a disuse rat model [2, 3]. In order to develop the translational potentials of ImP, a non-invasive intervention with direct fluid flow coupling is necessary to develop new treatments for microgravity-induced osteopenia/osteoporosis.

In Vivo Mesenchymal Stem Cell Proliferation in Response to Dynamic Fluid Flow Stimulation

2012 ◽  
Author(s):  
M. Hu ◽  
R. Yeh ◽  
M. Lien ◽  
Y. X. Qin
Keyword(s):  
Fluid Flow ◽  
Bone Tissue ◽  
Bone Adaptation ◽  
Hindlimb Suspension ◽  
Osteoporotic Bone ◽  
Hydraulic Stimulation ◽  
Structural Deterioration ◽  
Bone Fluid Flow ◽  
Cord Injury

Osteoporosis is a debilitating disease characterized as decreased bone mass and structural deterioration of bone tissue. Osteoporotic bone tissue turns itself into altered structure, which leads to weaker bones that are more susceptible for fractures. While often happening in elderly, long-term bed-rest patients, e.g. spinal cord injury, and astronauts who participate in long-duration spaceflights, osteoporosis has been considered as a major public health thread and causes great medical cost impacts to the society. Mechanobiology and novel stimulation on regulating bone health have long been recognized. Loading induced bone fluid flow, as a critical mechanotransductive promoter, has been demonstrated to regulate cellular signaling, osteogenesis, and bone adaptation [4]. As one of the factors that mediate bone fluid flow, intromedullary pressure (ImP) creates a pressure gradient that further influence the magnitude of mechanotransductory signals [5]. As for a potential translational development of ImP, our group has recently introduced a novel, non-invasive dynamic hydraulic stimulation (DHS) on bone structural enhancement. Its promising effects on inhibition of disuse bone loss has been shown with 2 Hz loading through a 4-week hindlimb suspension rat study followed by microCT analysis. At the cellular level, mesenchymal stem cells (MSCs) are defined by their self-renewal ability and that to potentially differentiate into the cells that form tissues such as bone [1]. To further elucidate the cellular effects of DHS and its potential mechanism on bone quality enhancement, the objective of this study was to measure MSC quantification in response to the in vivo mechanical signals driven by DHS.

Inhibition of Bone Loss and Muscle Atrophy by Dynamic Muscle Contractions With Rest Periods in a Functional Disuse Mouse Model

2008 ◽  
Author(s):  
Adiba Ali ◽  
Yi-Xian Qin
Keyword(s):  
Bone Loss ◽  
Mouse Model ◽  
Muscle Atrophy ◽  
High Frequency ◽  
Synergistic Effects ◽  
Bone Adaptation ◽  
Muscle Contractions ◽  
Rest Periods ◽  
Bone Fluid Flow ◽  
Intramedullary Pressure

Osteoporosis, induced by aging and long-term disuse, often occurs together with muscle loss. Musculoskeletal disuse causes severe physiologic changes and it has been proposed the synergistic effects of muscle function and bone adaptation. Bone fluid flow has been shown to be induced during mechanical loading, and is proposed to be a critical mediator of bone adaptation. The skeletal muscle may serve as a muscle pump that may mediate bone mechanotransduction via modulation of intramedullary pressure. Thus, muscular stimulation is proposed to be used to simultaneously treat both muscle and bone loss, but the optimal parameters required for such treatment is unclear. Studies have separately investigated the optimal signal parameters for bone or muscle. Insertion of recovery periods during high frequency stimulations have shown potential to reduce muscle atrophy by minimizing fatigue and mimicking physiologic contractions, and demonstrated enhancement of bone remodeling. Our preliminary research has indicated that dynamic muscle contractions within an optimal frequency range can significantly recover disuse induced bone loss. However, the optimal rest periods required to prevent muscle fatigue during stimulations are not clear. The overall objective of this study was to evaluate optimized dynamic muscle stimulations at relatively high frequency, e.g., 20 Hz, and to test the role of varying the rest duration on muscle mass and bone morphology in a functional hind limb disuse mouse model.

scholarly journals Bone strain magnitude is correlated with bone strain rate in tetrapods: implications for models of mechanotransduction

2015 ◽  
Vol 282 (1810) ◽  
pp. 20150321 ◽  
Author(s):  
B. R. Aiello ◽  
J. Iriarte-Diaz ◽  
R. W. Blob ◽  
M. T. Butcher ◽  
M. T. Carrano ◽  
...  
Keyword(s):  
Fluid Flow ◽  
Strain Rate ◽  
Flow Rate ◽  
Structural Integrity ◽  
Tissue Level ◽  
Bone Adaptation ◽  
Bone Strain ◽  
Mechanical Stimuli ◽  
Fluid Flow Rate ◽  
Strain Magnitude

Hypotheses suggest that structural integrity of vertebrate bones is maintained by controlling bone strain magnitude via adaptive modelling in response to mechanical stimuli. Increased tissue-level strain magnitude and rate have both been identified as potent stimuli leading to increased bone formation. Mechanotransduction models hypothesize that osteocytes sense bone deformation by detecting fluid flow-induced drag in the bone's lacunar–canalicular porosity. This model suggests that the osteocyte's intracellular response depends on fluid-flow rate, a product of bone strain rate and gradient, but does not provide a mechanism for detection of strain magnitude. Such a mechanism is necessary for bone modelling to adapt to loads, because strain magnitude is an important determinant of skeletal fracture. Using strain gauge data from the limb bones of amphibians, reptiles, birds and mammals, we identified strong correlations between strain rate and magnitude across clades employing diverse locomotor styles and degrees of rhythmicity. The breadth of our sample suggests that this pattern is likely to be a common feature of tetrapod bone loading. Moreover, finding that bone strain magnitude is encoded in strain rate at the tissue level is consistent with the hypothesis that it might be encoded in fluid-flow rate at the cellular level, facilitating bone adaptation via mechanotransduction.

Oscillatory Bone Fluid Flow and its Role in Initiating Remodeling in the Absence of Matrix Strain

2001 ◽  
Author(s):  
Yixian Qin ◽  
Anita Saldanha ◽  
Tamara Kaplan
Keyword(s):  
Fluid Flow ◽  
Cellular Response ◽  
Fluid Shear Stress ◽  
Bone Matrix ◽  
Fluid Pressure ◽  
Streaming Potential ◽  
Bone Adaptation ◽  
Interstitial Fluid Flow ◽  
Bone Fluid Flow ◽  
Matrix Deformation

Abstract Load-generated intracortical fluid flow is proposed to be an important mediator for regulating bone mass and morphology [1]. Although the mechanism of cellular response to induced flow parameters, i.e., fluid pressure, pressure gradient, velocity, and fluid shear stress, are not yet clear, interstitial fluid flow driven by loading may be necessary to explain the adaptive response of bone, which is either coupled with load-induced strain magnitude or independent with matrix strain per se [2]. It has been demonstrated that load-induced intracortical fluid flow is contributed by both bone matrix deformation and induced intramedullary (IM) pressure [3]. To examine the hypothesis of fluid flow generated adaptation, it is necessary to test the mechanism under the circumstances of solely fluid induced bone adaptation in the absence of matrix deformation. While our previous data has demonstrated that bone fluid flow and its associated streaming potential product can be influenced by the dynamic IM pressure quantitatively [4], the objective of this study was to evaluate fluid induced bone adaptation in an avian ulna model using oscillatory IM fluid pressure loading in the absence of bone matrix strain. The potential fluid pathway was measured in the model.

The Effects of Loading Rate and Duration on Mitigation of Osteopenia by Dynamic Muscle Stimulation

2009 ◽  
Author(s):  
Yi-Xian Qin ◽  
Hoyan Lam ◽  
Murtaza Malbari
Keyword(s):  
Bone Loss ◽  
Muscle Atrophy ◽  
High Frequency ◽  
Synergistic Effects ◽  
Bone Adaptation ◽  
Muscle Adaptation ◽  
Skeletal Health ◽  
Skeletal Tissue ◽  
Bone Fluid Flow ◽  
Intramedullary Pressure

Musculoskeletal adaptations to aging and disuse environment have significant physiological effects on skeletal health, i.e., osteopenia and bone loss. Osteoporosis often occurs together with muscle loss. Such musculoskeletal complications cause severe physiologic changes and have been proposed the synergistic effects of muscle function and bone adaptation. The role of mechanobiology in the skeletal tissue may be closely related to load-induced transductive signals, e.g., bone fluid flow, which is proposed to be a critical mediator of bone and muscle adaptation. The skeletal muscle may serve as a muscle pump that may mediate bone mechanotransduction via modulation of intramedullary pressure. Muscular stimulation (MS) is proposed to be used to simultaneously treat both muscle and bone loss. Indeed, our recent data have demonstrated that high frequency, short duration stimulation can inhibit bone loss and muscle atrophy. Although 10 min dynamic loading can effectively attenuate bone loss, it cannot totally recover disuse osteopenia. The optimal parameters required for such treatment are unclear. Studies have separately investigated the optimal signal parameters for bone or muscle. Insertion of recovery periods during high frequency stimulations to extend the loading cycles have shown potential to reduce muscle atrophy by minimizing fatigue and mimicking physiologic contractions, and demonstrated enhancement of bone remodeling. The overall hypothesis for this study is that dynamic MS can enhance anabolic activity in bone, and inhibit bone loss in a functional disuse condition. Combined high frequency and sufficient loading cycle may be able to completely mitigate bone loss induced by disuse osteopenia.

Bone Formation and Inhibition of Bone Loss by Dynamic Muscle Stimulation With Altered Interstitial Fluid Pressure

2007 ◽  
Author(s):  
Yi-Xian Qin ◽  
Hoyan Lam
Keyword(s):  
Fluid Flow ◽  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Tissue Level ◽  
Bone Strain ◽  
Bone Fluid Flow ◽  
Muscle Dynamics ◽  
Key Players ◽  
Flow Through ◽  
Bone Physiology

Tissue-level mechanisms and functions, including bone strain and muscle, are the potential key players in bone physiology and adaptation [1,2,3]. However, the mechanisms are not yet fully understood. Exercise such as muscle contraction appears to increase blood flow to the skeletal tissues, i.e., bone and muscle. These evidences imply that bone fluid flow induced by muscle dynamics may be an important role in regulating fluid flow through coupling of muscle and bone via microvascular system.

Effects of Intravenous Anesthetics on Atrial Wavelength and Atrioventricular Nodal Conduction in Guinea Pig Heart

1996 ◽  
Vol 85 (2) ◽  
pp. 393-402 ◽  
Author(s):  
Charles A. Napolitano ◽  
Pekka M. J. Raatikainen ◽  
Jeffrey R. Martens ◽  
Donn M. Dennis
Keyword(s):  
Guinea Pig ◽  
Conduction Velocity ◽  
Cycle Length ◽  
Rank Order ◽  
Interelectrode Distance ◽  
Atrial Pacing ◽  
Dependent Manner ◽  
Frequency Dependent ◽  
His Bundle ◽  
Atrioventricular Nodal Conduction

Background Supraventricular tachydysrhythmias such as atrial fibrillation frequently complicate the perioperative period. Two electrophysiologic factors critical to the pathogenesis of supraventricular tachydysrhythmias are: 1) atrial wavelength, the product of atrial conduction velocity (CV) and effective refractory period (ERP), and 2) atrioventricular nodal conduction. Modulation of these factors by drugs has important clinical ramifications. The authors studied the effects of propofol, thiopental, and ketamine on atrial wavelength and atrioventricular nodal function in guinea pig isolated atrial trabeculae and hearts, respectively. Methods Electrocardiogram recordings in superfused atrial tissue were obtained using hanging microelectrodes. A stimulating and two recording electrodes were placed on a single atrial trabecula, and the interelectrode distance was measured. Atrial ERP determinations were made using a premature stimulus protocol. The time (t) required for a propagated impulse to traverse the interelectrode distance (d) was measured. Conduction velocity was calculated as d/t. Langendorff-perfused guinea pig hearts were instrumented for low atrial pacing (cycle length = 300 ms) and for measurements of stimulusto-His bundle interval, an index of atrioventricular nodal conduction. To investigate the frequency-dependent behavior of the atrioventricular node, computer-based measurements were made of Wenckebach cycle length (WCL) and atrioventricular nodal ERP. Results Thiopental significantly prolonged atrial ERP in a concentration-dependent manner, whereas propofol and ketamine had no significant effect on atrial refractoriness. In contrast, ketamine caused a dose-dependent decrease in atrial CV, but propofol and thiopental had no significant effect on CV. Therefore, thiopental, ketamine, and propofol caused an increase, a decrease, and no change, respectively, in atrial wavelength. All anesthetics caused a concentration-dependent prolongation of the stimulus-to-His bundle interval, atrioventricular nodal ERP, and WCL. However, on an equimolar basis, significant differences in potencies were found. The concentrations of drug that caused a 20% increase in ERP (ERP20) and WCL (WCL20) for propofol, thiopental, and ketamine were 14 +/- 2 microM, 26 +/- 3 microM, and 62 +/- 11 microM, and 17 +/- 2 microM, 50 +/- 1 microM, and 123 +/- 19 microM (mean +/- SEM), respectively. Therefore, the rank order of potency for frequency-dependent atrioventricular nodal effects is propofol > thiopental > ketamine. Conclusion The authors' results indicate that propofol would be most effective at filtering atrial impulses during supraventricular tachydysrhythmias, whereas thiopental would be most effective at preventing atrial reentrant dysrhythmias. In contrast, ketamine may be most likely to promote atrial reentry while having minimal effect on atrioventricular nodal conduction.

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