一个在体内收缩引起的损伤，非侵入性的监测恢复啮齿动物模型
Summary
一个<em>在体内</em>损伤的动物模型是描述。该方法采用腓骨神经的皮下位置的优势。测速，授时肌肉活化，圆弧运动，所有预先确定的，并同步使用商业软件。伤后的变化进行监测<em>在体内</em>，使用磁共振成像/光谱。
Abstract
肌肉拉伤，医生治疗最常见的投诉之一。一个肌肉损伤通常是单独从患者的病史和体检诊断，但可以不同的临床表现大大取决于在评估肌肉损伤肌肉损伤或肌肉疾病，患者程度的损伤，病人的疼痛的耐受力等临床体征，如压痛，强度，范围的议案，最近，影像学检查，通常是有限的。生物标志物，如血清肌酸磷酸激酶水平，通常与肌肉损伤升高，但他们的水平并不总是力生产的损失相关联。这是来自动物，它提供了一个“直接的措施”损害的组织学研究结果即使如此，但没有考虑到所有的功能丧失。有些人认为，肌肉收缩力的整体健康状况的最全面的衡量。由于肌肉损伤是一个随机事件发生的各种生物力学条件下，它是很难研究。在这里，我们描述了在体内动物模型来测量扭矩，并产生一个可靠的肌肉损伤。我们还描述了我们的模型，从一个在原地隔离肌肉力测量。此外，我们描述了我们的小动物磁共振成像过程。
Protocol
1， 在体内损伤模型和等距扭矩测量。 这些程序可用于大鼠或小鼠7,17,18。首先，放置在动物仰卧吸入麻醉，使用精确的蒸发器（CAT＃91103，兽医装备公司，普莱森（〜4-5％的异氟醚诱导感应室，然后，通过头锥维护〜2％异氟醚） ，CA）。应用无菌眼科霜（Paralube兽医软膏，PharmaDerm，Floham公园，新泽西州），每只眼睛的角膜，以防止干燥。在实验过程中，动物笼外放置了一?…
Discussion
“肌肉损伤”已定义，并在许多方面衡量。在6,9病理结果结构破坏是显而易见的，但许多用于评估肌肉损伤，包括在动物实验中使用的的生物标志物的问题，他们通常没有关联武力的损失。肌肉损伤通常被定义内用来检查它的检测的背景下，没有人发现，可以考虑在伤后的收缩变化。由于充分的收缩功能，能坚持，尽管损伤标志物的存在，可能会失去武力的最有效的措施，伤后3 …
Disclosures
The authors have nothing to disclose.
Acknowledgements
作者想感谢的核心罗伯特Bloch博士，他的实验室空间和设施，并拉奥博士Gullapalli和大施慷慨捐赠，在马里兰（C – TRIM）为转化成像和磁共振研究中心（MRRC）技术支持。这项工作得到了补助金，RML（K01AR053235和1R01AR059179）国家卫生研究院和肌肉萎缩症协会（＃4278），和赠款，耆那教基金会的JAR。
Materials
(All equipment is the same for mice and rats except for the footplate)
- BUD Value Line Cabinet (Newark, 06M4718)
- Multifunction l/O USB-6221M (National Instruments, 779808-01)
- Stepper motor controller (Newark, 16M4189)
- Stepper Motor (Newark, 16M4198)
- Strain Gauge Amplifier (Honeywell, Sensotec, DV-05)
- Torque Sensor (Honeywell, QWLC-8M)
- Foot plate and stabilization device (custom made, patent pending)
References
- Aldridge, R. Muscle pain after exercise is linked with an inorganic phosphate increase as shown by 31P. NMR. Biosci. Rep. 6, 663-663 (1986).
- Argov, Z., Lofberg, M., Arnold, D. L. Insights into muscle diseases gained by phosphorus magnetic resonance spectroscopy. Muscle Nerve. 23, 1316-1316 (2000).
- Brooks, S. V., Zerba, E., Faulkner, J. A. Injury to muscle fibres after single stretches of passive and maximally stimulated muscles in mice. J. Physiol. 488, 459-459 (1995).
- Burkholder, T. J. Relationship between muscle fiber types and sizes and muscle architectural properties in the mouse hindlimb. J. Morphol. 221, 177-177 (1994).
- Hakim, M. Dexamethasone and Recovery of Contractile Tension after a Muscle Injury. Clin. Orthop. Relat Res. 439, 235-235 (2005).
- Hamer, P. W. Evans Blue Dye as an in vivo marker of myofibre damage: optimising parameters for detecting initial myofibre membrane permeability. J. Anat. 200, 69-69 (2002).
- Hammond, J. W. Use of Autologous Platelet-rich Plasma to Treat Muscle Strain Injuries. Am. J. Sports Med. , (2009).
- Heemskerk, A. M. Determination of mouse skeletal muscle architecture using three-dimensional diffusion tensor imaging. Magn Reson. Med. 53, 1333-1333 (2005).
- Ho, K. W. Skeletal muscle fiber splitting with weight-lifting exercise in rats. Am. J. Anat. 157, 433-433 (1980).
- Huijing, P. A., Baan, G. C. Myofascial force transmission causes interaction between adjacent muscles and connective tissue: effects of blunt dissection and compartmental fasciotomy on length force characteristics of rat extensor digitorum longus muscle. Arch. Physiol Biochem. 109, 97-97 (2001).
- Ingalls, C. P. Dihydropyridine and ryanodine receptor binding after eccentric contractions in mouse skeletal muscle. J. Appl. Physiol. 96, 1619-1619 (2004).
- Lee, D., Marcinek, D. Noninvasive in vivo small animal MRI and MRS: basic experimental procedures. J. Vis. Exp. , (2009).
- Lovering, R. M., Deyne, P. G. D. e. Contractile function, sarcolemma integrity, and the loss of dystrophin after skeletal muscle eccentric contraction-induced injury. Am. J. Physiol Cell Physiol. 286, C230-C238 (2004).
- Lovering, R. M. The contribution of contractile pre-activation to loss of function after a single lengthening contraction. J. Biomech. 38, 1501-1501 (2005).
- Lovering, R. M. Recovery of function in skeletal muscle following 2 different contraction-induced injuries. Arch. Phys. Med. Rehabil. 88, 617-617 (2007).
- Provencher, S. W. Automatic quantitation of localized in vivo 1H spectra with LCModel. NMR Biomed. 14, 260-260 (2001).
- Roche, J. A., Lovering, R. M., Bloch, R. J. Impaired recovery of dysferlin-null skeletal muscle after contraction-induced injury in vivo. Neuroreport. 19, 1579-1579 (2008).
- Stone, M. R. Absence of keratin 19 in mice causes skeletal myopathy with mitochondrial and sarcolemmal reorganization. J. Cell Sci. 120, 3999-3999 (2007).
- Van Donkelaar, C. C. Diffusion tensor imaging in biomechanical studies of skeletal muscle function. J. Anat. 194, 79-79 (1999).
- Vogl, T. J. The value of in-vivo 31-phosphorus spectroscopy in the diagnosis of generalized muscular diseases. The clinical results and the differential diagnostic aspects. Rofo. 162, 455-455 (1995).
Tags
In Vivo Rodent ModelContraction-induced InjuryNon-invasive MonitoringRecoveryMuscle StrainsMuscle Injury DiagnosisClinical PresentationMuscle Damage AssessmentBiological MarkersSerum Creatine Kinase LevelsLoss Of Force ProductionHistological FindingsOverall Health Of The MuscleContractile ForceBiomechanical ConditionsIn Vivo Animal ModelTorque MeasurementReliable Muscle InjuryIsolated Muscle MeasurementSmall Animal MRI Procedure
Cite This Article
Lovering, R. M., Roche, J. A., Goodall, M. H., Clark, B. B., McMillan, A. An in vivo Rodent Model of Contraction-induced Injury and Non-invasive Monitoring of Recovery. J. Vis. Exp. (51), e2782, doi:10.3791/2782 (2011).