Acute Effects of Nucleus Pulposus on Blood Flow and Endoneurial Fluid Pressure in Rat Dorsal Root Ganglia

Yabuki, Shoji; Kikuchi, Shinichi; Olmarker, Kjell; Myers, Robert R.

doi:10.1097/00007632-199812010-00006

Cited by 125 publications

(62 citation statements)

References 37 publications

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“…Such intraneural edema is associated with a reduction in nerve blood flow [15]. Yabuki et al [30] harvested autologous nucleus pulposus and applied it to the nerve root just proximal to the DRG, with continuous monitoring of the blood flow using a laser Doppler flow probe. They reported that application of nucleus pulposus to the nerve root decreased blood flow in the dorsal root ganglia.…”

Section: Discussionmentioning

confidence: 99%

Effects of lumbar sympathectomy on pain behavioral changes caused by nucleus pulposus-induced spinal nerve damage in rats

Murata

Olmarker²,

Takahashi

et al. 2005

Eur Spine J

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IntroductionIt has been reported that nucleus pulposus in the epidural space induces spinal nerve root damage, not only by mechanical but also by chemical mechanisms as nucleus pulposus is capable of producing proinflammatory cytokines [5,14,16,17,19,21,23,29]. There have been a number of recent reports regarding the pain behavior due to lumbar disk herniation in rats [7,18,20,24]. One well-characterized model involves L4/5 disk incision and/or displacement of the adjacent spinal nerve in rats. These studies indicated that the combination of chemical and mechanical damage results in behavioral changes, mechanical allodynia, thermal hyperalgesia, increased lifting of the hind paw on the operated side, and increased rotation of the head toward the operated side [18].Tight and loose ligation with or without transection of the nerve are well-known neuropathic pain models in rats [1,9]. These models show mechanical allodynia and thermal hyperalgesia. It has been reported that lumbar sympathectomy, which was performed in these pain models, can decrease the pain behavior [2,8,10]. Kim et al. reported the prevention of pain behavioral changes by sympathectomy prior to nerve ligation [10]. In contrast, it has also been reported that intraperitoneal injection of phentolamine hydrochloride, an alphaadrenoceptor blocker, or surgical sympathectomy does Abstract It has been suggested that lumbar sympathectomy can reduce pain behavior, including mechanical allodynia and thermal hyperalgesia, caused by ligation of the spinal nerve. One well-characterized model, which involves application of nucleus pulposus to the spinal nerve and displacement of the adjacent nerve, shows behavioral changes in rats. However, there have been no previous reports regarding sympathectomy performed in this model. Disk incision and adjacent spinal nerve displacement were performed with (n=6) or without (n=6) sympathectomy. Sham surgery was also performed with (n=6) or without (n=6) sympathectomy. The animals were tested for 3 days before surgery and on days 1, 3, 7, 14, and 21 after surgery. Non-noxious mechanical thresholds were tested by determining the hind paw withdrawal response to von Frey hair stimulation of the plantar surface of the footpad using a touch stimulator. Thermal nociceptive thresholds were tested using a sensitive thermal-testing device. While rats in the disk incision with displacement surgery group showed allodynia and hyperalgesia after surgery on the experimental side, sympathectomized animals did not. No allodynia was observed in the sham groups. Sympathectomy seemed to prevent the pain behavioral changes caused by the combination of disk incision and nerve displacement.

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Section: Discussionmentioning

confidence: 99%

Effects of lumbar sympathectomy on pain behavioral changes caused by nucleus pulposus-induced spinal nerve damage in rats

Murata

Olmarker²,

Takahashi

et al. 2005

Eur Spine J

Self Cite

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“…In a follow-up study, ultrastructural changes such as swelling of Schwann cells were demonstrated using electron microscopy [34]. The capacity of nucleus pulposus to induce both structural and functional changes in spinal nerve roots has been verified in several recent studies evaluating the biologic effects of nucleus pulposus [1,3,4,20,21,22,35,38,39,44,47,52]. Nucleus pulposus' role in pain induction has recently been evaluated [22,36,37].…”

Section: Discussionmentioning

confidence: 99%

“…Spinal nerve root injury can be induced by chronic compression and/or the presence of nucleus pulposus [1, 3, 4, 5,20,21,22,26,31,32,33,34,35,36,37,38,39,46,52]. It has been demonstrated experimentally that epidurally applied autologous nucleus pulposus, without any compression, can induce significant changes in nerve root morphology and function in animal models [4, 5,21,22,31,34,35].…”

Section: Introductionmentioning

confidence: 99%

Nucleus pulposus-induced nerve root injury: effects of diclofenac and ketoprofen

et al. 2001

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IntroductionSpinal nerve root injury can be induced by chronic compression and/or the presence of nucleus pulposus [1, 3, 4, 5,20,21,22,26,31,32,33,34,35,36,37,38,39,46,52]. It has been demonstrated experimentally that epidurally applied autologous nucleus pulposus, without any compression, can induce significant changes in nerve root morphology and function in animal models [4, 5,21,22,31,34,35]. Nucleus pulposus has been demonstrated to have inflammatogenic properties [33] and abundant macrophages and interleukin-1β immunoreactive cells have been demonstrated in human disc hernias, suggesting an active inflammation [11, 13]. Inflammatory mechanisms have been suggested to be of pathogenetic significance in sciatAbstract Main problem. Nucleus pulposus and/or chronic compression can induce spinal nerve root injury. Inflammation has been proposed as having major importance in the pathophysiologic mechanisms involved in the induction of such injuries. Corticosteroids, potent anti-inflammatory drugs, have been demonstrated to reduce nucleus pulposusinduced spinal nerve root injury. The aim of the present study was to assess the effects of two potent nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac and ketoprofen, in experimental nucleus pulposus-induced spinal nerve root injury in a pig model. Methods. Eighteen pigs were included in the study. Autologous nucleus pulposus was harvested from a lumbar disc and applied locally around the first sacral nerve root after a partial laminectomy of the first and second sacral vertebrae. Six pigs were treated with daily intramuscular injections of diclofenac, 3 mg/kg body weight, for 7 days. Six other pigs were treated with daily intramuscular injections of ketoprofen, 4 mg/kg body weight, for 7 days. As controls, six pigs received injections with physiologic saline. After 7 days, the pigs were reanesthetized and the nerve conduction velocity over the exposed nerve root area was determined. Results. The nerve conduction velocity was significantly higher in pigs treated with diclofenac than in the salinetreated controls, (57±6 m/s vs 38± 18 m/s, P<0.05, Student's t-test). The velocity in pigs treated with ketoprofen, 42±24 m/s, did not differ significantly from that of controls. Conclusions. This study of two potent NSAIDs indicates that nucleus pulposus-induced nerve root dysfunction may be reduced by diclofenac but not by ketoprofen. The reason for this difference is not known, but it might be related to the fact that ketoprofen and diclofenac belong to different NSAID subgroups and have a different selectivity for the two cyclo-oxygenases COX-1 and COX-2.

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“…In animals and humans, pure compression of a non-inflamed nerve produces sensory and motor changes without pain, whereas pain is elicited with manipulation of an inflamed nerve [1,2]. The effects induced by the contact of the NP with the epidural elements have been observed in experimental studies and compelling evidence of histological alterations, changes in the nervous electrical activity, and in the intraneural blood flux after such contact has been obtained [2][3][4][5][6]. The NP structure mainly comprises proteoglycans, collagen and support cells, which are able to produce inflammatory mediators after injury, such as cytokines [7].…”

Section: Introductionmentioning

confidence: 99%

Cytokine inhibition and time-related influence of inflammatory stimuli on the hyperalgesia induced by the nucleus pulposus

2011

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Introduction The symptoms of lumbar disc herniation, such as low back pain and sciatica, have been associated with local release of cytokines following the inflammatory process induced by the contact of the nucleus pulposus (NP) with the spinal nerve. Material and methods Using an animal experimental model of intervertebral disc herniation and behavioral tests to evaluate mechanical (electronic von Frey test) and thermal (Hargreaves Plantar test) hyperalgesia in the hind paw of rats submitted to the surgical model, this study aimed to detect in normal intervertebral disc the cytokines known to be involved in the mechanisms of inflammatory hyperalgesia, to observe if previous exposure of the intervertebral disc tissue to specific antibodies could affect the pain behavior (mechanical and thermal hyperalgesia) induced by the NP, and to observe the influence of the time of contact of the NP with the fifth lumbar dorsal root ganglion (L5-DRG) in the mechanical and thermal hyperalgesia. Results The cytokines present at highest concentrations in the rat NP were TNF-a, IL-1b and CINC-1. Rats submitted to the disc herniation experimental model, in which a NP from the sacrococcygeal region is deposited over the right L5-DRG, showed increased mechanical and thermal hyperalgesia that lasted at least 7 weeks. When the autologous NP was treated with antibodies against the three cytokines found at highest concentrations in the NP (TNF-a, IL-1b and CINC-1), there was decrease in both mechanical and thermal hyperalgesia in different time points, suggesting that each cytokine may be important for the hyperalgesia in different steps of the inflammatory process. The surgical remotion of the NP from herniated rats 1 week after the implantation reduced the hyperalgesia to the level similar to the control group. This reduction in the hyperalgesia was also observed in the group that had the NP removed 3 weeks after the implantation, although the intensity of the hyperalgesia did not decreased totally. The removal of the NP after 5 weeks did not changed the hyperalgesia observed in the hind paw, which suggests that the longer the contact of the NP with the DRG, the greater is the possibility of development of chronic pain. Conclusion Together our results indicate that specific cytokines released during the inflammatory process induced by the herniated intervertebral disc play fundamental role in the development of the two modalities of hyperalgesia (mechanical and thermal) and that the maintenance of this inflammation may be the most important point for the chronification of the pain.

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Acute Effects of Nucleus Pulposus on Blood Flow and Endoneurial Fluid Pressure in Rat Dorsal Root Ganglia

Cited by 125 publications

References 37 publications

Effects of lumbar sympathectomy on pain behavioral changes caused by nucleus pulposus-induced spinal nerve damage in rats

Effects of lumbar sympathectomy on pain behavioral changes caused by nucleus pulposus-induced spinal nerve damage in rats

Nucleus pulposus-induced nerve root injury: effects of diclofenac and ketoprofen

Cytokine inhibition and time-related influence of inflammatory stimuli on the hyperalgesia induced by the nucleus pulposus

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