Sutures of Fibrin Glue for Divided Rat Nerves: Schwann Cell and Muscle Metabolism

Becker, Corinne; Gueuning, C; Graff, G. L. A.

doi:10.1055/s-2007-1007066

Cited by 23 publications

(19 citation statements)

References 6 publications

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“…Small amounts of fibrin glue may be easily applied in order to perform nerve anastomosis. Fibrin glue does not cause foreign body reaction or scar tissue formation, and it also reduces nerve stump manipulation and avoids the use of nylon wires, that remain in close contact with the nerve tissue 2,16,[25][26][27][28][29][30] . In order to check the results attained in the studies about reinnervation dynamics, we can do histologic and functional evaluations.…”

Section: Introductionmentioning

confidence: 99%

Anastomose do nervo facial de coelhos com cola de fibrina: estudo da velocidade de condução nervosa

Sandrini¹,

Pereira-Júnior

Gay‐Escoda

2007

Rev. Bras. Otorrinolaringol.

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Ai m: The aim of this study was to evaluate the use of fibrin glue on nerve anastomosis, and study conduction velocity obtained by surface electrodes. Methods: In this experimental model we evaluated nerve conduction velocity differences in the preoperative and postoperative periods, for the left facial nerve of 12 rabbits. Then, we evaluated whether there were correlations between conduction velocity and the number of postoperative regenerated axons. The sectioned nerves were anastomosed with fibrin glue. The muscle action potentials were obtained from surface electrodes. The stimulation electrode was placed immediately before the ear pinna (facial nerve trunk) and the recording surface electrode was placed on the quadratus labii inferioris muscle. Results: The facial nerve normal conduction velocity mean value was of 36.53 m/sec. On the postoperative period, the mean conduction velocity was approximately 81% of the normal mean value. A significant correlation was not observed between the postoperative conduction velocity and the number of regenerated axons (p=0.146). Conclusion:The fibrin glue can be used on nerve anastomosis in this animal model and nerve.

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Section: Introductionmentioning

confidence: 99%

Anastomose do nervo facial de coelhos com cola de fibrina: estudo da velocidade de condução nervosa

Sandrini¹,

Pereira-Júnior

Gay‐Escoda

2007

Rev. Bras. Otorrinolaringol.

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“…Among the extracellular matrix factors are laminin and chondroitin sulphate proteoglycans (CSPGs) [22,256,257]. While laminin and neurotrophic factors promote axon regeneration, CSPGs inhibits axon regeneration [70,258]. Although the overall balance of axon regeneration-promoting and -inhibiting favors axon regeneration, if the CSPG in a denervated nerve is eliminated, axon regeneration is faster and more extensive [26, [258][259][260][261].…”

Section: Inhibition Of Axon Regeneration Into the Distal Denervated Nmentioning

confidence: 99%

“…While laminin and neurotrophic factors promote axon regeneration, CSPGs inhibits axon regeneration [70,258]. Although the overall balance of axon regeneration-promoting and -inhibiting favors axon regeneration, if the CSPG in a denervated nerve is eliminated, axon regeneration is faster and more extensive [26, [258][259][260][261]. Therefore, to enhance neurological recovery, lesioned axons must first be induced axons to regenerate across a nerve gap, and then down the distal nerve, which requires eliminating the factors that inhibit axon regeneration [258].…”

Section: Inhibition Of Axon Regeneration Into the Distal Denervated Nmentioning

confidence: 99%

“…Although the overall balance of axon regeneration-promoting and -inhibiting favors axon regeneration, if the CSPG in a denervated nerve is eliminated, axon regeneration is faster and more extensive [26, [258][259][260][261]. Therefore, to enhance neurological recovery, lesioned axons must first be induced axons to regenerate across a nerve gap, and then down the distal nerve, which requires eliminating the factors that inhibit axon regeneration [258]. CSPGs can be eliminated by the application of the enzyme C-ABC that digests CSPG or by blocking its synthesis via intramuscular injections of β-D-xyloside [259,260].…”

Section: Inhibition Of Axon Regeneration Into the Distal Denervated Nmentioning

confidence: 99%

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Promoting Axon Regeneration and Neurological Recovery Following Traumatic Peripheral Nerve Injuries

Kuffler¹

2015

Int J Neurorehabilitation Eng

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Repairing Peripheral Nerves following Traumas Nerve crushWithin several days of crushing a peripheral nerve, the injured axons begin to regenerate through their distal pathway until they reach their original targets with which they restore neurological function. The larger the number of axons that regenerate through the distal nerve, the greater the extent of neurological recovery [1][2][3]. The number of axons that regenerate, and thus neurological recovery, is influenced by the physiological state of the distal denervated nerve pathway [4][5][6][7].Following a peripheral nerve crush, the injured axons begin to regenerate within 2 days of injury [8]. They may regenerate to their targets through their original pathway in association with and promoted by its Schwann cells, the neurotrophic factors they release, and the Schwann cell extracellular matrix [1,4,[9][10][11][12][13][14]. Thus, the distal nerve provides a simple means for promoting and directing the regenerating axons to their original targets [15][16][17][18]. However, when a nerve has a gap, the gap must be bridged with a material that is permissive to and promotes axon regeneration across the entire gap to reach the distal nerve stump, through which the axons must then be able to regenerate.The Schwann cells in the denervated distal nerve release neurotrophic factors that promote axon regeneration, but also release extracellular matrix components that promote and inhibit axon regeneration [19][20][21][22][23][24][25][26]. Thus, regeneration through the distal nerve is a balance of the influences of factors that both promote and inhibit regeneration. If the Schwann cells are present, such as after a simple nerve crush, virtually 100% of the axons regenerate and they innervate all the denervated synaptic sites. If the Schwann cells within the distal nerve pathway are killed, leaving only the extracellular matrix intact, the number of axons that regenerates to their targets decreases by 94%. This is because the factors required to trigger the regenerating axons to branch at extracellular matrix branch points are missing, axons do not branch, and therefore each axon reinnervates only a single denervated muscle fiber. Thus, Schwann cells along the distal nerve pathway and a AbstractFollowing a peripheral nerve crush, or when a peripheral the nerve is transected and the nerve stumps anastomosed, neurological recovery is generally excellent. This is because the axons merely have to regenerate through the distal portion of the nerve through the existing extracellular matrix of the denervated Schwann cells that direct and promote them to their distant denervated motor and sensory targets. However, when a length of a peripheral nerve is destroyed, and anastomosis is not possible, the standard surgical repair technique is to graft a length/s of autologous sensory nerve into the gap. Neurological recovery is generally good if the nerve gap is <2 cm in length, the repair is performed <4 months post trauma, and the patients are <25 years of age. Because the nerve ...

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“…The less than optimal results obtained af ter surgical division of the sciatic nerve in the rat and repair by either the classical microneurosurgical sutures or the new fibrinogen adhesive method -both repair methods in volving a significant degree of cross-reinner vation and being equally inferior to the spon taneous recovery occurring after a simple nerve crush [3] -has led to the search for neurotrophic factors. Consideration of hu man material has led Lundborg [12] to the same general conclusion, i.e.…”

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confidence: 99%

Nerve and Muscle Regeneration after Axonal Division in Rats Treated with Isaxonine Phosphate (Isopropylamino-2-Pyrimidine Phosphate)

Becker¹,

Gueuning²,

Graff³

1986

Eur Surg Res

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Isaxonine phosphate (isopropylamino-2-pyrimidine phosphate), a neurotrophic agent, was tested on Schwann cell and muscle metabolism as evidenced by radiophosphate uptake in the inorganic phosphate and organic-bound acid-soluble phosphate fractions. It had no demonstrable effect either on sciatic nerve Schwann cells above and below an experimental crush or on the corresponding gastrocnemius and soleus muscles in their denervated and reinnervated state (7th to 28th postoperative day). It also failed to influence the end results (150th postoperative day) at nerve and muscle level after surgical division of the nerve and repair by either microsuture or fibrinogen adhesive.

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Sutures of Fibrin Glue for Divided Rat Nerves: Schwann Cell and Muscle Metabolism

Cited by 23 publications

References 6 publications

Anastomose do nervo facial de coelhos com cola de fibrina: estudo da velocidade de condução nervosa

Anastomose do nervo facial de coelhos com cola de fibrina: estudo da velocidade de condução nervosa

Promoting Axon Regeneration and Neurological Recovery Following Traumatic Peripheral Nerve Injuries

Nerve and Muscle Regeneration after Axonal Division in Rats Treated with Isaxonine Phosphate (Isopropylamino-2-Pyrimidine Phosphate)

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