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PubMed1992

Microsurgical nerve graft repair of the ablated cavernosal nerves in the rat.

Erectile dysfunction is a significant complication of radical pelvic surgery in men. Using the rat as an experimental model, we investigated the feasibility of repairing surgically ablated cavernosal nerves. Known fertile male Sprague-Dawley rats were randomly divided into three surgical groups of 30 animals (60 study nerves) per group consisting of nerve ablation, immediate nerve reconstruction, and control groups. The nerve ablation group had 5-mm sections of the cavernosal nerve excised bilaterally. The nerve graft group had 5-mm sections of the cavernosal nerve excised bilaterally, followed by immediate microsurgical reconstruction with an autologous interposition nerve graft utilizing the ipsilateral genitofemoral nerve bilaterally. The anastomoses were performed with 10-O nylon sutures at 16 to 25x magnification. The control group underwent sham operations with the cavernosal nerves being exposed only. Erectile function was evaluated at 1, 2, 4, and 6 months postoperatively. Return of erectile function was defined as tumescence of the corporal bodies with application of direct electrical stimulation (3 V of 5 msec pulses at 20 Hertz) to the proximal cavernosal nerves. The 4- and 6-month electrical stimulation studies resulted in tumescence from 65 and 75% of the grafted nerves, which represented a significant difference compared to the ablated group 11 and 5%, respectively (P less than 0.001 at 4 and 6 months). Behavioral copulatory studies, performed prior to electrical stimulation testing, corresponded closely with the results of electrically induced tumescence. We conclude that in this experimental model immediate nerve graft repair appears to be a successful method of salvaging erectile function when the cavernosal nerves have been divided.

Animals↗
PubMed1994

Effects of mast cell degranulation on blood-nerve barrier permeability and nerve conduction in vivo.

Changes in blood-nerve barrier (BNB) integrity and nerve conduction were assessed in rat tibial nerves in which mast cell degranulation was induced by intraneural injection of Compound 48/80 (C48/80). BNB permeability changes were quantitated by the endoneurial accumulation of Evan's blue-labelled albumin (EBA). Over 24 h following intraneural injections, nerves receiving saline showed a 6-fold increase in endoneurial extravasated EBA compared to non-injected nerves. Injection of 250 ng C48/80 produced a similar level of EBA accumulation as saline injections. Increasing the C48/80 dose to 1 microgram produced twice the EBA accumulation as control saline injections and a 12-fold increase over non-injected nerves. Tibial nerves injected with these C48/80 doses showed completely normal nerve conduction. In contrast, increasing the dose to 5 micrograms C48/80 induced, again, increased EBA accumulation over lower doses, but also significant axonal degeneration indicated by profound decreases in compound muscle action potential amplitudes measured with nerve stimulation distal to the injection site. Co-injection of Leupeptin and neutralizing anti-TNF-alpha antibodies with C48/80 failed to mitigate conduction abnormalities suggesting a direct toxic effect of C48/80 on nerve fibres. Time-kinetic studies showed rapid restoration of BNB integrity 24-48 h after injections in all nerves, but at these timepoints C48/80 injected nerves still showed significantly increased BNB permeability compared to nerves injected with saline. Neural mast cell stimulation in the absence of a primed immune response can produce profound temporary changes in blood-nerve barrier permeability and endoneurial fluid composition without affecting nerve conduction.

Animals↗
PubMed1998

Partial cortical devascularization results in elevations of cortical nerve growth factor and increases nerve growth factor protein within basal forebrain cholinergic neurons.

Previous studies have demonstrated that partial cortical devascularization results in increased levels of nerve growth factor protein within the tissue immediately surrounding the infarcted region. In the present study, we have used this lesion model to further characterize the nerve growth factor increase by investigating: (i) the time course for this phenomenon; (ii) the impact of the devascularizing lesion on cortical regions not directly impinged upon by the lesion; and (iii) the response of nerve growth factor-sensitive nucleus basalis neurons providing afferent cortical innervation to the increased availability of nerve growth factor within their target territory. Our results indicate that, within the infarcted cortex, nerve growth factor levels increase rapidly following the lesion (up 51% by one day post lesion), reach a maximum of 136% above controls by three days and undergo a slow decline back to baseline levels by 23 days. Within the frontal and cingulate cortices, which are not devascularized by the lesion and show no signs of pathological damage, nerve growth factor levels increase over a similar time course, and with a similar magnitude, to those in the lesioned cortex. Nerve growth factor-sensitive nucleus basalis neurons on the side ipsilateral to the lesion respond to increased cortical nerve growth factor levels with an increased accumulation of nerve growth factor within their cell bodies (revealed by nerve growth factor immunohistochemistry and quantitative enzyme-linked immunosorbent assay) which was apparent at three days following the lesion, but no longer discernible at seven or 14 days or later. The present study investigated a model of cortical devascularization for its ability to alter nerve growth factor levels within the cortex. Nerve growth factor levels were rapidly increased within the infarcted cortical tissue beneath the lesion but were also elevated to a similar extent, and with a similar time course, in cortical regions not directly impinged upon by the lesion. The retrograde impact of elevated cortical nerve growth factor levels was demonstrated by an increased accumulation of nerve growth factor within the cell bodies of nucleus basalis neurons providing innervation to the cortex. This lesion model should provide a potential avenue for investigating the functional role(s) of nerve growth factor in the intact and lesioned adult central nervous system, as well as the internal mechanisms for regulating its synthesis, release, uptake, and degradation.

Animals↗
PubMed1977

The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

We have shown that when one of the spinal nerves supplying the salamander hind limb is cut or treated with colchicine, the fields of the remaining nerves enlarge in area; whereas nerve section produces Wallerian degeneration, the colchicine-treated nerves conducted action potentials normally and their peripheral fields remained unchanged in area (Aguilar, Bisby, Cooper & Diamond, 1973). Since colchicine-treatment reduced neuronal transport, and nerve-section eliminated it, we proposed that nerve sprouting is regulated by factors normally conveyed to the endings by axoplasmic transport. 1. We have now investigated the effects of colchicine on the thresholds and distribution of individual mechanosensory endings in the skin. If reduction of neuronal transport were enough to cause the threshold to be increased to the point of total unresponsiveness, then this could be a sign of an early stage of degernation in those terminals. It could then be hypothesized that products of degeneration were providing a stimulus for adjacent nerves to sprout. 2. Quantitative physiological studies of the effects of colchicine doses known to interfere with fast axoplasmic transport, indicate that in some experiments the terminal field of the treated nerve was invaded by sprouting fibres from neighbouring axons, when its own endings were unchanged in number, distribution and sensory thresholds. In other experiments the colchicine-treated nerve endings showed an increase in threshold but their function was otherwise unchanged; a similar adjacent nerve sprouting occurred. In a final group, colchicine caused total unresponsiveness of some endings of the treated nerve. 3. When a region of skin was partially denervated by nerve section, the physiological analysis indicated that the number of new mechanosensory endings which sprouted from the remaining axons exactly matched the number lost by nerve degeneration: furthermore the distribution of the endings was normal. It therefore appears that sprouting ceased when the original density of mechanosensory endings in the skin was restored. 4. The possibility that the drug induced sprouting as a consequense of a direct action on the skin is unlikely. With [3H]colchicine, we found that the accumulation of label in the skin of the untreated limb, in which sprouting did not occur, equalled that of the opposite limb. 5. The present results lend support to the original hypothesis of Aguilar et al. (1973), which proposed that collateral sprouting of intact nerves occurs when the supply of neuronally transported factors becomes inadequate to balance out the effects of a postulated target-tissue stimulus. In the Discussion other examples of collateral nerve sprouting, such as that following adjacent denervation, are shown to be explainable by this hypothesis.

Action Potentials↗
PubMed1990

Nerve sprouting induced by a piece of peripheral nerve placed over a normally innervated frog muscle.

1. The effects of a segment of peripheral nerve on the innervation of a skeletal muscle were investigated in the cutaneous pectoris muscle of the frog Rana esculenta. An explant of the sciatic nerve was placed in an aneural region of the muscle at a distance of 1-3 mm from the zone of neuromuscular junctions. The muscles were examined morphologically and electrophysiologically at different post-operative times. 2. After the first month nerve sprouts were seen arising from both nerve terminals and intramuscular nodes of Ranvier. Both the number of sites of sprouting and the relative distance to the explant tip increased with time (up to 5 months), suggesting spread of a nerve sprouting-promoting stimulus. 3. Most neurites resulting from sprouting were seen growing towards the nerve explant, in the vicinity of which active neurite proliferation occurred. Some of them entered the explant as observed in semi-thin and thin sections which revealed the presence of both myelinated and unmyelinated nerve fibres. 4. Electrical stimulation of the nerve explant in preparations autografted for more than 2 months resulted in the contraction of bundles of muscle fibres. Endplate potentials of similar amplitudes were recorded intracellularly in some muscle fibres of such preparations when stimulating either the nerve explant or the cutaneous pectoris nerve. When two stimuli were paired by gradually reducing the interval of time between them, the second response was gradually facilitated. This confirmed that nerve fibres stimulated through the explant corresponded to new neuritic processes resulting from motor nerve sprouting. 5. Pieces of perineural tissue and segments of peripheral nerve killed by alcohol treatment or by repeated freezing and thawing were used as controls. They did not induce any nerve sprouting. 6. The results indicate that cells surviving in a segment of peripheral nerve trunk actively induce intact axons to sprout both from their terminals and intramuscular nodes of Ranvier; moreover these cells promote attraction and proliferation of growing neurites. The possibility of release of a diffusible factor by glial cells is discussed.

Animals↗
PubMed2004

Microsurgical repair of the sural nerve after nerve biopsy to avoid associated sensory morbidity: a preliminary report.

OBJECTIVE: The purpose of this article is to report our preliminary results regarding microsurgical repair of the sural nerve after nerve biopsy, in an attempt to reduce the well-described sensory morbidity and neuroma formation. METHODS: Three patients with a suspected diagnosis of peripheral neuropathy underwent sural nerve biopsies to establish definitive diagnoses. A 10-mm segment of the sural nerve was resected with local anesthesia. After harvesting of the specimen, the proximal and distal nerve stumps were carefully mobilized and united with epineural suture techniques, under a surgical microscope. Sensory evaluations (assessing the presence of hypesthesia/dysesthesia or pain) of the lateral aspect of the foot, in regions designated Areas 1, 2, and 3, were performed before and 6 and 12 months after the biopsies. A visual analog scale was used for pain estimation. RESULTS: The biopsy material was sufficient for histopathological examinations in all cases, leading to conclusive diagnoses (vasculitis in two cases and amyloidosis in one case). The early post-biopsy hypesthesia, which was present for 4 to 8 weeks, improved to preoperative levels as early as 6 months after the nerve repair. Sensory evaluations performed at 6- and 12-month follow-up times demonstrated that none of the patients complained of pain at the biopsy site or distally in the area innervated by the sural nerve. Ultrasonography performed at the 12-month follow-up examination revealed normal sural nerve morphological features, with no neuroma formation, comparable to findings for the contralateral site. CONCLUSION: Microsurgical repair of the sural nerve after biopsy can eliminate or reduce sensory disturbances such as paraesthesia, hypesthesia, and dysesthesia distal to the biopsy site, in the distribution of the sensory innervation of the sural nerve, and can prevent painful neuroma formation. To our knowledge, this article is the first in the literature to report on microsurgical repair of the sural nerve after nerve biopsy. Decreased side effects suggest that this technique can become a standard procedure after sural nerve biopsy, which is commonly required to establish the diagnosis of various diseases, such as peripheral nerve pathological conditions, vasculitis, and amyloidosis. More cases should be analyzed, however, to explore the usefulness of the technique and the reliability of sural nerve biopsy samples in attempts to obtain conclusive diagnoses.

Aged↗
PubMed2000

Prevention and treatment of painful neuromas of the superficial radial nerve by the end-to-side nerve repair concept: an experimental study and preliminary clinical experience.

This article studies the utilization of the end-to-side neurorrhaphy concept in the prevention and treatment of painful neuromas. A total of 20 rats were divided into 2 groups (10 rats per group). In group A, the tibial nerve was divided and left lying in the subcutaneous tissue. In group B, the cut ends of the tibial nerve were sutured to the adjacent peroneal nerve in an end-to-side fashion. Evaluation was performed 90 days after nerve injury. For group A, the proximal end of the tibial nerve formed a "classic" neuroma and the distal end showed a degenerated nerve. In group B, the proximal end of the tibial nerve formed a "non-classic" neuroma and the nerve healed into the peroneal nerve with continuity of the epineurium of the 2 nerves. The distal end of the tibial nerve in group B showed evidence of axonal regeneration. Preliminary clinical experience utilizing the same technique in the prevention and treatment of painful neuromas of the superficial radial nerve is presented and other techniques of nerve-to-nerve implantation are discussed.

Adult↗
PubMed1993

Nerve innervation of the hand and associated nerve dominance aggregates in the somatosensory cortex of a primate (squirrel monkey).

The cutaneous innervation territories of the median, ulnar, and radial nerves to the hand were determined from neurophysiological recordings of peripheral mechanoreceptor axons in adult squirrel monkeys. These territories were then related to cutaneous receptive fields of cortical area 3b neurons to determine how low-threshold inputs from each hand nerve map onto the primary somatosensory cortex. The results indicate that mechanoreceptor axons in each nerve innervate a continuous skin territory covering about 40% of the hand surface. The total territory of each nerve contains subregions of skin that are either autonomously innervated by that nerve or that receive overlapping innervation from more than one nerve. The autonomous, overlap, and total territories of each nerve are relatively constant from hand to hand. In the area 3b cortex, low-threshold afferents from each nerve provide inputs to aggregates of cortical neurons. The cortical aggregates relating to the median and ulnar nerves are arranged as continuous, rostrocaudally oriented bands, whereas aggregates relating to the radial nerve are discontinuous and more patch-like. Similar patterns of bands and patches, and similar compression ratios of skin/cortical area, are seen across different monkeys. These findings demonstrate that the primary somatosensory cortex of normal adult primates contains bands or patches of neurons that are dominantly activated by low-threshold inputs from specific hand nerves. This approach of delineating nerve territories and their related cortical dominance aggregates provides a useful means of analyzing cortical images of nerves and of quantitating peripheral and central patterns of deprivation after nerve injury.

Animals↗
PubMed1982

Nerve growth activities in rat peripheral nerve.

Nerve growth activities in rat sciatic nerves were assayed by recording the neuritic outgrowth from chick embryonic ganglia cultured in collagen gels beside nerve fragments for two days. Living nerve explants released activity that resembled nerve growth factor (NGF) in its effect on sympathetic ganglia and that was almost totally blocked by an antiserum to 2.5 S mouse NGF. Frozen and thawed specimens from normal nerves elicited responses from sympathetic ganglia that were only partially suppressed by anti-NGF and also induced neuritic outgrowth from ciliary ganglia. Thus, from observations on normal nerves, at least two agents promoting axonal extension in vitro were deduced to exist; one substance similar to NGF plus another, non-NGF factor. The level of NGF-like activity was low in killed segments of normal nerves but higher in autologous nerve grafts and degenerating nerves two days after grafting or cutting. However, one or two weeks after nerve transection, distal nerve segments contained little nerve growth activity of either kind. Furthermore, when endoneurial fragments from chronically denervated stumps were cultured, they appeared to have lost some of their capacity to produce NGF-like activity in vitro although the production of activity had, if anything, increased in the perineurial region. In summary, rat peripheral nervous tissue releases two or more soluble substances that stimulate neuritic outgrowth. The level of one or both activities in the endoneurium can be altered by manipulation of nerves in vivo.

Animals↗
PubMed2000

Sorbitol and myo-inositol levels and morphology of sural nerve in relation to peripheral nerve function and clinical neuropathy in men with diabetic, impaired, and normal glucose tolerance.

AIMS: Sorbitol and myo-inositol levels and morphology of sural nerve were compared with nerve function and clinical neuropathy in men with diabetic, impaired (IGT), and normal glucose tolerance. METHODS: After neurography of sural nerve and determinations of sensory thresholds for vibration, warm and cold on the foot, whole nerve sural nerve biopsy was performed in 10 men with Type 1 diabetes mellitus, 10 with IGT, and 10 with normal glucose tolerance. Polyol levels were assessed by gas-liquid chromatography/mass spectrometry. RESULTS: Sural nerve amplitudes were significantly lower and sorbitol levels significantly higher in diabetic patients (median (interquartile range)) (3.7 (3.5) microV and 643 (412) pmol/mg protein, respectively) both compared with IGT (11.3 (10.6)microV; P = 0.04 and 286 (83) pmol/mg protein; P = 0.0032, respectively) and normally glucose tolerant (10.0 (11.6); P = 0.0142 and 296 (250) pmol/mg protein; P = 0.0191, respectively) subjects. There were no differences in nerve morphology between the three groups. Nerve myo-inositol levels correlated, however, positively with cluster density (rs = 0.56; P = 0.0054). In diabetic and IGT subjects, sural nerve amplitudes (2.6 (3.8) vs. 12.1 (10.6) microV; P = 0.0246) and myelinated nerve fibre density (MNFD; 4,076 (1091) vs. 5,219 (668) nerve fibres/mm2; P = 0.0021) were significantly lower in nine subjects with clinical neuropathy than in 10 without. CONCLUSIONS: Nerve degeneration (i.e. MNFD) correlated with clinical neuropathy but not with glucose tolerance status whereas nerve myo-inositol levels positively correlated with signs of nerve regeneration (i.e. increased cluster density).

Diabetes Mellitus, Type 1↗
PubMed1988

Comparative electrophysiologic evaluation of nerve grafts and autogenous vein grafts as nerve conduits: an experimental study.

This study was carried out to compare electrophysiologically the efficacy of autogenous vein grafts, with autogenous nerve grafts as conduits for nerve regeneration. A 0.75-cm segment of sciatic nerve was resected in two groups of Sprague-Dawley rats of equivalent maturity. The nerve gaps were bridged with an autogenous vein graft in the first group (31 rats), and an autogenous nerve graft in the second group (24 rats). Serial in vivo nerve conduction velocity studies and terminal in vitro nerve conduction velocity and nerve action potential measurements were performed. An additional group of 21 animals who had undergone no surgical procedures, were similarly studied to establish an age-adjusted baseline for comparison. Twelve animals in the first group, 14 in the second group, and 13 in the baseline group survived the full year of study. In vivo conduction velocities between the two experimental groups compared favorably. Nerve conduction velocity determined by in vitro technique confirmed this finding and measured similarly at about 78 percent of the baseline. Nerve action potential amplitude in the vein-grafted group was 12.0 percent of the baseline, while the nerve-grafted group was 23.9 percent of the baseline. This study demonstrated that the vein graft compares well with the nerve graft in nerve conduction velocity, but only one-half as well in nerve action potential.

Action Potentials↗
PubMed1998

Effects of prelesioned peripheral nerve graft on nerve regeneration in the rat spinal cord.

OBJECTIVE: The aim of this study was to examine the effects of prelesioned peripheral nerve grafts on central nerve regeneration compared with the freshly transected peripheral nerve grafts in the dorsal funiculus of the rat spinal cord. METHODS: The experimental paradigm consisted of ligating the common peroneal nerve at the midthigh level for 7 days, while the adjacent tibial nerve was left intact. Numerous Schwann cells appeared accompanying regenerating axons in the proximal stump of the ligated nerve. The proximal stumps of the ligated (prelesioned) common peroneal nerve and the intact (untreated) tibial nerve were excised as one tissue block and autografted into the dorsal funiculi of the upper cervical cord. The graft was placed so that the prelesioned common peroneal nerve was positioned on the left dorsal funiculus and the untreated tibial nerve was positioned to the right of the midsagittal plane. Nerve regeneration was examined by light and transmission electron microscopy 1 to 16 weeks after grafting, comparing the effectiveness of prelesioned and untreated nerve grafts. RESULTS: Numerous regenerating axons were observed in the caudal border of both grafts 1 to 2 weeks after grafting. Astrocyte proliferation was suppressed in the prelesioned grafts compared to the untreated grafts. Four to 16 weeks later, the number of regenerating axons was approximately 10-fold as large in the prelesioned grafts as in the untreated grafts. The regenerating axons were myelinated by Schwann cells. Astrocytic glial scar formation was inconspicuous in the prelesioned grafts, whereas it was prominent in the untreated grafts. Schwann cells were contiguous with astrocytes along regenerating axons, forming a continuous conduit from the central to peripheral nerve microenvironments for the outgrowth of regenerating axons. CONCLUSION: The prelesioned peripheral nerve graft is more effective than the untreated graft in suppressing astrocytic scar formation and in supporting the outgrowth of regenerating axons in the dorsal funiculus of rat spinal cord.

Animals↗
PubMed2001

Effects of age on nerve fibers in the rhesus monkey optic nerve.

During normal aging there is a reduction in white matter volume in the cerebral hemispheres and structural abnormalities in myelin in some parts of the central nervous system, but whether nerve fibers are lost with age and whether the myelin changes are ubiquitous is not known. Studying the optic nerve, which is a circumscribed bundle of nerve fibers, offers an opportunity to gain further insight into the effects of normal aging on white matter. The present study examined the optic nerves from young (4-10 years) and old (27-33 years) rhesus monkeys using light and electron microscopy. These nerves had been perfused transcardially to obtain optimal preservation of the tissue. Varying degrees of degeneration were encountered in all the optic nerves from the old monkeys. The changes included myelin abnormalities, similar to those reported in other parts of the central nervous system; the presence of degenerating axons and their sheaths; changes in neuroglial cells; and thickening of the trabeculae of connective tissue in the nerve. The total number of nerve fibers was reduced from an average of 1.6 x 10(6) in the young optic nerves to as few as 4 x 10(5) in one old monkey, and with one exception in all of the old optic nerves the packing density of nerve fibers was less than in any of the young optic nerves. The degenerative changes were most marked in those optic nerves that contained the fewest nerve fibers.

Age Factors↗
PubMed2006

Effect of oblique nerve grafting on peripheral nerve regeneration in rats.

Current methods of peripheral nerve repair are to rejoin cut nerve stumps directly or to bridge large gaps with autologous nerve grafts. In both cases the surface of nerve stump endings is typically cut perpendicularly to the long axis of the nerve. The outcome of such operations, however, is still not satisfactory. In this study, we examine the effect of oblique nerve cutting and grafting on morphological as well as functional features of regeneration. In adult rats, sciatic nerve was cut and rejoined either directly or using an autologous graft, at 90 degrees or 30 degrees angle. Functional regeneration was assessed by walking track analysis during 12-week follow-up. Afterwards muscle weight was measured and histological studies were performed. The latter included nerve fibers and Schwann cells counting, as well as visualization of scar formation and epineural fibrosis. Nerves cut obliquely and rejoined showed better functional recovery than perpendicularly transected. Similar effect was observed after oblique grafting when compared to perpendicular one. Numbers of nerve fibers growing into the distal stump of the nerve as well as the number of Schwann cells were significantly higher in obliquely than in perpendicularly operated nerves. Moreover, growing axons were arranged more regularly following oblique treatment. These data indicate that joining or grafting the nerve stumps at acute angle is a more profitable method of nerve repair than the standard procedure performed at right angle.

Animals↗
PubMed1991

Calbindin-immunoreactive nerve terminals in the guinea pig coeliac ganglion originate from colonic nerve cells.

Previous work has shown that calbindin-immunoreactive (calbindin-IR) nerve terminals are numerous in guinea pig prevertebral ganglia. A high proportion of those colonic nerve cells that project to the inferior mesenteric ganglia are calbindin-IR, but none of the neurons that project from the small intestine to the coeliac ganglion are immunoreactive for calbindin. The present work was designed to determine the source of the calbindin-IR fibres and the pathways by which they reach the coeliac ganglion. Sections through the major nerve trunks that connect with the coeliac ganglion revealed numerous calbindin-IR fibres in the inferior coeliac nerves and in the intermesenteric nerves, while there were very few fibres in the splanchnic or superior coeliac nerves. When all peripheral nerve connections to a lobe of the coeliac ganglion were cut, all calbindin-IR terminals degenerated. Cutting the ileo-caeco-colic nerves caused a substantial reduction in the density of nerve fibres in the coeliac ganglion, whereas no significant reduction could be detected when the intermesenteric nerves were cut. However, lesion of both the ileo-caeco-colic and intermesenteric nerves caused all the calbindin-IR nerve fibres in the coeliac ganglion to degenerate. It is concluded that most or all of the calbindin-reactive nerve terminals in the coeliac ganglion originate from the large intestine and that most reach the ganglion via the ileo-caeco-colic nerves. Thus many colonic intestinofugal neurons, supplying both the coeliac and inferior mesenteric ganglia, are immunoreactive for calbindin, whereas small intestinal intestinofugal neurons are not immunoreactive for this protein.

Animals↗
PubMed2003

Recovery of muscle contractile function following nerve gap repair with chemically acellularized peripheral nerve grafts.

Acellular nerve grafts have emerged as a possible alternative for reconstruction of short (<2 cm) peripheral nerve gaps. Axonal regeneration has been demonstrated within the nerve constructs. However, very little work has been done to demonstrate both axonal regeneration and recovery of motor function following peripheral nerve gap repair with acellular nerve constructs. The authors hypothesized that chemically acellularized nerve grafts can support axonal regeneration and provide functional reinnervation of rat hindlimb muscles with equivalent efficiency to peripheral nerve autografts. Peroneal nerves were harvested from adult rats and chemically acellularized. Two- and 4-cm peroneal nerve gaps were reconstructed with either a cellular autograft or an acellular isograft. Functional recovery was evaluated with walking-track analyses and measurement of maximum tetanic isometric force (F 0 ) of the extensor digitorum longus (EDL) muscle. Walking-track analysis revealed no statistically significant difference in functional recovery in rats undergoing reconstruction of 2-cm nerve gaps with acellular isografts or cellular autografts. Maximum tetanic isometric force measurements revealed a 60 percent force deficit in EDL muscles reinnervated by 2-cm acellular nerve grafts, compared to cellular autografts. Four-centimeter acellular grafts failed to support any significant EDL muscle reinnervation. This study demonstrates that chemically acellularized peripheral nerve supports axonal regeneration and functional reinnervation across 2-cm nerve gaps, and may potentially serve as an appropriate scaffold for reintroducing cellular elements, adhesion molecules, or growth factors for repair of longer nerve gaps.

Animals↗
PubMed1996

Host nerve fibers that regenerate and reside long-term in a rejected nerve allograft are not protected by permability barriers.

We investigated whether permeability barriers develop and protect host nerve fibers that regenerate and reside long-term in a rejected nerve allograft. In order for the barriers to form, host cells have to enter the rejected allograft and differentiate into new endothelial and perineurial cells that respectively form the impermeable endoneurial blood-nerve and the perineurium-nerve barriers that are present in normal nerve. A 2-cm long graft of peroneal nerve was taken from American Cancer Institute (ACI) or Fischer (FR) rats and transplanted to bridge a 2-cm gap between the cut ends of the peroneal nerve of other FR rats. Six months postoperatively, histology revealed that regenerated host nerve fibers in ACI allografts were compartmentalized into numerous minifascicles by perineurial cells and that blood vessels were located outside rather than inside the perineurial compartments among the nerve fibers. Administration of the permeability indicator horseradish peroxidase to allograft recipients (intravenously or topically to the graft in situ) revealed that it entered the endoneurium of microcompartments and spread around the nerve fibers. In contrast, none of the indicator reached nerve fibers in FR syngrafts or normal ACI or FR nerves which were not microcompartmentalized. We concluded that host nerve fibers that regenerate and reside long-term in a rejected nerve allograft are not protected by permeability barriers.

Animals↗
PubMed1997

Blood flow in mobilized nerves: results in a rabbit sciatic nerve model.

The purpose of this study was to evaluate the immediate effect on capillary blood flow of surgical mobilization of 15 cm of the rabbit sciatic and tibial nerve. Capillary nerve blood flow was determined with 16-micron radioactive microspheres. Thirty-seven rabbits were divided into six groups. In the control group A (n = 7), the in situ nerve blood flow was determined. In group B (n = 7), the nerve was mobilized, leaving only the proximal and distal endoneurial vascular supplies; blood flow increased compared with in situ values in most segments. In group C (n = 5), the nerve was mobilized as in group B, but also transected distally; blood flow was markedly decreased in the distal segments but was maintained up to a diameter-to-length ratio of 1:63. In group D (n = 6), the nerve was not mobilized, but was transected proximally and distally; blood flow increased in all segments. In group E (n = 5), the nerve was mobilized and transected proximally and distally, leaving only nerve branches intact; blood flow was significantly higher in segments of the nerve from which nerve branches originated with the nerve receiving blood flow through its branches. In group F (n = 6), the nerve was mobilized, all extrinsic vessels except one were transected, and the proximal and distal nerve was transected; flow was maintained to a diameter:length ratio of 1:41 from the source of blood flow. Therefore, it does appear that long lengths of nerve may be mobilized and transposed while maintaining sufficient blood flow.

Animals↗