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At least 19 recordsLinked to original sources
PubMed1991

Decreased density of beta-adrenergic and muscarinic cholinergic receptor sites in the vasa nervorum of aged rats.

The pharmacological profile and the anatomical localization of beta-adrenergic and muscarinic cholinergic receptors of the vasa nervorum were studied in sections of sciatic nerve using radioreceptor binding and light microscope autoradiography techniques. Sprague-Dawley rats of 4 and 24 months of age were used. [3H]Dihydroalprenolol (DHA) and [3H]quinuclidinyl benzilate (QNB) were used to label beta-adrenergic and muscarinic cholinergic receptors, respectively. The ligands were bound to sections of rat sciatic nerve in a manner consistent with the labelling of beta-adrenergic or muscarinic cholinergic receptors in the 2 age groups investigated. The dissociation constant (Kd) values (about 1.37 nM for [3H]DHA and 0.75 nM for [3H]QNB) did not significantly change between 4- and 24-month-old rats. The maximum concentration of binding sites (Bmax) for [3H]DHA was decreased by about 35% in 24 in comparison with 4-month-old rats. The Bmax value for [3H]QNB was reduced by about 50% in the aged rats. Light microscope autoradiography revealed the development of specific silver grains in the medial layer of epineurial and perineurial arteries in sections of sciatic nerve exposed either to [3H]DHA or [3H]QNB. The number of silver grains developed in epineurial and perineurial arteries of rats of 24 months is significantly lower than in animals of 4 months. The above results suggest the occurrence of an age-dependent loss in the density of beta-adrenergic and muscarinic cholinergic receptors of vasa nervorum. Vasa nervorum are the blood vessels which supply peripheral nerve trunks. They are constituted by outer (epineurial) and inner (perineurial) arteries and veins as well as by a capillary (endoneurial) plexus. Vasa nervorum are innervated by both sympathetic and non-sympathetic nerves which probably play a role in the pathogenesis of some neuropathies. Several different neurotransmitter containing nerve fibres have been identified in the vasa nervorum perivascular plexuses. However, no information is so far available concerning the neurotransmitter receptors of vasa nervorum. Moreover, although the occurrence of age-dependent changes in peripheral nerve morphology and function is well documented, very few reports were centered on the age-dependent changes of the vasa nervorum. The aims of the present study were to characterize pharmacologically and to localize anatomically the beta-adrenergic and muscarinic cholinergic receptors in the rat vasa nervorum. Moreover, the effect of ageing on the density and pattern of these receptors was investigated.

Aging↗
PubMed2001

Do denervated peripheral nerve trunks become ischemic? The impact of chronic denervation on vasa nervorum.

The long-term relationship between the peripheral nerve trunk and its vascular supply, the vasa nervorum, has not been considered in the context of denervation and regeneration. While the microvessels of peripheral nerve are not thought to influence Wallerian degeneration itself, in this work we explored how vasa nervorum respond to denervation of the nerve trunk. Our hypotheses were that the presence of axons had a significant impact on the vasa nervorum and that the absence of reinnervation might eventually lead to an unfavorable ischemic regenerative microenvironment. We studied rat sciatic nerve trunks for up to 6 months following transection and either prevented regeneration or allowed it to proceed. Vasa nervorum were studied in several ways: (i) measurements of local endoneurial blood flow using microelectrode hydrogen clearance polarography; (ii) measurements of erythrocyte flux (flow) in the extrinsic nerve plexus using laser Doppler flowmetry; (iii) India ink perfusion of microvessels in unfixed nerve; (iv) mRNA expression of vascular endothelial growth factor (VEGF) using reverse transcription polymerase chain reaction. Early after injury, there were rises in endoneurial and extrinsic flow, microvessel numbers, and VEGF mRNA expression. Angiogenesis was apparently confined to the epineurial and perineurial compartments. Later, however, there were substantial declines in flow observed in long-term (6-month) denervated sciatic nerve trunks associated with declines in the caliber of new microvessels. Reinnervated sciatic nerves had restored endoneurial blood flow. The findings confirm important relationships between axon presence and local blood flow. Angiogenesis is a feature of the injured peripheral nerve, but long term denervated nerve trunks have declines of flow despite retaining new microvessels.

Animals↗
PubMed1987

The noradrenergic innervation of the vasa nervorum in old rats: a fluorescence histochemical study.

The effect of ageing on the density and pattern of noradrenergic nerves in the perivascular nerve plexus supplying the vasa nervorum of the rat sciatic nerve was studied using combined catecholamine histofluorescence and quantitative image analysis techniques. The density of noradrenergic fibres around arteries and arterioles of the rat sciatic nerve vasa nervorum increased in the old animals. In contrast, no changes in perivascular nerve fibres supplying the veins and venules were found in the vasa nervorum of old rats. The increase in old age of noradrenergic innervation of arteries and arterioles of the vasa nervorum may be related to the pathogenesis of some peripheral nerve diseases.

Age Factors↗
PubMed1989

The vasa nervorum: microcorrosion casts for scanning electron microscopy.

Studies on the vasa nervorum have a long history, not least because of their beneficial application in surgical practice and in understanding the pathogenesis of some neuropathies. In the present study a method is described for the preparation of microcorrosion casts of the vasa nervorum suitable for examination by scanning electron microscopy. The results confirm the findings of earlier investigations but also demonstrate the advantages of an immediate three-dimensional representation of the vascular architecture together with the additional magnification and resolving power of electron microscopy.

Animals↗
PubMed1993

Vasa nervorum constriction from substance P and calcitonin gene-related peptide antagonists: sensitivity to phentolamine and nimodipine.

Previous work has suggested that vasa nervorum are 'tonically' vasodilated by substance P (SP) and calcitonin gene-related peptide (CGRP) arising from perivascular afferent nerve fibers. Local application of specific receptor antagonists of SP or CGRP results in constriction of vasa nervorum. In this work, we examined the responsiveness of vasa nervorum to epineurial spantide and spantide II (SP antagonists) and hCGRP (8-37) (CGRP antagonist) using serial hydrogen clearance curves in the rat sciatic nerve. Vasoconstriction from spantide and hCGRP (8-37) was dose-dependent, and was slightly greater with spantide than hCGRP (8-37). Spantide II induced vasoconstriction comparable to that of spantide. The vasoconstrictive effects of both spantide and hCGRP (8-37) were eliminated by concurrent systemic treatment with with either phentolamine or nimodipine. The findings support the hypothesis that SP or CGRP blockade interrupts 'tonic' peptide vasodilatation and permits vasoconstriction, perhaps by unopposed adrenergic action mediated through calcium channels. The findings however do not exclude a unique direct vasoconstrictive action of the peptide antagonists.

Animals↗
PubMed1992

Differential vulnerability of neuropeptides in nerves of the vasa nervorum to streptozotocin-induced diabetes.

Neuropeptides in perivascular nerves of vasa nervorum supplying blood to rat optic, sciatic, vagus and sympathetic chain nerve trunks are differentially vulnerable to streptozotocin (STZ)-induced diabetes. Immunohistochemical analysis of epineurial/perineurial nerve sheaths showed that 8 weeks after induction of diabetes, the density of neuropeptide Y (NPY)-immunoreactive nerve fibres in optic nerve sheaths was increased, while it was decreased in sciatic, vagus and sympathetic nerve sheaths. Vasoactive intestinal polypeptide (VIP)-immunoreactivity was increased in vasa and nervi nervorum of optic, sciatic, vagus and sympathetic chain nerve sheaths. Immunoassay of NPY confirmed increased levels in optic nerve sheaths and showed that substance P and calcitonin gene-related peptide levels increased in sciatic but not optic nerve sheaths. Neuropeptide levels in the intrafascicular nerve fibres were unaffected. This provides further evidence for a disturbance in the autonomic control of blood flow to peripheral and cranial nerve trunks via vasa nervorum in STZ-induced diabetes, which may lead to ischaemic changes, alter local axon reflexes and contribute to the pathogenesis of the disease.

Animals↗
PubMed1985

Tangier disease. A case with sensorimotor distal polyneuropathy and lipid accumulation in striated muscle and vasa nervorum.

A 65-year-old man with Tangier disease (analphalipoproteinemia) had had a progressive sensorimotor distal neuropathy with sensory ataxia for 1 year. Muscle biopsy demonstrated excess lipid vacuoles on histochemical and electron-microscopic techniques. Sural nerve biopsy showed a marked loss of large fibers and an increase in small myelinated fibers, with presence of remyelinating fibers and clusters of regeneration; a few aspects of active demyelination and some onion-like formations were also present. Lipid accumulation chiefly affected the Schwann cells of unmyelinated fibers and, to a lesser degree, of myelinated fibers, endoneurial fibroblast, and vasa nervorum. Teased fibers showed prevalent aspects of de-/remyelination and, often in association, marked myelin wrinkling suggesting axonal atrophy. This Tangier patient differs from known cases for the presence of a distal symmetrical sensorimotor polyneuropathy (not previously reported in Tangier disease) and because of the morphological findings of de-/remyelination coexisting with aspects of axonal atrophy and previous degeneration, and of lipid accumulation within striated muscle and vasa nervorum. This latter finding contrasts with the assumption that in Tangier disease vessel walls are not a site of lipid storage: probably the vasa nervorum are different, in this respect, from other vessels, because of the intense lipid metabolism of the nervous tissue. Thus we suggest that involvement of vasa nervorum in Tangier disease may be more important than previously suspected, possibly playing a role in the causation of neuropathy.

Aged↗
PubMed1993

Evidence that capsaicin hyperaemia of rat sciatic vasa nervorum is local, opiate-sensitive and involves mast cells.

1. In previous work, we identified a prolonged and intense hyperaemic response of rat sciatic endoneurial vasa nervorum produced by epineurial application of capsaicin. We postulated that this response, which was blocked by substance P (SP) or calcitonin gene-related peptide (CGRP) antagonists, was a result of local release of neuropeptides on the 'feeding' epineurial vascular plexus. 2. In the present study, we evaluated factors that might influence capsaicin-induced hyperaemia of the rat sciatic endoneurium as measured by hydrogen clearance: central afferent connections, the epineurial vascular plexus, the release of histamine and administration of opiates. 3. Interruption of central afferent connections by proximal nerve section or removal of the epineurial vascular plexus did not influence baseline endoneurial perfusion. Plexus removal, but not proximal section, prevented capsaicin hyperaemia. 4. The epineurial vascular plexus was desensitized to the effect of capsaicin by prior application of capsaicin. Capsaicin hyperaemia was also prevented by: topical treatment with Spantide II ((D-NicLys1,3-Pal3,D-Cl2Phe5,Asn6,D-Trp7,9,Nl e11) substance P) an SP antagonist, systemic pretreatment with a combination of H1 and H2 histamine receptor antagonists, systemic pretreatment with cromolyn sodium or systemic pretreatment with morphine. None of these pretreatments influenced baseline perfusion. When systemic morphine was given together with systemic naloxone, an opiate antagonist, capsaicin-induced hyperaemia was restored. 5. These findings indicate that the capsaicin hyperaemia of vasa nervorum is locally mediated, is independent of central afferent connections and is sensitive to a variety of interventions. It requires an intact epineurial plexus that 'feeds' endoneurial microvessels and the release of histamine by mast cells. Its inhibition by morphine suggests that there are local opiate receptors on epineurial perivascular peptidergic fibres.

Afferent Pathways↗
PubMed1983

The autonomic innervation of the vasa nervorum.

Using catecholamine fluorescence and histochemical cholinesterase staining combined with quantitative image analysis a direct autonomic innervation of arteries, arterioles, venules, veins and arterio-venous anastomoses within peripheral nerves was demonstrated in normal as well as in chemically sympathectomized rats. The adrenergic nerves carry varicosities and were more diffused than acetylcholinesterase-containing nerves; the arteries and the arterio -venous anastomoses were more richly innervated. The findings that acetylcholinesterase-positive nerve fibres were unalterated by chemical sympathectomy and were revealed by short incubation times are indicative of a true cholinergic, and probably parasympathetic, innervation of the vasa nervorum. The possible importance of the autonomic innervation of the vasa nervorum in the pathogenesis of some diseases of peripheral nerves is discussed.

Acetylcholine↗
PubMed2007

Therapeutic angiogenesis inhibits or rescues chemotherapy-induced peripheral neuropathy: taxol- and thalidomide-induced injury of vasa nervorum is ameliorated by VEGF.

Toxic neuropathy represents an important clinical problem in the use of the chemotherapeutic substances Taxol and thalidomide. Sensory neuropathy has a high incidence, lacks an effective treatment and is the dose-limiting factor for these drugs. The pathogenic basis of these neuropathies is unknown. We investigated the hypothesis that the experimental toxic neuropathies from Taxol and thalidomide results from destruction of vasa nervorum and can be reversed by the administration of an angiogenic cytokine. In animal models of Taxol- and thalidomide-induced neuropathy, nerve blood flow has been attenuated and the number of vasa nervorum has been reduced. Intramuscular gene transfer of naked plasmid DNA encoding VEGF-1 administered in parallel with Taxol injections completely inhibited deterioration of nerve function and diminution of the peripheral nerve vasculature. Gene therapy in animals with established Taxol- or thalidomide-induced neuropathies resulted in recovery of vascularity and improved nerve electrophysiology. These findings implicate microvascular damage as the basis for toxic neuropathy and suggest that angiogenic growth factors may constitute a novel treatment for this disorder.

Animals↗
PubMedDate not supplied

Effects of diabetes on reactivity of sciatic vasa nervorum in rats.

The aim was to investigate the effects of 2 months of streptozotocin-induced diabetes mellitus in rats on the responses of sciatic vasa nervorum to vasoactive drugs. Changes in perineural blood flow were monitored by laser-Doppler flowmetry during drug superfusion in vivo. Laser-Doppler flux was reduced by 53.3% after 2 months of diabetes. A 38-fold increase in norepinephrine sensitivity was found in diabetic compared to nondiabetic rats. Co-superfusion of norepinephrine and a high dose (100 microM) of the nitric oxide synthase inhibitor, NG-nitro-L-arginine, resulted in 116-fold and 3.6-fold increases in norepinephrine sensitivity in nondiabetic and diabetic rats, respectively, such that dose-response curves for changes in vascular conductance were superimposed. This suggests that the increased norepinephrine sensitivity in diabetes was caused by defective endothelial nitric oxide production or action. After norepinephrine preconstriction, acetylcholine caused dose-dependent increases in vascular conductance, sensitivity being 8.1-fold greater in nondiabetic than diabetic rats. In contrast, endothelium-independent responses to the nitrovasodilator, glyceryl trinitrate, were relatively unaffected by diabetes. Thus, diabetes causes a deficit in nitric oxide mediated endothelium-dependent relaxation of vasa nervorum, resulting in increased vasoconstrictor sensitivity which is likely to impair perfusion and contribute to the pathogenesis of neuropathy.

Animals↗
PubMed1984

The nerves to blood vessels supplying blood to nerves: the innervation of vasa nervorum.

Noradrenergic, serotoninergic and peptidergic nerves have been demonstrated in perivascular plexuses of vasa nervorum of sympathetic, parasympathetic and somatic nerve trunks. 5-Hydroxytryptamine-, vasoactive intestinal polypeptide- and substance P-containing fibers were found by immunohistochemistry to variable extents in whole mounts of the epineurium of sciatic, vagus and paravertebral sympathetic chains of rabbits. Innervation increased with age. This suggests an hitherto unsuspected role for these vasoactive substances in normal blood flow to nerves and in the genesis of experimental and human neuropathies.

Age Factors↗
PubMed1993

Effects of nimodipine on sciatic nerve blood flow and vasa nervorum responsiveness in the diabetic rat.

Evidence is accumulating that impairment of nerve blood flow is a key factor in the pathogenesis of diabetic neuropathy. Nimodipine, a 1,4-dihydropyridine type Ca2+ channel antagonist, has been shown to ameliorate an existing neuropathy in the streptozotocin-induced diabetic rat. In the present study the effect of diabetes mellitus itself and the effect of chronic nimodipine treatment on the sciatic nerve blood flow of streptozotocin-induced diabetic rats were investigated. Nerve blood flow was assessed using laser-Doppler flowmetry. Nerve blood flow gradually decreased during the first 10 weeks of diabetes mellitus and remained relatively stable thereafter. Intervention with nimodipine significantly improved the flow deficit observed in the diabetic rats. Vasa nervorum adrenergic responsiveness was also investigated. Diabetic rats showed a postsynaptic adrenergic hyporesponsiveness. Treatment with nimodipine restored the reduced presynaptic responsiveness independent of the postsynaptic adrenergic hyporesponsiveness. It was concluded that, in addition to direct neuroprotective effects, nimodipine exerts beneficial effects on disturbed nerve blood flow and on reduced presynaptic adrenergic responsiveness of the vasa nervorum in experimental diabetic neuropathy.

Analysis of Variance↗
PubMed1986

Transient focal conduction block following experimental occlusion of the vasa nervorum.

Injection of low-dose arachidonic acid into the rat femoral artery occludes the vasa nervorum of the tibial nerve and produces focal and generalized ischemia with transient effects on nerve conduction. Across a severely ischemic segment of the proximal tibial nerve there is a marked fall in amplitude of the compound muscle action potential (CMAP), indicating focal conduction block. There is also significant slowing of maximal motor conduction velocity (MCV) through this nerve segment, but no dispersion of the proximally elicited response. Distally, in a region of less severe ischemia, there is mild slowing of MCV, but no further decrement in the CMAP amplitude. The conduction block begins 5-15 minutes after injection, reaches a nadir at 30 minutes, and persists in more severe cases for at least 2 hours. Despite these prolonged electrophysiologic abnormalities, there is no evidence of axonal degeneration or segmental demyelination.

Action Potentials↗
PubMed1984

Microangiopathy of vasa nervorum in dysglobulinemic neuropathy.

Thickening of vessel walls resulting from endothelial proliferation was observed in the vasa nervorum of eleven patients with peripheral neuropathy associated with dysglobulinemia. Electron microscopy showed endothelial proliferation accompanied by abnormal accumulation of masses of intracytoplasmic filaments in each case. Of the eleven patients with dysglobulinemia, nine had monoclonal gammopathy and two were found to have polyclonal elevation of gamma globulin levels. Symptoms of neuropathy characteristically preceded detection of serum protein abnormalities by months to years. Nerve fiber lesions involved primarily the axon in four cases; segmental demyelination was the principal abnormality in the other seven. Both abnormalities were present to some degree in all eleven patients. Biphasic myelinopathy with uniform separation of myelin lamellae attributable to globulin deposition was observed in four cases. The microvascular changes included endothelial cytoplasmic enlargement, virtually obliterating the vessel lumen in many instances, with thickening of pericytes, in which intracytoplasmic filaments were prominent and pinocytotic vesicles numerous. No extracellular filaments were noted, and amyloid stains were negative. Possible effects of these microvascular changes include ischemia resulting from severe vascular luminal narrowing, and altered vascular permeability. Severe loss of axons in this group of neuropathies may be the result of ischemia, whereas altered vascular permeability may admit globulin into the endoneurium, where it may directly affect the myelin sheath and precipitate demyelination.

Adult↗
PubMed1992

Innervation of the vasa nervorum: changes in human diabetics.

Transperineurial and epineurial vessels are innervated by plexuses of unmyelinated axons. Human sural nerve biopsies were examined ultrastructurally and immunocytochemically with an antibody which recognizes a neuronal and neuroendocrine protein, PGP 9.5, to characterize perivascular axons of these plexuses. Diabetics exhibited a greater degree of abnormal innervation of the vasa nervorum than nondiabetics with and without neuropathy. Abnormal innervation included: a reduction in the percentage of vessels exhibiting perivascular axons and a concomitant increase in the percentage of vessels having denervated Schwann cell units, particularly around vessels confined to perineurial compartments, and remaining axons in nerves from diabetics exhibited fewer varicosities. Denervated arterioles of diabetics also displayed structural changes indicating injury. The arteriolar structural defects and loss of neurogenic control of neural blood flow may lead to or aggravate endoneurial ischemia or hypoxia. The patchy, focal endoneurial fiber loss that is prominent in proximal nerves and associated with the distal myelinated fiber loss of some diabetic patients may be due in part to perivascular denervation of the vasa nervorum.

Aged↗
PubMed2005

Neuronal nitric oxide synthase mediates statin-induced restoration of vasa nervorum and reversal of diabetic neuropathy.

BACKGROUND: Peripheral neuropathy is a frequent and major complication of diabetes. METHODS AND RESULTS: Severe peripheral neuropathy developed in type II diabetic mice, characterized by significant slowing of motor and sensory nerve conduction velocities. Rosuvastatin restored nerve vascularity, including vessel size, and nerve function also recovered to the levels of nondiabetic mice. Neuronal nitric oxide synthase expression in sciatic nerves was reduced in diabetic mice but was preserved by rosuvastatin. Coadministration of a nitric oxide synthase inhibitor with rosuvastatin attenuated the beneficial effects of rosuvastatin on nerve function and limited the recovery of vasa nervorum and nerve function. In vitro, rosuvastatin inhibited downregulation of neuronal nitric oxide synthase expression induced by high-glucose conditions in cultured Schwann cells. Furthermore, Akt phosphorylation in Schwann cells, downregulated by high-glucose conditions, was also restored by rosuvastatin, consistent with the change of neuronal nitric oxide synthase expression. Akt inhibition independently reduced neuronal nitric oxide synthase expression in Schwann cells in low-glucose cultures. CONCLUSIONS: These data indicate that the HMG-CoA reductase inhibitor rosuvastatin has a favorable effect on diabetic neuropathy independent of its cholesterol-lowering effect. Our data provide evidence that this effect may be mediated in part via neuronal nitric oxide synthase/nitric oxide and phosphatidylinositol 3-kinase/Akt-signaling pathways and also suggest that restoration or preservation of the microcirculation of the sciatic nerve may be involved.

Animals↗