The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform
Douglas W. Zochodne - One of the best experts on this subject based on the ideXlab platform.
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neurobiology of peripheral nerve regeneration regeneration and the Vasa Nervorum
2008Co-Authors: Douglas W. ZochodneAbstract:Peripheral nerves are living dynamic tissues that thrive on a nutritive blood supply. The vascular supply of the peripheral nerve, termed “Vasa Nervorum” participates intimately in regenerative events and influences their success. There are important morphological and physiological differences among microvessels that supply nerve trunk, ganglia, and brain. Each entrains and regulates its vascular supply from differing physiological perspectives, depending on their need for metabolic support. Following injury, Vasa Nervorum alter their behavior in unique ways that reflect their exposure to molecules released within the microenvironment and that offer insights into the repair process. Blood flow and microvessels of intact nerve trunks Nerve trunk blood vessels, or Vasa Nervorum, are supplied by upstream arterial branches of major limb vessels. Sometimes these arteries and nerves course together as neurovascular bundles. Peripheral nerves also share their abundant blood supply with other structures in limbs such as bone, connective tissue, skin, and muscle. For this reason, major ischemic lesions are likely to target several tissues and cause widespread damage. The redundant and abundant blood suppy of nerve trunks, however, can be advantageous because the interruption of a single artery is unlikely to cause significant ischemia. There are some sites where there is ischemic vulnerability, known as watershed zones. These are found at areas supplied by terminal branches of overlapping arterial trees. For example, a nerve watershed zone has been identified in the proximal tibial nerve of rats [458].
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do denervated peripheral nerve trunks become ischemic the impact of chronic denervation on Vasa Nervorum
Experimental Neurology, 2001Co-Authors: Ahmet Hoke, Hong S Sun, Tessa Gordon, Douglas W. ZochodneAbstract: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.
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Vasa Nervorum constriction from substance P and calcitonin gene-related peptide antagonists: sensitivity to phentolamine and nimodipine.
Regulatory Peptides, 1993Co-Authors: Douglas W. Zochodne, Lam T. HoAbstract:Abstract 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 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.
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Evidence that capsaicin hyperaemia of rat sciatic Vasa Nervorum is local, opiate-sensitive and involves mast cells.
The Journal of Physiology, 1993Co-Authors: Douglas W. ZochodneAbstract: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.
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stimulation induced peripheral nerve hyperemia mediation by fibers innervating Vasa Nervorum
Brain Research, 1991Co-Authors: Douglas W. ZochodneAbstract:Abstract We studied the influence of graded nerve trunk stimulation on endoneurial blood flow (NBF), oxygen tension and pH in the rat sciatic nerve. The purpose of the investigation was to explore changes in the in vivo microenvironment of axons which result from their metabolic activation. Using endoneurial microelectrodes, we made serial measurements before, during and after varying stimulation protocols in curarized animals. NBF was increased by stimulation and the effect was directly related to the frequency, length and intensity of the stimulation train. At an intensity designed to supramaximally recruit myelinated fibers, high frequency (50 and 100 Hz) and prolonged duration (5–15 min) stimulation increased NBF. The effect was partly blocked by infiltration of lidocaine at the stimulating site. High intensity stimulation, designed to also recruit unmyelinated fibers, was particularly effective in enhancing NBF and lowering microvascular resistance. Continuous measurements of endoneurial oxygen and pH tension failed to identify associated declines with stimulation irrespective of the protocol. Both oxygen tension and pH tended to rise with stimulation. These studies confirm the presence of stimulation-induced endoneurial hyperemia but provide no evidence that local hypoxia or acidosis are mechanisms. Stimulation recruitment of vasodilatory axons innervating Vasa Nervorum may be an alternative explanation.
Norman E Cameron - One of the best experts on this subject based on the ideXlab platform.
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vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy
Diabetologia, 2001Co-Authors: Norman E Cameron, Mary A. Cotter, Sem Eaton, Solomon TesfayeAbstract:Diabetes mellitus is a major cause of peripheral neuropathy, commonly manifested as distal symmetrical polyneuropathy. This review examines evidence for the importance of vascular factors and their metabolic substrate from human and animal studies. Diabetic neuropathy is associated with risk factors for macrovascular disease and with other microvascular complications such as poor metabolic control, dyslipidaemia, body mass index, smoking, microalbuminuria and retinopathy. Studies in human and animal models have shown reduced nerve perfusion and endoneurial hypoxia. Investigations on biopsy material from patients with mild to severe neuropathy show graded structural changes in nerve microvasculature including basement membrane thickening, pericyte degeneration and endothelial cell hyperplasia. Arterio-venous shunting also contributes to reduced endoneurial perfusion. These vascular changes strongly correlate with clinical defects and nerve pathology. Vasodilator treatment in patients and animals improves nerve function. Early Vasa Nervorum functional changes are caused by the metabolic insults of diabetes, the balance between vasodilation and vasoconstriction is altered. Vascular endothelium is particularly vulnerable, with deficits in the major endothelial vasodilators, nitric oxide, endothelium-derived hyperpolarising factor and prostacyclin. Hyperglycaemia and dyslipidaemia driven oxidative stress is a major contributor, enhanced by advanced glycation end product formation and polyol pathway activation. These are coupled to protein kinase C activation and omega-6 essential fatty acid dysmetabolism. Together, this complex of interacting metabolic factors accounts for endothelial dysfunction, reduced nerve perfusion and function. Thus, the evidence emphasises the importance of vascular dysfunction, driven by metabolic change, as a cause of diabetic neuropathy, and highlights potential therapeutic approaches.
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correction of nerve conduction and endoneurial blood flow deficits by the aldose reductase inhibitor tolrestat in diabetic rats
Journal of The Peripheral Nervous System, 1998Co-Authors: Murray A Cotter, Norman E Cameron, T. C. HohmanAbstract:Increased activation of the first half of the polyol pathway, the conversion of glucose to sorbitol by aldose reductase, has been implicated in aldose reductase inhibitor-preventable neurochemical changes that may contribute to the aetiology of diabetic neuropathy. Tolrestat has been used as a standard aldose reductase inhibitor to dissect out polyol pathway-dependent mechanisms in many experimental studies; however, doubt has been cast upon its ability to prevent nerve conduction velocity deficits in diabetic rats. Nerve dysfunction has also been linked to abnormal endoneurial blood flow and oxygenation via increased Vasa Nervorum polyol pathway flux. The aim of this study was to test whether tolrestat could correct sciatic conduction velocity and perfusion defects in diabetic rats. Sciatic motor conduction velocity, 21% reduced by 1 month of streptozotocin-induced diabetes, was corrected by 23% and 84% with 1 month of tolrestat treatment at doses of 7 and 35 mg/kg/day respectively. Endoneurial blood flow, 44-52% reduced by untreated diabetes, was within the nondiabetic range with high-dose tolrestat treatment and the flow deficit was 39% corrected by the low dose. Sciatic sorbitol and fructose concentrations were approximately 13-fold and approximately 4-fold elevated by untreated diabetes. This was 32-50% attenuated by low-dose tolrestat and sorbitol and fructose content was suppressed below the nondiabetic level by high dose treatment. A 58% nerve myo-inositol deficit was partially (32%) corrected by high-dose tolrestat treatment. We conclude that tolrestat restores defective conduction and blood flow in diabetic rats and is a good pharmacological tool for studies on polyol pathway effects in peripheral nerve.
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effects of diabetes on reactivity of sciatic Vasa Nervorum in rats
Journal of Diabetes and Its Complications, 1997Co-Authors: Emily K Maxfield, Norman E Cameron, Mary A. CotterAbstract:Abstract 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 perineurial 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 μM) of the nitric oxide synthase inhibitor, N G -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.
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the effects of evening primrose oil on nerve function and capillarization in streptozotocin diabetic rats modulation by the cyclo oxygenase inhibitor flurbiprofen
British Journal of Pharmacology, 1993Co-Authors: Norman E Cameron, Mary A. Cotter, K. C. Dines, S. Robertson, Dominic CoxAbstract:1 The aims of this study were first, to examine whether deficits in nerve conduction in streptozotocin-diabetic rats could be reversed by a 10% dietary supplement of evening primrose oil. Second, to determine the time-course of reversal, and third, to assess whether the effects could be blocked by the cylco-oxygenase inhibitor flurbiprofen (5 mg kg−1 day−1). 2 One-month diabetes produced 20% and 15% deficits in sciatic motor and saphenous sensory conduction velocity respectively, which were maintained over 2 months diabetes. 3 The effect of 1-month evening primrose oil treatment on abnormalities caused by an initial month of untreated diabetes was examined. Motor and sensory nerve conduction velocity were restored to the non-diabetic level. 4 Resistance to hypoxic conduction failure was investigated for sciatic nerve trunk in vitro. The 80% conduction failure times were 29% and 55% prolonged by 1- and 2-month diabetes respectively. Evening primrose oil did not reverse the increased hypoxic resistance following 1-month untreated diabetes. 5 Sciatic nerve endoneurial capillary density was not significantly affected by diabetes, but was 16% increased in diabetic rats with reversal by evening primrose oil treatment for 1 month compared to 2-month untreated diabetes. 6 Serial motor conduction velocity measurement after 3-month untreated diabetes revealed complete normalization by evening primrose oil within 4 days. Cessation of treatment resulted in a rapid decline in conduction velocity over 24 h. 7 In a preventive study of 2-month duration, 6 groups of rats were used. These comprised non-diabetic controls, diabetic rats, and evening primrose oil-treated diabetic rats, both with and without flurbiprofen treatment. Flurbiprofen had no significant effect in non-diabetic rats, but produced an 11% worsening of motor conduction velocity and a 21% reduction of sciatic capillary density in diabetic rats. Evening primrose oil prevented the decreases in conduction velocity and increased hypoxic resistance with diabetes, and caused a 23% increase in capillary density. Flurbiprofen completely blocked the effect of evening primrose oil on conduction velocity, resistance to hypoxia, and capillarization. 8 Six main conclusions were reached. First, evening primrose oil rapidly reverses conduction deficits in diabetic rats. Second, the effects of treatment may be very short-lived, suggesting a primary metabolic action. Third, evening primrose oil cannot reverse established changes in hypoxic resistance over 1-month treatment. Fourth, long-term treatment causes angiogenesis, suggesting a vascular action. Fifth, products of cyclo-oxygenase-mediated metabolism are necessary for maintaining Vasa Nervorum integrity in diabetic rats. Sixth, evening primrose oil probably acts by providing substrate for vasodilator prostanoid synthesis by Vasa Nervorum.
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essential fatty acid diet supplementation effects on peripheral nerve and skeletal muscle function and capillarization in streptozocin induced diabetic rats
Diabetes, 1991Co-Authors: Norman E Cameron, Mary A. Cotter, S. RobertsonAbstract:Effects of essential fatty acids on nerve conduction, hypoxic resistance, skeletal muscle contractile properties, and capillary density were examined in streptozocin-induced diabetic rats. Nondiabetic and diabetic controls and three diabetic groups treated with 10% supplements of corn oil, evening primrose oil (Efamol), or a mixture of 80% evening primrose oil and 20% fish oil (Efamol Marine) for 2 mo were used. Efamol and Efamol Marine increased plasma gamma-linolenic acid levels, but arachidonic acid was elevated only with Efamol. Diabetes resulted in 15-29% reductions in sciatic motor and sensory saphenous nerve conduction velocity. Efamol prevented conduction deficits more effectively than Efamol Marine, and corn oil had no effect. In vitro measurement of sciatic nerve hypoxic resistance revealed a 49% increase in the time taken for action potential amplitude to decline by 50% with diabetes. Corn oil had no significant effect. With Efamol, hypoxic resistance was within the nondiabetic range. Efamol Marine produced intermediate results. Functional improvements may relate to enhanced Vasa Nervorum perfusion, because endoneurial capillary density increased by 22% with Efamol, angiogenesis perhaps resulting from eicosanoid production from arachidonic acid. Soleus muscle contractions were prolonged by diabetes. This was partially corrected by treatment, Efamol being most effective. Extensor digitorum longus muscle had reduced tetanic tension with diabetes, and this was prevented by all treatments. Soleus showed a modest increase in capillarization with Efamol, which may have contributed to reduced susceptibility to fatigue. The data suggest involvement of abnormal fatty acid metabolism in the etiology of diabetic neuropathy and myopathy.
Mary A. Cotter - One of the best experts on this subject based on the ideXlab platform.
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vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy
Diabetologia, 2001Co-Authors: Norman E Cameron, Mary A. Cotter, Sem Eaton, Solomon TesfayeAbstract:Diabetes mellitus is a major cause of peripheral neuropathy, commonly manifested as distal symmetrical polyneuropathy. This review examines evidence for the importance of vascular factors and their metabolic substrate from human and animal studies. Diabetic neuropathy is associated with risk factors for macrovascular disease and with other microvascular complications such as poor metabolic control, dyslipidaemia, body mass index, smoking, microalbuminuria and retinopathy. Studies in human and animal models have shown reduced nerve perfusion and endoneurial hypoxia. Investigations on biopsy material from patients with mild to severe neuropathy show graded structural changes in nerve microvasculature including basement membrane thickening, pericyte degeneration and endothelial cell hyperplasia. Arterio-venous shunting also contributes to reduced endoneurial perfusion. These vascular changes strongly correlate with clinical defects and nerve pathology. Vasodilator treatment in patients and animals improves nerve function. Early Vasa Nervorum functional changes are caused by the metabolic insults of diabetes, the balance between vasodilation and vasoconstriction is altered. Vascular endothelium is particularly vulnerable, with deficits in the major endothelial vasodilators, nitric oxide, endothelium-derived hyperpolarising factor and prostacyclin. Hyperglycaemia and dyslipidaemia driven oxidative stress is a major contributor, enhanced by advanced glycation end product formation and polyol pathway activation. These are coupled to protein kinase C activation and omega-6 essential fatty acid dysmetabolism. Together, this complex of interacting metabolic factors accounts for endothelial dysfunction, reduced nerve perfusion and function. Thus, the evidence emphasises the importance of vascular dysfunction, driven by metabolic change, as a cause of diabetic neuropathy, and highlights potential therapeutic approaches.
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effects of diabetes on reactivity of sciatic Vasa Nervorum in rats
Journal of Diabetes and Its Complications, 1997Co-Authors: Emily K Maxfield, Norman E Cameron, Mary A. CotterAbstract:Abstract 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 perineurial 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 μM) of the nitric oxide synthase inhibitor, N G -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.
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the effects of evening primrose oil on nerve function and capillarization in streptozotocin diabetic rats modulation by the cyclo oxygenase inhibitor flurbiprofen
British Journal of Pharmacology, 1993Co-Authors: Norman E Cameron, Mary A. Cotter, K. C. Dines, S. Robertson, Dominic CoxAbstract:1 The aims of this study were first, to examine whether deficits in nerve conduction in streptozotocin-diabetic rats could be reversed by a 10% dietary supplement of evening primrose oil. Second, to determine the time-course of reversal, and third, to assess whether the effects could be blocked by the cylco-oxygenase inhibitor flurbiprofen (5 mg kg−1 day−1). 2 One-month diabetes produced 20% and 15% deficits in sciatic motor and saphenous sensory conduction velocity respectively, which were maintained over 2 months diabetes. 3 The effect of 1-month evening primrose oil treatment on abnormalities caused by an initial month of untreated diabetes was examined. Motor and sensory nerve conduction velocity were restored to the non-diabetic level. 4 Resistance to hypoxic conduction failure was investigated for sciatic nerve trunk in vitro. The 80% conduction failure times were 29% and 55% prolonged by 1- and 2-month diabetes respectively. Evening primrose oil did not reverse the increased hypoxic resistance following 1-month untreated diabetes. 5 Sciatic nerve endoneurial capillary density was not significantly affected by diabetes, but was 16% increased in diabetic rats with reversal by evening primrose oil treatment for 1 month compared to 2-month untreated diabetes. 6 Serial motor conduction velocity measurement after 3-month untreated diabetes revealed complete normalization by evening primrose oil within 4 days. Cessation of treatment resulted in a rapid decline in conduction velocity over 24 h. 7 In a preventive study of 2-month duration, 6 groups of rats were used. These comprised non-diabetic controls, diabetic rats, and evening primrose oil-treated diabetic rats, both with and without flurbiprofen treatment. Flurbiprofen had no significant effect in non-diabetic rats, but produced an 11% worsening of motor conduction velocity and a 21% reduction of sciatic capillary density in diabetic rats. Evening primrose oil prevented the decreases in conduction velocity and increased hypoxic resistance with diabetes, and caused a 23% increase in capillary density. Flurbiprofen completely blocked the effect of evening primrose oil on conduction velocity, resistance to hypoxia, and capillarization. 8 Six main conclusions were reached. First, evening primrose oil rapidly reverses conduction deficits in diabetic rats. Second, the effects of treatment may be very short-lived, suggesting a primary metabolic action. Third, evening primrose oil cannot reverse established changes in hypoxic resistance over 1-month treatment. Fourth, long-term treatment causes angiogenesis, suggesting a vascular action. Fifth, products of cyclo-oxygenase-mediated metabolism are necessary for maintaining Vasa Nervorum integrity in diabetic rats. Sixth, evening primrose oil probably acts by providing substrate for vasodilator prostanoid synthesis by Vasa Nervorum.
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essential fatty acid diet supplementation effects on peripheral nerve and skeletal muscle function and capillarization in streptozocin induced diabetic rats
Diabetes, 1991Co-Authors: Norman E Cameron, Mary A. Cotter, S. RobertsonAbstract:Effects of essential fatty acids on nerve conduction, hypoxic resistance, skeletal muscle contractile properties, and capillary density were examined in streptozocin-induced diabetic rats. Nondiabetic and diabetic controls and three diabetic groups treated with 10% supplements of corn oil, evening primrose oil (Efamol), or a mixture of 80% evening primrose oil and 20% fish oil (Efamol Marine) for 2 mo were used. Efamol and Efamol Marine increased plasma gamma-linolenic acid levels, but arachidonic acid was elevated only with Efamol. Diabetes resulted in 15-29% reductions in sciatic motor and sensory saphenous nerve conduction velocity. Efamol prevented conduction deficits more effectively than Efamol Marine, and corn oil had no effect. In vitro measurement of sciatic nerve hypoxic resistance revealed a 49% increase in the time taken for action potential amplitude to decline by 50% with diabetes. Corn oil had no significant effect. With Efamol, hypoxic resistance was within the nondiabetic range. Efamol Marine produced intermediate results. Functional improvements may relate to enhanced Vasa Nervorum perfusion, because endoneurial capillary density increased by 22% with Efamol, angiogenesis perhaps resulting from eicosanoid production from arachidonic acid. Soleus muscle contractions were prolonged by diabetes. This was partially corrected by treatment, Efamol being most effective. Extensor digitorum longus muscle had reduced tetanic tension with diabetes, and this was prevented by all treatments. Soleus showed a modest increase in capillarization with Efamol, which may have contributed to reduced susceptibility to fatigue. The data suggest involvement of abnormal fatty acid metabolism in the etiology of diabetic neuropathy and myopathy.
Harumi Hotta - One of the best experts on this subject based on the ideXlab platform.
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stimulation of saphenous afferent nerve produces vasodilatation of the Vasa Nervorum via an axon reflex like mechanism in the sciatic nerve of anesthetized rats
Neuroscience Research, 1996Co-Authors: Harumi Hotta, Akio Sato, Yuko Sato, Sae UchidaAbstract:Abstract The present study was intended to examine the physiological relevance of peptidergic afferent vasodilative fibers in the regulation of blood flow in the Vasa Nervorum, with special reference to the axon reflex. The response of nerve blood flow (NBF) in the sciatic nerve to electrical stimulation of saphenous nerve afferents was examined using laser Doppler flowmetry in anesthetized rats whose lumbosacral afferents and efferents had been disconnected from the spinal cord. Repetitive electrical stimulation of unmyelinated fibers in the central cut end of the saphenous nerve produced an increase in NBF in the sciatic nerve ipsilateral to the stimulation, independent of changes in mean arterial blood pressure. This increase was abolished by topical application of a calcitonin gene-related peptide (CGRP) receptor antagonist, hCGRP (8–37). In conclusion, NBF in the sciatic nerve is regulated via an axon reflex-like mechanism by unmyelinated afferent CGRP containing vasodilators with collaterals in the saphenous nerve.
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Stimulation of lumbar sympathetic trunk produces vasoconstriction of the Vasa Nervorum in the sciatic nerve via α-adrenergic receptors in rats
Neuroscience letters, 1991Co-Authors: Harumi Hotta, Akio Sato, K. Nishijo, Yuko Sato, S. TanzawaAbstract:Abstract The effects of repetitive electrical stimulation of a lumbar sympathetic trunk (LST) for 30 s at various frequencies and supramaximum intensity on the nerve blood flow in a sciatic nerve were studied by laser Doppler flowmetry in anesthetized Fischer-344 male rats. The response was biphasic; i.e. an initial increase and then a decrease. The maximum mean increase after 2 Hz stimulation was 22 ± 8%, while the maximum mean decrease after 20–50 Hz stimulation was 79 ± 3%, of the prestimulus control level. The initial increase, which was greater at lower frequencies and existed even after loca sympathetic denervation, was passive, and was caused by the systemic pressor response to LST stimulation. The decrease, which was nearly abolished by an i.v. α-adrenergic blocker, phentolamine (10 mg/kg), resulted from vasoconstriction in the Vasa Nervorum, mainly via activation of α-adrenergic receptors.
Kevin J Shoemaker - One of the best experts on this subject based on the ideXlab platform.
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evidence of bidirectional flow in the sciatic Vasa Nervorum
Microvascular Research, 2014Co-Authors: Dylan T Olver, James C Lacefield, Kevin J ShoemakerAbstract:The purpose of this study was to determine whether bidirectional flow exists in the sciatic Vasa Nervorum. Images obtained using high-frequency color Doppler ultrasound in duplex imaging mode (Vevo 2100) were studied retroactively. In Fig. 1 (left panel; rat 1), the color Doppler signal and flow-velocity waveforms are indicative of pulsatile flow traveling towards (B) and away (C) from the probe. In the right panel (Fig. 1; rat 2), there appears to be three distinct vessels, reflective of non-pulsatile negative flow (D), and pulsatile positive (E) and negative (F) flows. These data confirm the presence of bidirectional arterial flow in the sciatic Vasa Nervorum. Investigating bidirectional flow in the intact whole nerve may be helpful in elucidating novel features of nerve blood flow control in healthy and diseased states.
