Topic
Vasa nervorum
About: Vasa nervorum is a research topic. Over the lifetime, 264 publications have been published within this topic receiving 9001 citations. The topic is also known as: set of vessels of nerves.
Papers published on a yearly basis
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Papers
TL;DR: The evidence emphasises the importance of vascular dysfunction, driven by metabolic change, as a cause of diabetic neuropathy, and highlights potential therapeutic approaches.
Abstract: 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.
729 citations
TL;DR: Metabolic abnormalities combine to produce deleterious changes in nerve perfusion that make a major contribution to the etiology of diabetic neuropathy.
Abstract: Reduced nerve perfusion is an important factor in the etiology of diabetic neuropathy. Studies in streptozotocin-induced diabetic rats show that nerve conduction velocity (NCV) and blood flow deficits are corrected by treatment with vasodilator drugs, with angiotensin II and endothelin-1 antagonists being particularly important. The AT 1 antagonist ZD7155 also prevents diabetic deficits in regeneration following nerve damage, indicating that hypoperfusion is an important limitation for nerve repair. Metabolic changes include high polyol pathway flux, increased advanced glycosylation, elevated oxidative stress, and impaired ω-6 essential fatty acid metabolism. Aldose reductase inhibitors (ARIs) restore NCV via their effects on perfusion. ARI action probably depends on blocking the conversion of glucose to sorbitol, thus preventing depletion of vasa nervorum glutathione, an important endogenous free radical scavenger. Free radicals cause vascular endothelium damage and reduced nitric oxide vasodilation. Inhibition of advanced glycosylation and autoxidation (autoxidative glycosylation), major sources of free radicals, by aminoguanidine or transition metal chelators, corrects neurovascular dysfunction. Evening primrose oil supplies γ-linolenic acid (GLA) to improve vasodilator eicosanoid synthesis in diabetes, correcting nerve blood flow and NCV deficits. Interactions between some of these mechanisms have therapeutic implications. Thus, combined ARI and evening primrose oil treatment produced a 10-fold amplification of NCV and blood flow responses. Similarly, GLA effects are markedly enhanced when given in combination with ascorbate as ascorbyl-GLA. Thus, metabolic abnormalities combine to produce deleterious changes in nerve perfusion that make a major contribution to the etiology of diabetic neuropathy. The potential importance of multi-action therapy is stressed.
338 citations
TL;DR: The present study was designed to investigate whether peripheral nerves present changes in the permeability of blood vessels for labelled serum albumin following crush lesion and sectioning.
Abstract: I t is well known that traumatic lesions of peripheral nerves are followed by a rapid macroscopic swelling of the affected part ( D ~ Y B ~ o w ~ and B ~ , ~ , 1944b; BAT]~AN; G ~ F I ~ L D ) . Experimental studies have also revealed an increase in the wet weight of sectioned sciatic nerves (MoTT and HALLIBVRTON, 1901a, b; MAY; A~E~0~OMm~ and JOttNssoN; JoH~sso~ et al., 1949, 1950; MA2NELL; MAJNO and KaRNows~Y, 1958; ROSSlT~) and of organophosphorons induced peripheral neuropathy (MAJ~o and KAR/gows~:Y, 1961). Several morphological investigations have demonstrated that there is a separation of the nerve fibres in the distal part of sectioned nerves (W~Iss, 1943; W~Iss and DAVIS, 1943; D n ~ Y B ~ o w ~ and B a ~ E ~ , 1944a, b; BLAC~:wooI) and HoL~i~s) and on both sides of a constriction of a peripheral nerve trunk (W~Iss, 1943). This separation of the nerve fibres is thought to be caused by oedema. Various opinions have been put forward concerning the origin of this oedema. W~Iss (1943, 1945) considered that the endoneurial oedema, which is formed above a constriction of a peripheral nerve, is due to obstruction of the centrifugal flow of fluid in the endoneurium, which normally takes place along the whole nerve trunk. Others have proposed that oedema in compressed nerves derives directly from the neural blood vessels ( D ] ~ c B ~ o w ~ and B ~ E ~ n , 1944a, b; WmsL and 0s~omqE). Vasodilatation and increased permeability for serum proteins, leading to a protein rich exudate can be produced by a number of stimuli capable of inducing an inflammatory response in various tissues (for references see SPnc~on and WILLOVG~BY 1963, 1964, 1965; MAJ~O; W I L ~ L ~ 1962, 1965). Albumin labelled with a fluorescent marker has been used previously for tracing the extravascular passage of albumin in various experimental conditions of the central nervous system (KLATZO et al., 1961, 1962, 1964; K~A~zo and ST~rSW~LL ; S TREICItER et al.). The present study was designed to investigate whether peripheral nerves present changes in the permeability of blood vessels for labelled serum albumin following crush lesion and sectioning.
242 citations
TL;DR: In this paper, the authors studied the permeability changes of vasa nervorum and exudation of serum albumin in a nutritional peripheral neuropathy induced by isonicotinic acid hydrazide (INH) in rats.
Abstract: Permeability changes of vasa nervorum and exudation of serum albumin in a nutritional peripheral neuropathy induced by isonicotinic acid hydrazide (INH) in rats were studied by menas of fluorescence microscopic tracing of intravenously injected albumin tagged with Evans blue or with fluorescein isothiocyanate.
220 citations
213 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2021 | 5 |
| 2020 | 11 |
| 2019 | 10 |
| 2018 | 6 |
| 2017 | 7 |
| 2016 | 3 |