diabetic neuropathies/hypoxia

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Hypoxic neuropathy: does hypoxia play a role in diabetic neuropathy? The 1988 Robert Wartenberg lecture.

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Prijava / prijava

In this report I review: (1) the blood supply and endoneurial microenvironment of nerve; (2) the class, type, and spatial distribution of nerve fiber degeneration as a function of number, site, and class of vessels occluded; (3) the putative mechanisms of nerve hypoxia; and (4) the role of hypoxia

Central hypoxaemia in rats provokes neurological defects similar to those seen in experimental diabetes mellitus: evidence for a partial role of endoneurial hypoxia in diabetic neuropathy.

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Endoneurial hypoxia has been put forward as a factor contributing to diabetic neuropathy. The aim of this study was to determine whether alterations in motor nerve conduction velocity, Na+/K(+)-ATPase activity and substance P content of nerve and skin tissue, characteristic of the diabetic rat,

Science to practice: Renal hypoxia and fat deposition in diabetic neuropathy--new insights with functional renal MR imaging.

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Prijava / prijava

Despite being a valuable tool for evaluation of the kidneys, renal magnetic resonance (MR) imaging in clinical practice has been limited to depiction of anatomy and provides little diagnostic information about the health and function of the kidney in patients with chronic kidney disease (CKD) and

Erythropoietin response to hypoxia in patients with diabetic autonomic neuropathy and non-diabetic chronic renal failure.

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OBJECTIVE An erythropoietin (EPO)-deficient anaemia is recognized in Type 1 diabetic patients with early nephropathy and symptomatic autonomic neuropathy (DN). The aim of this study was to determine whether the EPO response to hypoxia was deficient in order to clarify the mechanisms involved in this

[Intersensory correlations in diabetic neuropathy during adaptation to intervalic normobaric hypoxia].

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The state of vibration sensitivity and of gustatory perception as well as the influence of interval hypoxic training on these indices were estimated in 21 patients with insulin-independent diabetes mellitus (IIDM) without neuropathic manifestations, in 21 analogous patients with neuropathic

Neuropathology and pathogenesis of diabetic autonomic neuropathy.

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Autonomic neuropathy is a significant complication of diabetes resulting in increased patient morbidity and mortality. A number of studies, which have shown correspondence between neuropathologic findings in experimental animals and human subjects, have demonstrated that axonal and dendritic

Transperineurial capillary abnormalities in the sural nerve of patients with diabetic neuropathy.

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Morphometric techniques were employed to assess perineurial capillary abnormalities in the sural nerve of 20 diabetic patients with neuropathy and 10 normal control subjects. Structural abnormalities were related to quantitative neurophysiological and neuropathological measures of neuropathy.

Reduced vascular endothelial growth factor expression and intra-epidermal nerve fiber loss in human diabetic neuropathy.

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OBJECTIVE To assess the relevance of vascular endothelial growth factor (VEGF) in the maintenance of peripheral nerve integrity in diabetic neuropathy we have assessed the expression of VEGF and intra-epidermal nerve fiber density (IENFD) in skin biopsy samples from diabetic

Effects of hypoxia and severity of diabetes on Na,K-ATPase activity and arachidonoyl-containing glycerophospholipid molecular species in nerve from streptozotocin diabetic rats.

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The pathogenesis of experimental diabetic neuropathy is associated with the development of endoneurial hypoxia. Exposure of normal rats to hypoxic conditions has previously been shown to reduce nerve conduction velocity. To study the biochemical effects of hypoxia further, streptozotocin-induced

Hypoxia-induced apoptosis of dorsal root ganglion neurons is associated with DNA damage recognition and cell cycle disruption in rats.

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The metabolic effects of hyperglycemia and hypoxia are important in the pathogenesis of diabetic neuropathy. We demonstrated apoptosis in dorsal root ganglion neurons in vitro by employing an oxygen-glucose deprivation model that uses dorsal root ganglia incubated in room air (pO2=150 torr) followed

Improvement of endoneurial lipid abnormalities in experimental diabetic neuropathy by oxygen modification.

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Endoneurial hypoxia and a high frequency of closed capillaries have been found in chronic experimental diabetes and human diabetic sural nerve, respectively. These findings have led to the hypothesis that the pathogenesis of diabetic neuropathy is due to endoneurial hypoxia. To evaluate the role of

Hypoxia and high glucose activate tetrodotoxin-resistant Na(+) currents through PKA and PKC.

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Prijava / prijava

Voltage-gated sodium channels are critical for the initiation and propagation of action potentials and for the regulation of neuronal excitability. Hyperglycemia and hypoxia are two main changes in diabetes frequently associated with several complications. Although many studies on

Differences in sensitivity to hyperglycemic hypoxia of isolated rat sensory and motor nerve fibers.

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We explore whether the prevalence of sensory deficits in diabetic neuropathy can be explained by diffuse endoneurial hypoxia. Isolated ventral and dorsal rat spinal roots incubated in 2.5 or 25 mM extracellular glucose were transiently exposed to hypoxia (30 min) in a solution of low buffering

Abnormal chemoreceptor response to hypoxia in patients with tabes dorsalis.

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Nine patients with tabes dorsalis and one patient with diabetic autonomic neuropathy were subjected to hypoxia to test the integrity of their carotid chemoreceptors. Ventilation and pulse rate changes were monitored and compared with those of a group of normal subjects of comparable age and sex.

Preservation of the hypoxic drive to breathing in diabetic autonomic neuropathy.

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1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia (Ve/Peto2) during exercise in 22 male diabetic patients,

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