Les neuropathies periphériques du diabète sucré

Vital, C; Jm, Vallat; M, Le Blanc; Martín, Francisco Javier Escalada San; Coquet, M

doi:10.1016/0022-510x(73)90133-0

Cited by 13 publications

(2 citation statements)

References 17 publications

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“…Even assuming that there is some autoregulation, the reduced Pno2 argues in favor of a primary basis of NBF reduction in EDN; if the reduction were secondary (to reduced 02 requirements), then Pno2 should be increased or normal. We suggest that the low Pno2 in experimental diabetes is secondary to reduced NBF and to impairment of diffusion of 02 across the thickened capillary walls (21)(22)(23)(24)(25) and through the increased endoneurial space (27). Tissue 02 tension would also be reduced if erythrocyte 02 affinity were increased.…”

Section: Discussionmentioning

confidence: 99%

“…Reduced erythrocyte deformability and increased erythrocyte adhesion to endothelial cells, which also occur in diabetes (18)(19)(20), may also impair NBF. Microangiopathy, which is well developed in endoneurial blood vessels of humans (21,22) and has been reported in experimental (23)(24)(25) diabetes, might also increase resistance to NBF by reducing the caliber of these vessels (22). In tissues that autoregulate, such as brain (26), blood flow reduction may be primary or secondary (to reduced metabolic demands).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Prevention of some electrophysiologic and biochemical abnormalities with oxygen supplementation in experimental diabetic neuropathy.

Low¹,

Tuck²,

Dyck³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

108

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Endoneurial hypoxia has been suggested as a mechanism of human and experimental diabetic neuropathy (EDN). We found that rats rendered diabetic for 4 months had reduced nerve blood flow (NBF) and nerve oxygen tension (Pno2). The NBF was reduced by at least 33% in EDN and 60% of the oxygen tensions in the endoneurial 02 histogram were less than 25 mm Hg (3.3 kPa) in EDN compared with only 19% in the controls. To test the hypothesis that EDN may in part be due to hypoxia, we studied the effectiveness of oxygen supplementation in preventing some electrophysiologic and biochemical abnormalities. Rats with EDN had reduced caudal nerve conduction velocity and had a resistance to ischemic conduction block. When a matched groups of rats with EDN were 02 supplemented for 4 weeks, the time to 50% block of nerve conduction and nerve conduction velocity was no longer statistically different from controls. Endoneurial free sugars (glucose, fructose, sorbitol) were markedly increased in EDN. Oxygen supplementation resulted in no change in plasma glucose; by contrast, these increased endoneurial free sugars were significantly reduced (towards normal) by 60%, 33%, and 34%, respectively. myo-Inositol, however, was further decreased by oxygen supplementation. These findings of a partial prevention of electrophysiologic and biochemical abnormalities support a role of hypoxia in the pathogenesis of EDN.While the pathogenesis of diabetic neuropathy remains obscure (1), certain clues have been provided by some recent studies. These include reduced energy utilization (2), increased sorbitol and decreased nerve free myo-inositol concentrations (2, 3), increased intra-axonal sodium levels (4), and a reduced rate of incorporation of lipid and amino acids into myelin (5). Axonal transport rates are also reduced in experimental diabetic neuropathy (6, 4.5 (50 mg-ml-1; dose 1 ml-kg-1). The control groups received an intraperitoneal injection of citrate buffer (1 ml-kg-') alone. The rats were housed in cages with plastic floors covered with sawdust and wood shavings and were fed Purina Rat Chow (no. 5001) with an unrestricted supply of water. Rats were accepted as diabetic if fasting glucose exceeded 300 mg/dl 2 days after streptozotocin and remained >300 mg/dl at the time of sacrifice. NBF and Oxygen Tension Measurements. NBF was measured by using the hydrogen (H2) clearance method (8, 9); H2 and 02 were sensed in nerve with platinum microelectrodes (3-to 5-gm tip diameter) polarized +0.25 V and -0.65 V, respectively, using the principle of polarography (9-11). NBF was calculated from the time constant of the H2 washout curve (9-11). Sciatic Pno2 was sampled as for H2 by using identical microelectrodes but polarized -0.65 V. After in vitro calibration, the electrode was inserted into the nerve fascicle until the tip was at the center of the fascicle. Recordings were repeated at steps of 0.1 x radius as the micropipet was withdrawn. The electrode was recalibrated and the process was repeated at a different site three to five times...

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