scholarly journals Exercise-induced conduction velocity increment: a marker of impaired peripheral nerve blood flow in diabetic neuropathy

Diabetologia ◽  
1992 ◽  
Vol 35 (2) ◽  
pp. 155-159 ◽  
Author(s):  
S. Tesfaye ◽  
N. D. Harris ◽  
R. M. Wilson ◽  
J. D. Ward
Keyword(s):  
Blood Flow ◽  
Diabetic Neuropathy ◽  
Peripheral Nerve ◽  
Conduction Velocity ◽  
Nerve Blood Flow ◽  
Velocity Increment ◽  
Exercise Induced

Hypoxic effect of exogenous insulin on normal and diabetic peripheral nerve

1994 ◽  
Vol 266 (6) ◽  
pp. E980-E985 ◽  
Author(s):  
M. Kihara ◽  
P. J. Zollman ◽  
I. L. Smithson ◽  
T. D. Lagerlund ◽  
P. A. Low
Keyword(s):  
Blood Flow ◽  
Peripheral Nerve ◽  
Oxygen Tension ◽  
Glycosylated Hemoglobin ◽  
Diabetic Rats ◽  
Insulin Administration ◽  
Dissociation Curve ◽  
Nerve Blood Flow ◽  
Intravenous Insulin ◽  
Arteriovenous Shunts

Insulin administration can cause or worsen experimental and human diabetic neuropathy ("insulin neuritis"). In this study, we tested the hypothesis that insulin administration impairs tissue oxygenation. We infused insulin under nonhypoglycemic conditions and evaluated its effect on endoneurial oxygen tension, nerve blood flow, and the oxyhemoglobin dissociation curve of peripheral nerve in normal and diabetic rats. Intravenous insulin infusion resulted in a dose-dependent reduction in endoneurial oxygen tension in normal nerves (from 26% at 0.04 U/kg insulin to 55% at 32 U/kg). The nerves of rats with streptozotocin-induced diabetes were resistant, but with control of hyperglycemia this susceptibility to the endoneurial hypoxic effect of insulin returned. The reduction in endoneurial oxygen tension regressed with glycosylated hemoglobin (Y = 53.8-2.7X, where Y = %reduction in endoneurial oxygen tension and X = HbA1; r = 0.87; P = < 0.001). Diabetes or insulin administration resulted in only minimal and physiologically insignificant alterations in the oxygen dissociation curve and 2,3-diphosphoglycerate of sciatic nerve. Instead, insulin administration resulted in a reduction in nerve nutritive blood flow and an increase in arteriovenous shunt flow. When the latter was eliminated by the closure of arteriovenous shunts (infusion of 5-hydroxytryptamine), endoneurial oxygen reverted to normal. These findings indicate a deleterious vasoactive effect of insulin and may explain the development of insulin neuritis.

scholarly journals Gentiopicroside Ameliorates Diabetic Peripheral Neuropathy by Modulating PPAR- Γ/AMPK/ACC Signaling Pathway

2018 ◽  
Vol 50 (2) ◽  
pp. 585-596 ◽  
Author(s):  
Yi Lu ◽  
Jiayin Yao ◽  
Chulian Gong ◽  
Bao Wang ◽  
Piao Zhou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Peripheral Neuropathy ◽  
Signaling Pathway ◽  
Conduction Velocity ◽  
Nerve Conduction ◽  
Diabetic Peripheral Neuropathy ◽  
Nerve Conduction Velocity ◽  
Nerve Blood Flow ◽  
Ppar Γ ◽  
Compound C

Background/Aims: Gentiopicroside is promising as an important secoiridoid compound against pain. The present study aimed to investigate the analgesic effect and the probable mechanism of Gentiopicroside on Diabetic Peripheral Neuropathy (DPN), and to figure out the association among Gentiopicroside, dyslipidemia and PPAR- γ/AMPK/ACC signaling pathway. Methods: DPN rat models were established by streptozotocin and RSC96 cells were cultured. Hot, cold and mechanical tactile allodynia were conducted. Blood lipids, nerve blood flow, Motor Nerve Conduction Velocity (MNCV) and Sensory Nerve Conduction Velocity (SNCV) were detected. Gene and protein expression of PPAR- γ/AMPK/ACC pathway was analyzed by reverse transcription-quan titative polymerase chain reaction (RT-qPCR) and Westernblot. Besides, PPAR-γ antagonist GW9662 and agonist rosiglitazone, AMPK antagonist compound C and activator AICAR as well as ACC inhibitor TOFA were used to further confirm the relationship between PPAR-γ and AMPK. Results: The results demonstrated that Gentiopicroside markedly ameliorated hyperalgesia with prolonged paw withdrawal latency to heat and cold stimuli and fewer responses to mechanical allodynia compared with DPN model group. Gentiopicroside regulated dyslipidemia, enhanced nerve blood flow and improved MNCV as well as SNCV. Gentiopicroside suppressed ACC expression through the activation of AMPK and PPAR-γ mediated the activation of AMPK and subsequent inhibition of ACC expression. Conclusion: In conclusion, the present study demon strated that Gentiopicroside exerted nerve-protective effect and attenuated experimental DPN by restoring dyslipidmia and improved nerve blood flow through regulating PPAR-γ/AMPK/ACC signal pathway. These results provided a promising potential treatment of DPN.

Iodoantipyrine and Rb86 Cl uptake by brain, cord, and sciatic nerve in the rat

1963 ◽  
Vol 204 (2) ◽  
pp. 327-329 ◽  
Author(s):  
Morris J. Mandel ◽  
Francesco Arcidiacono ◽  
Leo A. Sapirstein
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Nervous System ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Anatomical Entity ◽  
Nerve Blood Flow ◽  
The Brain

Rb86 and Iodo131 antipyrine were injected together by vein in rats. The brain, spinal cord, and nerve contents of each label were measured 30 or 60 sec later. Iodoantipyrine values were used to calculate blood flow to these portions of the nervous system. The ratio of Rb86 to iodoantipyrine uptake was used as an index of the efficacy of the hematoneural barrier. The barrier is most complete in the brain, less complete in the spinal cord, and absent in peripheral nerve. Blood flow values per gram are: brain .41 ml/g min; cord .28 ml/g min, and nerve .11 ml/g min. It is suggested that the blood-brain barrier is an anatomical entity rather than a functional one.

Sonographic assessment of nerve blood flow in diabetic neuropathy

2019 ◽  
Vol 37 (2) ◽  
pp. 343-349
Author(s):  
A. A. Borire ◽  
T. Issar ◽  
N. C. Kwai ◽  
L. H. Visser ◽  
N. G. Simon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diabetic Neuropathy ◽  
Nerve Blood Flow ◽  
Sonographic Assessment

scholarly journals Pentoxifylline Effects on Nerve Conduction Velocity and Blood Flow in Diabetic Rats

2000 ◽  
Vol 1 (1) ◽  
pp. 49-58 ◽  
Author(s):  
Heather Flint ◽  
Mary A. Cotter ◽  
Norman E. Cameron
Keyword(s):  
Blood Flow ◽  
Diabetic Neuropathy ◽  
Conduction Velocity ◽  
Nerve Conduction ◽  
Nerve Conduction Velocity ◽  
Sensory Nerve ◽  
Blood Rheology ◽  
Tissue Perfusion ◽  
Diabetic Rats ◽  
Nitric Oxide Synthase Inhibitor

Pentoxifylline has several actions that improve blood rheology and tissue perfusion and may therefore potentially be applicable to diabetic neuropathy. The aims of this study were to ascertain whether 2 weeks of treatment with pentoxifylline could correct nerve conduction velocity and blood flow deficits in 6-week streptozotocin-diabetic rats and to examine whether the effects were blocked by co-treatment with the cyclooxygenase inhibitor, flurbiprofen, or the nitric oxide synthase inhibitor,NG-nitro-ʟ-arginine. Diabetic deficits in sciatic motor and saphenous sensory nerve conduction velocity were 56.5% and 69.8% corrected, respectively, with pentoxifylline treatment. Sciatic endoneurial blood flow was approximately halved by diabetes and this deficit was 50.4% corrected by pentoxifylline. Flurbiprofen co-treatment markedly attenuated these actions of pentoxifylline on nerve conduction and blood flow whereasNG-nitro-ʟ-arginine was without effect. Thus, pentoxifylline treatment confers neurovascular benefits in experimental diabetic neuropathy, which are linked at least in part to cyclooxygenasemediated metabolism.

104 Effect of Hemorrhagic Shock on Cerebral and Peripheral Nerve Blood Flow in the Rat

1999 ◽  
Vol 11 (4) ◽  
pp. 309
Author(s):  
Shunichi Takagi ◽  
Koji Tateishi ◽  
Takaaki Kilano ◽  
Gabriel Lu ◽  
Vladmir Kvetan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Peripheral Nerve ◽  
Hemorrhagic Shock ◽  
Nerve Blood Flow

Absence of autoregulation in peripheral nerve blood flow

1977 ◽  
Vol 33 (3) ◽  
pp. 347-352 ◽  
Author(s):  
Donald R. Smith ◽  
Arthur I. Kobrine ◽  
Hugo V. Rizzoli
Keyword(s):  
Blood Flow ◽  
Peripheral Nerve ◽  
Nerve Blood Flow
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