Glutathione and α-lipoate in diabetic rats: nerve function, blood flow and oxidative state

2001 ◽  
Vol 31 (5) ◽  
pp. 417-424 ◽  
Author(s):  
P. S. Van Dam ◽  
B. S. Van Asbeck ◽  
J. F. L. M. Van Oirschot ◽  
G. J. Biessels ◽  
F. P. T. Hamers ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diabetic Rats ◽  
Nerve Function ◽  
Oxidative State

Nerve function and regeneration in diabetic rats: effects of ZD-7155, an AT1 receptor antagonist

1995 ◽  
Vol 269 (3) ◽  
pp. E530-E537 ◽  
Author(s):  
E. K. Maxfield ◽  
A. Love ◽  
M. A. Cotter ◽  
N. E. Cameron
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Renin Angiotensin System ◽  
Capillary Density ◽  
Diabetic Rats ◽  
At1 Receptor ◽  
Myelinated Fiber ◽  
Nerve Function ◽  
Endoneurial Blood Flow ◽  
Nerve Dysfunction

Effects of the angiotensin II AT1 receptor antagonist ZD-7155 on nerve function, blood flow, capillarization, oxygenation, and regenerative capacity after injury were studied in streptozocin-diabetic rats. Deficits in saphenous sensory and sciatic motor conduction velocity measured after 1 or 2 mo of diabetes in anesthetized rats were prevented and corrected by ZD-7155. Sciatic resistance to hypoxic conduction failure, which was increased by 71% by 2 mo of diabetes, was attenuated by 39% with ZD-7155. Endoneurial capillary density, which was unaffected by diabetes, was increased by 34% with 2 mo of ZD-7155 treatment. Sciatic nutritive endoneurial blood flow, which was reduced by 45% by 2 mo of diabetes, remained in the nondiabetic range with ZD-7155. Mean endoneurial O2 tension was reduced 38% by diabetes, which was attenuated by ZD-7155. Punctate freeze damage of sciatic nerve caused complete fiber degeneration. Fourteen days postlesion, there was a 26% deficit in myelinated fiber regeneration distance after 2 mo of diabetes, which was prevented by ZD-7155 treatment from diabetes induction. Thus alterations in the renin-angiotensin system contribute to the neurovascular etiology of nerve dysfunction in experimental diabetes.

The Influence of Oral Magnesium Sulfate on Skin Microvasculature Blood Flow in Diabetic Rats

2010 ◽  
Vol 143 (1) ◽  
pp. 344-350 ◽  
Author(s):  
Ali Heidarianpour ◽  
Efat Sadeghian ◽  
Ali Gorzi ◽  
Farzad Nazem
Keyword(s):  
Blood Flow ◽  
Magnesium Sulfate ◽  
Diabetic Rats ◽  
Oral Magnesium

Abstract WP498: Impaired Pericyte Constriction and Cerebral Blood Flow Autoregulationin Diabetes

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yedan Liu ◽  
Shaoxun Wang ◽  
Ya Guo ◽  
Huawei Zhang ◽  
Richard Roman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ex Vivo ◽  
Mitochondrial Dynamics ◽  
Vascular Cognitive Impairment ◽  
Treated Group ◽  
Diabetic Rats ◽  
Cerebrovascular Function

Diabetes is the primary pathological factor attributed to Alzheimer’s disease and vascular cognitive impairment. Previous studies demonstrated that hyperglycemia promoted oxidative stress in the cerebral vasculature. Cerebrovascular pericytes contribute to maintaining blood-brain barrier (BBB) integrity and regulating cerebral blood flow (CBF). However, whether hyperglycemia diminishes the contractile capability of pericytes, impairs CBF autoregulation and increases BBB permeability are unclear. In the present study, we examined the role of pericytes in cerebrovascular function and cognition in diabetes using cell culture in vitro , isolated penetrating arterioles ex vivo and CBF autoregulation in vivo . Reactive oxygen species were elevated in high glucose (HG, 30 mM) treated vs. normal glucose (NG, 5.5 mM) treated pericytes. Further, mitochondrial superoxide production was increased in HG-treated vs. NG-treated group (13.24 ± 1.01 arbitrary unit (a.u.)/30min vs. 6.98 ± 0.36 a.u./30min). Mitochondrial respiration decreased in HG-treated vs. NG-treated pericytes (3718 ± 185.9 pmol/min/mg, n=10 vs. 4742 ± 284.5 pmol/min/mg, n=10) as measured by a Seahorse XFe24 analyzer. HG-treated pericytes displayed fragmented mitochondria in association with increased fission protein (DRP1) and decreased fusion protein (OPA1) expression. HG-treated pericytes displayed lower contractile capability than NG-treated cells (20.23 ± 7.15% vs. 29.46 ± 9.41%). The myogenic response was impaired in penetrating arterioles isolated from diabetic rats in comparison with non-diabetic rats. Autoregulation of CBF measured by a laser Doppler flowmeter was impaired in diabetic rats compared with non-diabetic rats. Diabetic rats exhibited greater BBB leakage than control rats. The cognitive function was examined using an eight-arm water maze. Diabetic rats took longer time to escape than the non-diabetic rats indicating learning and memory deficits. In conclusion, hyperglycemia induces pericyte dysfunction by altering mitochondrial dynamics and diminishing contractile capability, which promotes BBB leakage, decreases CBF autoregulation and contributes to diabetes-related dementia.

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.

Cerebral vascular autoregulation of blood flow and tissue PO2 in diabetic rats

1985 ◽  
Vol 249 (3) ◽  
pp. H540-H546 ◽  
Author(s):  
M. J. Rubin ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Flow Regulation ◽  
Diabetic Rats ◽  
Adult Rats ◽  
Wall Area ◽  
Normal Limits ◽  
Blood Flow Regulation ◽  
Severe Diabetes ◽  
Tissue Po2 ◽  
Vessel Wall Area

The effect of chronic, severe diabetes mellitus on the morphology, blood flow regulation, and tissue PO2 of the cerebral cortex was evaluated in adult rats. The arterioles of the diabetic animals were enlarged in terms of both lumen diameter and vessel wall area. Although resting blood flow in the diabetic rats was greater than in the normal rats, the autoregulation of cerebral blood flow was very good within an arterial pressure range of 40-150 mmHg, just as in normal rats. The resting tissue PO2 in diabetic rats was 14.9 +/- 0.5 (SEM) compared with 12.7 +/- 0.6 mmHg in normal animals and in both groups remained at or near the resting PO2 at arterial pressures from 40 to 150 mmHg. There was no apparent loss of arterioles on the cortex surface or change in length of individual arterioles in diabetic animals but there was a 20-30% decrease in the number of venules and no change in the length of individual venules. These data indicate that although the arteriolar morphology and number of venules change in the brain during diabetes, physiological function in terms of tissue PO2 and blood flow regulation is maintained within normal limits.

Endoneurial Blood Flow Changes in Diabetic Rats

1993 ◽  
Vol 10 (S2) ◽  
pp. 49S-51S ◽  
Author(s):  
J.R. Williamson ◽  
K. Chang ◽  
W. Allison ◽  
C. Kilo
Keyword(s):  
Blood Flow ◽  
Diabetic Rats ◽  
Endoneurial Blood Flow ◽  
Flow Changes
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