Is resistance to ischaemic conduction failure induced by hypoxia?

Masson, E. A.; Church, S.; Woodcock, Ashley; Hanley, S P; Boulton, A. J. M.

doi:10.1007/bf00274780

Cited by 40 publications

(23 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The underlying rheological changes and vasa nervorum microangiopathy produce an ATP supply deficit and increased dependence on anaerobic metabolism in diabetic animals (1), leading to reduced CV and increased RICF. Similar functional changes have been noted in nondiabetic rats and patients with chronic hypoxia (7,8).…”

supporting

confidence: 66%

Effects of Chronic α-Adrenergic Receptor Blockade on Peripheral Nerve Conduction, Hypoxic Resistance, Polyols, Na+-K+-ATPase Activity, and Vascular Supply in STZ-D Rats

et al. 1991

View full text Add to dashboard Cite

The effects of alpha-receptor blockade on nerve conduction, hypoxic resistance, ouabain-sensitive Na(+)-K(+)-ATPase, nerve polyols, and capillary density were examined in streptozocin-induced diabetic (STZ-D) rats. Nondiabetic and untreated diabetic control groups were used. Diabetes duration was 2 mo. There were two treated diabetic groups. A "prevention" group received 5 mg/kg prazosin for 2 mo from the induction of diabetes. A "reversal" group was untreated for the 1st mo and was given prazosin for the subsequent month. Conduction was measured in motor nerves supplying tibialis anterior and gastrocnemius muscles and sensory saphenous nerve. Diabetes resulted in 15-29% reductions in conduction velocity (P less than 0.01). In the prevention group, conduction deficits were minimal compared with untreated diabetes (P less than 0.01). In the reversal group, motor conduction was also substantially improved, although sensory conduction was not significantly affected. In vitro measurement of sciatic nerve hypoxic resistance revealed a 49% increase in the time taken for compound action potential amplitude to reach half its initial value with diabetes (P less than 0.01). This was largely prevented by prazosin treatment (P less than 0.01), although treatment had a lesser effect in the reversal group. Treatment had no effect on nerve polyol levels or Na(+)-K(+)-ATPase activity. Functional improvements with prazosin were probably based on increased vasa nervorum perfusion. There was a 20% elevation of endoneurial capillary density (P less than 0.01) in both prevention and reversal groups. We conclude that vascular factors play an important role in the etiology of experimental diabetic neuropathy, and functional changes may be corrected by chronic vasodilator treatment.

show abstract

supporting

confidence: 66%

Effects of Chronic α-Adrenergic Receptor Blockade on Peripheral Nerve Conduction, Hypoxic Resistance, Polyols, Na+-K+-ATPase Activity, and Vascular Supply in STZ-D Rats

et al. 1991

View full text Add to dashboard Cite

show abstract

“…Others have suggested that increased resistance to hypoxia reflects an adaptation of the diabetic nerve to prolonged incipient hypoxia as a result of decreased nerve blood flow (Low et al, 1985(Low et al, , 1986a. This suggestion is supported by the demonstration of similar abnormalities in patients with lung or cardiac disease leading to hypoxaemia (Hampton et al, 1989;Masson et al, 1988) and in rats subjected to chronic hypoxia (Low et al, 1986b). The present study, however, demonstrates an improvement of nerve perfusion in the absence of an effect on resistance to hypoxia, questioning reduced blood flow as the single causal factor for this phemonemon in diabetic nerve.…”

Section: Discussionmentioning

confidence: 91%

Insulin partially reverses deficits in peripheral nerve blood flow and conduction in experimental diabetes

Biessels¹,

Stevens²,

Mahmood³

et al. 1996

Journal of the Neurological Sciences

View full text Add to dashboard Cite

Decreased nerve blood flow may be a pathogenetic factor in diabetic neuropathy. Previously it was shown that insulin treatment, commenced at the onset of streptozotocin-diabetes, prevents the development of a nerve blood flow deficit in the diabetic rat. The present study sought to determine the effect of short-term (one month) and acute (one hour) insulin reversal treatment on nerve blood flow deficits in streptozotocin-diabetes. Sciatic nerve blood flow was assessed using laser Doppler flowmetry. Treatment was initiated after one month of diabetes. One month of reversal insulin treatment ameliorated nerve laser Doppler flux (NDF) deficits; in untreated diabetic rats NDF was 51% of that in control animals (P < 0.01) in insulin-treated diabetic rats NDF was 85% of control values (P < 0.01 vs. untreated diabetic, P < 0.05 vs. control). In association with blood flow increases, we found a significant amelioration of motor (P < 0.05 vs. untreated diabetic) and sensory (P < 0.01 vs. untreated diabetic) nerve conduction velocities but not of exaggerated resistance to hypoxic conduction block. Insulin partially reversed hyperglycaemia and sciatic nerve polyol and sugar levels. In a second experiment, in rats with one month of diabetes, acute infusion of insulin led to a 47% (P < 0.001 vs. pre-insulin values) reduction of plasma glucose. This fall in plasma glucose was accompanied by a 38% (P < 0.05 vs. pre-insulin values) increase in NDF. Sensory nerve conduction velocity was marginally increased (6%, P < 0.05 vs. pre-insulin values) after insulin infusion, but motor conduction velocity was not. The data indicate that insulin can partially reverse deficits in nerve blood flow and conduction in diabetic rats.

show abstract

“…The cause is uncertain and there is evidence in support of several alternative mechanisms or different components in the mechanism: (1) Diabetic nerve may be adapted to chronic hypoxia by modification of cytoplasmic metabolic enzymes or their regulation so that anerobic glycolysis is able to maintain energy metabolite levels for longer periods of acute hypoxia 16. This hypothesis is supported by the finding that resistance to acute ischaemic conduction block in non-diabetic subjects is strongly influenced by endoneureal oxygenation 14. Vasodilators increasing nerve blood flow have also been shown to attenuate the development of resistance to acute ischaemic conduction block in streptozotocin induced diabetic rats 17…”

Section: Discussionmentioning

confidence: 99%

Delayed recovery of nerve conduction and vibratory sensibility after ischaemic block in patients with diabetes mellitus

Lindström

Lindblom²,

Brismar³

1997

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

Objectives-To determine if the recovery of nerve function after ischaemic block is impaired in patients with diabetes mellitus relative to healthy controls. Methods-Median nerve impulse conduction and vibratory thresholds in the same innervation territory were studied in patients with diabetes mellitus (n = 16) and age matched controls (n = 10) during and after 30 minutes of cuYng of the forearm. Results-CuYng caused a 50% reduction of the compound nerve action potential (CNAP) after 21.9 (SEM 1.6) minutes in patients with diabetes mellitus and after 10.6 (0.7) minutes in controls. After release of the cuV the half life for CNAP recovery was 5.13 (0.45) minutes in patients with diabetes mellitus and <1 minute in controls. At seven minutes after release of the cuV CNAP was fully restored in the controls whereas in patients with diabetes mellitus CNAP had only reached 75.1 (4.1)% of its original amplitude. After onset of ischaemia it took 14.6 (1.9) minutes in patients with diabetes mellitus before the vibratory threshold was doubled, whereas this took 5.8 (0.8) minutes in controls. After release of the cuV half time for recovery of vibratory threshold was 8.8 (1.0) minutes in patients with diabetes mellitus and 2.6 (0.3) minutes in controls. Ten minutes after the cuff was released the threshold was still raised (2.0 (0.3)-fold) in the diabetes mellitus group, whereas it was normalised in controls. Among patients with diabetes mellitus the impaired recovery correlated with older age, higher HbA1c, and signs of neuropathy, but not with blood glucose. Conclusion-After ischaemia there is a delayed recovery of nerve conduction and the vibratory sensibility in patients with diabetes mellitus. Impaired recovery after ischaemic insults may contribute to the high frequency of entrapment neuropathy in patients with diabetes mellitus.

show abstract

Is resistance to ischaemic conduction failure induced by hypoxia?

Cited by 40 publications

References 22 publications

Effects of Chronic α-Adrenergic Receptor Blockade on Peripheral Nerve Conduction, Hypoxic Resistance, Polyols, Na+-K+-ATPase Activity, and Vascular Supply in STZ-D Rats

Effects of Chronic α-Adrenergic Receptor Blockade on Peripheral Nerve Conduction, Hypoxic Resistance, Polyols, Na+-K+-ATPase Activity, and Vascular Supply in STZ-D Rats

Insulin partially reverses deficits in peripheral nerve blood flow and conduction in experimental diabetes

Delayed recovery of nerve conduction and vibratory sensibility after ischaemic block in patients with diabetes mellitus

Contact Info

Product

Resources

About