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Biomedical subjects

N E Cameron

Publications and source records attributed to N E Cameron.

At least 55 records · Page 3Linked to original sources
PubMed1995

Chronic vitamin E treatment prevents defective endothelium-dependent relaxation in diabetic rat aorta.

We examined the effect in rats of 2 months of streptozotocin-induced diabetes mellitus on relaxation and contraction of aortas in vitro. A further diabetic group was treated from time of diabetes induction with a 1% dietary supplement of vitamin E. Diabetes caused a 26.5% deficit (p < 0.001) in maximum endothelium-dependent relaxation to acetylcholine in phenylephrine-precontracted aortas. This was 64.3% attenuated (p < 0.01) by vitamin E treatment; maximum relaxation was not significantly altered compared to non-diabetic rats. Vitamin E treatment of non-diabetic rats did not significantly affect acetylcholine-induced relaxation. Diabetes or treatment did not significantly alter acetylcholine sensitivity. Endothelium-independent relaxation response to glyceryl trinitrate was not affected by diabetes or vitamin E treatment, indicating that vascular smooth muscle responses to nitric oxide remained unaltered. There was a 35.4% reduction in the maximum contractile response to phenylephrine with diabetes (p < 0.05) which was unaffected by vitamin E treatment. The data suggest that the chronic deficit in nitric oxide-mediated endothelium-dependent relaxation in diabetes depends largely upon excess activity of reactive oxygen species. Treatment with vitamin E to increase free radical scavenging specifically protected vascular endothelium although it had no effect on deficits in vascular smooth muscle contractile responses.

Acetylcholine↗
PubMed1995

Effects of natural free radical scavengers on peripheral nerve and neurovascular function in diabetic rats.

Increased generation of reactive oxygen species, coupled with impaired endogenous scavenging mechanisms, plays a prominent role in the aetiology of neurovascular abnormalities in experimental diabetes mellitus. We examined the efficacy of the natural anti-oxidants vitamins C, E and beta-carotene in preventing nerve conduction and nutritive blood flow deficits in streptozotocin-diabetic rats. One month of diabetes caused a 19.1% reduction in sciatic motor conduction velocity (p < 0.001). This was approximately prevented 80-90% by high-dose (1000 mg.kg-1.day-1) vitamin E and beta-carotene treatments (p < 0.001). Vitamin C had lesser effects; the maximum protection found for motor conduction velocity was 36% using a dose of 150 mg.kg-1.day-1 (p < 0.001). High dose (500 mg.kg-1.day-1 (p < 0.001). High dose (500 mg.kg-1.day-1) vitamin C had a lesser effect on conduction than intermediate doses. Joint vitamin C and lower dose (500 mg.kg-1.day-1) vitamin E treatment had a predominantly additive preventive effect against nerve dysfunction. Resistance to hypoxic conduction failure for sciatic nerve in vitro was markedly increased by diabetes and this remained relatively unaffected by treatment. Sciatic nutritive endoneurial blood flow, measured using microelectrode polarography and hydrogen clearance, was reduced 46.1% by 1 month of diabetes (p < 0.001). This was prevented to the extent of 87%, 36% and 98% by vitamins E, C and beta-carotene, respectively (p < 0.01). These data emphasize the role of oxidative stress in the development of early neurovascular changes in experimental diabetes and show that naturally available scavengers have a neuroprotective action.

Action Potentials↗
PubMed1995

Effects of acetyl- and proprionyl-L-carnitine on peripheral nerve function and vascular supply in experimental diabetes.

L-Carnitine metabolism is abnormal in diabetes mellitus, and treatment with acetyl-L-carnitine (ALC) improves the function of cardiac muscle, retina, and peripheral nerve in experimental models. The aim was to compare the effects of ALC and proprionyl-L-carnitine (PLC) on motor and sensory nerve conduction in streptozotocin-diabetic rats and to ascertain whether their action could be mediated by a vascular mechanism. ALC and PLC treatment for 2 months after diabetes induction attenuated the development of sciatic motor nerve conduction velocity (NCV) deficits by 59.4% +/- 4.4% and 46.9% +/- 3.2%, respectively. There was a similar level of protection for sensory saphenous NCV (42.9% +/- 6.6% and 47.8% +/- 6.0%, respectively). Neither ALC nor PLC prevented the development of resistance to hypoxic conduction failure (RHCF) in sciatic nerve from diabetic rats. A 46.5% +/- 3.4% deficit in sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, in diabetic rats was partially prevented by both ALC (48.7% +/- 6.4%) and PLC (69.4% +/- 10.1%). ALC had no significant effect on blood flow in nondiabetic rats. Thus, the data show that these L-carnitine derivatives have a similar efficacy in preventing nerve dysfunction, which depends on a neurovascular action.

Acetylcarnitine↗
PubMed1995

Effects of chronic treatment with a nitric oxide donor on nerve conduction abnormalities and endoneurial blood flow in streptozotocin-diabetic rats.

This study examined the ability of nitrovasodilator treatment with isosorbide dinitrate to prevent the development of reduced nerve conduction velocity and nutritive blood flow in streptozotocin-induced diabetes mellitus in rats. Two month untreated diabetes caused approximately 23% and 13% reductions in sciatic motor and saphenous nerve sensory conduction velocity (P < 0.001). Isosorbide dinitrate treatment provided 64.6 and 67.6% protection for motor and sensory nerves, respectively (P < 0.01). Sciatic endoneurial nutritive blood flow was measured by microelectrode polarography and a hydrogen clearance technique. After 1 month untreated diabetes, flow was reduced by 41.9% (P < 0.001). Isosorbide dinitrate treatment for 1 month in non-diabetic and diabetic rats significantly increased blood flow (P < 0.01). When between-group variations in blood pressure were taken into account, vascular conductance increased by 29% and 31% in non-diabetic and diabetic rats, respectively (P < 0.01). Thus, nitrovasodilator treatment improves nerve perfusion and function in experimental diabetes, probably by compensating for reduced endothelium-derived nitric oxide release or action.

Animals↗
PubMed1995

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

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.

Angiotensin Receptor Antagonists↗
PubMed1995

Neurovascular dysfunction in diabetic rats. Potential contribution of autoxidation and free radicals examined using transition metal chelating agents.

Oxygen free radical activity is elevated in diabetes mellitus and has been implicated in the etiology of vascular complications. Recent studies have shown that impaired perfusion of nerve endoneurium is a major cause of nerve fiber dysfunction in experimental diabetes. Free radical scavenger treatment prevents the development of nerve conduction abnormalities in diabetic rats. In vitro experiments suggest that autoxidation reactions of glucose, catalyzed by free transition metal ions, are a potential source of free radicals in diabetes. We investigated whether chronic treatment with deferoxamine and trientine, transition metal chelating agents which can prevent autoxidation, could correct nerve conduction and blood flow changes in streptozotocin-diabetic rats. A 20% reduction in sciatic nerve motor conduction velocity after 2 mo diabetes was 90% ameliorated by 2 wk of treatment with deferoxamine or trientine. Sciatic endoneurial nutritive blood flow was 45% reduced by diabetes, but was completely corrected by treatment. In contrast, transition metal chelation had no effect on blood flow or conduction velocity in nondiabetic rats. Thus, the data support the hypothesis that increased free radical activity by glucose autoxidation as a result of impaired transition metal handling is a major cause of early neurovascular deficits in diabetes.

Animals↗
PubMed1995

Comparison of the effects of evening primrose oil and triglycerides containing gamma-linolenic acid on nerve conduction and blood flow in diabetic rats.

The aim was to ascertain whether the ability of evening primrose oil (EPO) treatment to correct peripheral nerve dysfunction in streptozotocin-diabetic rats depends on a gamma-linolenic acid (GLA)-containing triglyceride constituent, di-linolein mono-gamma-linolenate (DLMG). A second objective was to investigate whether the triglyceride conformation of GLA affects efficacy, using tri-gamma-linolenate (TGLA), which is not present in EPO. Third, we examined the actions of these omega-6 essential fatty acid-containing oils on sciatic nerve blood flow to establish a common mechanism. After 6 weeks of diabetes, sciatic motor nerve conduction velocity (NCV) was 21% reduced. EPO treatment caused dose-dependent increases in NCV that reached asymptote within 7 days. DLMG and TGLA, at doses matched for GLA content, had effects indistinguishable from those of EPO. Sciatic blood flow, 47.2% reduced by diabetes, was partially normalized by EPO, DLMG and TGLA. In contrast, sunflower oil (which does not contain GLA) did not alter NCV or blood flow. The data therefore provide strong evidence that DLMG is the active component of EPO and suggest that correction of nerve dysfunction involves a vascular action. The precise triglyceride configuration of GLA does not appear crucial to its effects in experimental diabetic neuropathy.

Animals↗
PubMed1994

The potential contribution of endothelin-1 to neurovascular abnormalities in streptozotocin-diabetic rats.

Abnormal vascular endothelium function may contribute to the reduced nerve perfusion implicated in the aetiology of neuropathy in diabetes mellitus. The aim was to test the hypothesis that a powerful vasoconstrictor, endothelin-1, could be involved in nerve dysfunction in streptozotocin-diabetic rats. After 6 weeks of untreated diabetes, rats were implanted with osmotic minipumps which continuously delivered the endothelin-1 antagonist, BQ-123, to the circulation via a jugular vein cannula. Sciatic motor conduction velocity, monitored serially, was increased after 4 days, treatment (p = 0.028), and reached asymptote by 9-11 days (p = 0.0001), when the degree of amelioration was approximately 60% of the initial diabetic deficit. Treatment of non-diabetic rats for 13 days with BQ-123 had no significant effect on motor conduction velocity. Sensory saphenous nerve conduction velocity was measured acutely after 20 days, BQ-123 treatment. The amelioration of a sensory deficit was approximately 80% (p < 0.001); the resultant conduction velocity value was not significantly different from that of a non-diabetic control group. After 20 days, treatment, sciatic nutritive endoneurial blood flow was measured by microelectrode polarography and hydrogen clearance. A 48% deficit with untreated diabetes (p < 0.001) was 64% ameliorated by BQ-123 treatment (p < 0.001). In non-diabetic rats, BQ-123 treatment had no effect on blood flow. We conclude that endothelin-1 does not seem to be involved in the control of nerve blood flow in non-diabetic rats; however, it makes a major contribution to the perfusion deficit in experimental diabetes. This has deleterious consequences for nerve conduction, and it is possible that endothelin-1 receptor blockade may have therapeutic potential in diabetic patients.

Analysis of Variance↗
PubMed1994

Aldose reductase inhibition, nerve perfusion, oxygenation and function in streptozotocin-diabetic rats: dose-response considerations and independence from a myo-inositol mechanism.

We examined the effects of aldose reductase inhibition on nerve biochemistry and function, blood flow and endoneurial oxygenation in experimental diabetes mellitus. After 1 month untreated diabetes in rats, treatment with the novel sulphonylnitromethane aldose reductase inhibitor, ZENECA ZD5522, prevented a progressive increase in sciatic nerve resistance to hypoxic conduction failure (p < 0.05). Motor conduction velocity deficits after 4 months untreated diabetes were rapidly returned to normal within 12 days (p < 0.0001) by ZD5522 treatment. Following 2-months untreated diabetes, examination of 1 month ZD5522 treatment dose-response relationships for correction of nerve sorbitol and fructose accumulations and reduction in myo-inositol concentration, sciatic motor and saphenous sensory conduction velocity and sciatic blood flow by laser-Doppler flowmetry revealed poor agreement between nerve function and biochemical indices. In addition, polyol accumulation differed between sciatic and saphenous nerves, the latter showing ten-fold lower sorbitol concentrations. Laser-Doppler blood flow was 60% decreased by untreated diabetes (p < 0.001) and there was a strong correlation between ZD5522-mediated increases in blood flow and conduction velocity (p < 0.0001). Measurement of nutritive endoneurial blood flow by microelectrode polarography and hydrogen clearance showed 44% and 45% deficits for 1 and 2 months untreated diabetes (p < 0.001) that were prevented by ponalrestat and ZD5522 treatments, respectively. In contrast, 2 months myo-inositol treatment from diabetes induction did not prevent reduction in blood flow or sciatic motor conduction velocity. A 37% reduction in endoneurial oxygen tension after 2 months diabetes (p < 0.001) was completely prevented by ZD5522 treatment (p < 0.001). The data show that a very high degree of polyol pathway blockade is necessary to correct nerve functional deficits and that aldose reductase inhibitors have a neurovascular action that does not depend on restoration of nerve myo-inositol.

Acetanilides↗
PubMed1994

Effects of evening primrose oil treatment on sciatic nerve blood flow and endoneurial oxygen tension in streptozotocin-diabetic rats.

Evening primrose oil (EPO) is rich in the omega-6 essential fatty acid component, gamma-linolenic acid. The aim of the investigation was to determine whether EPO treatment prevented a reduction in sciatic nerve perfusion and oxygenation in streptozotocin-diabetic rats. Rats were treated from diabetes induction with 10 g EPO kg-1 day-1. Sciatic blood flow was measured by microelectrode polarography and hydrogen clearance. Diabetes caused 47.7% +/- 3.4% (P < 0.001) and 58.8% +/- 4.8% (P < 0.001) reduction in the nutritive (capillary) and the non-nutritive (large vessel) components of endoneurial blood flow, respectively, which were prevented by EPO. Treatment had no significant effect on nutritive flow in non-diabetic rats; however, the rate of non-nutritive flow increased by 97.7% +/- 38.9% (P < 0.01). Sciatic endoneurial oxygen tension was measured by microelectrode polarography. Diabetes resulted in a 44.7% +/- 3.4% reduction in mean oxygen tension (P < 0.001), which was largely (82.3% +/- 10.2%) prevented by EPO treatment (P < 0.001). Thus, EPO prevents impairment of blood flow and endoneurial oxygenation in experimental diabetes. It is likely that this neurovascular action accounts for the beneficial effects of treatment on nerve function in diabetic rats and patients.

Animals↗
PubMed1994

Anti-oxidant and pro-oxidant effects on nerve conduction velocity, endoneurial blood flow and oxygen tension in non-diabetic and streptozotocin-diabetic rats.

Increased oxygen free radical activity, coupled with reduced protection against oxidative stress, could play a role in the aetiology of neurovascular abnormalities in experimental diabetes mellitus. To test this hypothesis, non-diabetic and streptozotocin-diabetic rats were treated with the anti-oxidant probucol or the pro-oxidant primaquine. One-month diabetes caused 21.4% and 13.6% reduction in sciatic motor and saphenous sensory conduction velocity (p < 0.001). These deficits were prevented by probucol treatment (p < 0.001). After 1-month untreated diabetes, conduction velocity deficits were reversed by a further month of probucol treatment (p < 0.001). For non-diabetic rats, primaquine treatment caused a 12.9% reduction in motor conduction velocity (p < 0.001), which was prevented by probucol treatment (p < 0.001). Primaquine treatment did not affect diabetic rats. Sciatic nerve nutritive endoneurial blood flow, measured using microelectrode polarography and hydrogen clearance, was 48.0% reduced by 2-month diabetes (p < 0.001). This was completely prevented by probucol treatment (p < 0.001). Primaquine treatment did not affect blood flow in diabetic rats. However, in non-diabetic rats it caused a 30.0% reduction (p < 0.01) which was prevented by probucol treatment (p < 0.05). Sciatic endoneurial oxygen tensions were also measured by microelectrode polarography. Mean tension was 38.8% reduced by diabetes (p < 0.001). This was prevented by probucol treatment. Non-diabetic rats given primaquine treatment showed a 21.7% reduction in endoneurial oxygen tension (p < 0.01). The data suggest that vascular-mediated nerve dysfunction in diabetes depends on oxidative stress, and that similar effects in non-diabetic rats may be produced by pro-oxidant treatment. This provides evidence for the potentially important role of oxygen free radical activity in diabetic neuropathy.

Animals↗
PubMed1994

The effect of immobilization on the recovery of rabbit soleus muscle from tenotomy: modulation by chronic electrical stimulation.

The effect of unilateral Achilles' tendon section on the soleus muscle of rabbits was examined after 2 and 4 weeks of unsutured recovery. Immobilization of the limb during recovery was also investigated. Following tendon section the limb was immobilized with an ankle angle of 90 deg, and final experiments were performed either after 2 weeks, or after the splints were removed and a further 2 weeks recovery allowed. Remobilized recovery was either allowed to occur naturally or with chronic low-frequency electrical stimulation of the soleus nerve. Achilles' tendon section resulted in very little change in the morphological profile of the soleus, but a marked decrease in tension production. Two weeks following tenotomy, tetanic tension was reduced to 50% of normal; this reduction persisted for the following 2 weeks of recovery. Imposition of immobilization after tendon section produced gross degeneration of the soleus. The fibres that remained had a mean fibre area of 20% of control values and displayed an immature staining pattern. This was accompanied by a reduction in tension production to less than 5% of normal and a marked speeding of contraction. Two weeks of passive recovery following splint removal slowed contraction and improved both the morphological profile and tension production of the soleus. Application of stimulation during this time restored contraction times to normal, reflecting the return to normal fibre-type proportions of this group, and improved the morphological profile and tension production beyond that of the unstimulated group. Thus immobilization worsened considerably the alterations occurring in the morphological and physiological properties of the soleus following Achilles' tendon section. Upon remobilization, chronic stimulation accelerated recovery of both parameters.

Achilles Tendon↗
PubMed1993

Contraction and relaxation of aortas from galactosaemic rats and the effects of aldose reductase inhibition.

Rats were fed for 10 days with a 40% galactose diet, in order to chronically stimulate the polyol pathway. Thoracic aorta contraction and relaxation were studied. Compared to controls, galactosaemia did not influence contractions to phenylephrine or serotonin. Acetylcholine produced concentration-dependent relaxation of aortic rectangles precontracted with phenylephrine; galactosaemia caused a 25% deficit in maximum relaxation to acetylcholine (P < 0.01) and a 168% increase in EC50. There was a similar 25% reduction in relaxation to 3 microM calcium ionophore A23187 (P < 0.05). By contrast, there were no significant differences in endothelium-independent relaxation to nitroglycerine or cromakalim. The abnormalities in endothelium-dependent relaxation were completely prevented by treating galactosaemic rats with the aldose reductase inhibitor, ponalrestat. Thus, the data demonstrate that elevated polyol pathway activity contributes to reduced endothelium production, release or the action of nitric oxide in experimental galactosaemia, and suggest that this mechanism could also contribute to the vascular defects seen in diabetes mellitus.

Aldehyde Reductase↗
PubMed1993

Prevention and reversal of motor and sensory peripheral nerve conduction abnormalities in streptozotocin-diabetic rats by the prostacyclin analogue iloprost.

The effects of the prostacyclin analogue iloprost on nerve function were examined in streptozotocin-diabetic rats. Rats were treated either with iloprost from induction of diabetes over 2 months in a preventive experiment, or for 1 month following a 1 month untreated period of diabetes in a reversal experiment. One and 2 months untreated diabetic control, non-diabetic control, and iloprost-treated non-diabetic groups were also used. Diabetes of 1 month duration caused a 21% (P < 0.001) reduction in sciatic motor conduction velocity and a 14% (P < 0.001) deficit in saphenous sensory conduction. This was not significantly changed over a subsequent month without treatment. Diabetic rats given iloprost treatment in both preventive and reversal studies had motor and sensory conduction velocities not significantly different from those of non-diabetic controls, but greater than for untreated diabetes (P < 0.01). Iloprost treatment did not have a significant effect on nerve conduction in non-diabetic rats. The time taken for sciatic nerve compound action potential amplitude to be reduced by 80% under hypoxic conditions in vitro was progressively elevated by 19% and 57% after 1 and 2 months diabetes respectively. Iloprost treatment significantly attenuated this for both preventive (47%, P < 0.001) and reversal (50%, P < 0.001) studies. There was no effect on hypoxic resistance for non-diabetic rats. In the preventive group there was a 28% increase in sciatic nerve endoneurial capillary density (P < 0.001), a lesser effect (16%, P < 0.05) in the reversal group, and no effect in non-diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1993

Anti-oxidant treatment prevents the development of peripheral nerve dysfunction in streptozotocin-diabetic rats.

We tested the notion that oxidative stress makes an important contribution to the aetiology of diabetic neuropathy. The effect of treatment with a 1% dietary supplement of the anti-oxidant butylated hydroxytoluene was studied during 2 months of streptozotocin-induced diabetes mellitus. In final experiments, sciatic motor and saphenous sensory conduction velocities were measured in vivo, and resistance to hypoxic conduction failure for sciatic trunk was examined in vitro. There were 20% and 12% decreases in motor and sensory conduction velocity, respectively after 2 months of diabetes (p < 0.001). There were completely prevented by butylated hydroxytoluene treatment (p < 0.001). Resistance to hypoxic conduction failure, shown by the time taken for sciatic compound action potential amplitude to decline by 80%, was 55% increased by diabetes, and this was limited to 31% (p < 0.01) by treatment. There were no significant effects of treatment on the 9-10 fold elevation of sciatic nerve sorbitol and fructose levels with diabetes, or on the non-significant 22% reduction in myoinositol content. Butylated hydroxytoluene treatment also did not affect sciatic nerve capillary density. We conclude that oxidative stress makes an important contribution to the aetiology of early experimental diabetic neuropathy. Amelioration of oxidative stress could potentially be a final common mechanism whereby a number of diverse treatments exert a beneficial effect on diabetic nerve function.

Action Potentials↗
PubMed1993

Angiotensin II receptor blockade improves nerve function, modulates nerve blood flow and stimulates endoneurial angiogenesis in streptozotocin-diabetic rats and nerve function.

We examined the effect of the angiotensin II receptor blocker, ZD 8731, on nerve function, capillary density, and blood flow in streptozotocin-diabetic rats. Deficits in sciatic motor and saphenous sensory nerve conduction velocity of 21% and 15%, respectively, were observed after 1 month of diabetes mellitus (p < 0.001). These were completely ameliorated by a further month of ZD 8731 treatment (p < 0.001). Treatment of non-diabetic rats for 1 month with ZD 8731 had no effect on motor or sensory conduction velocity. Sciatic nerve capillary density was not significantly affected by 1- or 2-month untreated diabetes, however, there was a 15% increase in density with ZD 8731 treatment (p < 0.001). Treatment of non-diabetic rats for 1 month had no effect on capillary density. Diabetes prolonged the time taken for 80% conduction failure by 19% (p < 0.05) and 49% (p < 0.001) for 1 and 2 months of diabetes, respectively, when sciatic nerve was exposed to hypoxia in vitro. ZD 8731 treatment during the second month of diabetes limited the prolongation to 22%, not significantly different from 1 month of untreated diabetes but less than for the 2-month diabetic group (p < 0.001). Concentrations of sciatic nerve polyol pathway metabolites were elevated six-fold and myo-inositol was reduced 40% by diabetes; ZD 8731 treatment was without effect. Acute experiments examined the effect of ZD 8731 on sciatic nerve blood flow using laser-Doppler flowmetry. In non-diabetic rats, blood flow changes followed the dose-dependent reductions in systemic arterial pressure and there were no significant variations in sciatic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1993

Contrasting effects of treatment with omega-3 and omega-6 essential fatty acids on peripheral nerve function and capillarization in streptozotocin-diabetic rats.

Essential fatty acid metabolism is impaired by diabetes mellitus and this may be important in the aetiology of peripheral nerve dysfunction. The effects of gamma-linolenic acid (omega-6) and fish oil (omega-3) alone, and in combination, on nerve function and capillarization were examined in 2-month streptozotocin-diabetic rats. Diabetes resulted in approximately 15% and 23% decreases in saphenous sensory and sciatic motor nerve conduction velocities, respectively (p < 0.001). Motor and sensory conduction velocities were in the non-diabetic range after both preventive and reversal omega-6 treatment of diabetic rats (p < 0.001). No significant changes occurred in omega-6 treated non-diabetic rats. Preventive omega-3 treatment was largely ineffective. Reversal treatment with a combination of omega-6 and omega-3 fatty acids was marginally effective and improved motor (p < 0.05), but not sensory conduction velocity. In vitro measurement of sciatic nerve resistance to hypoxic conduction failure in diabetic rats revealed a 56% increase in the time taken for the compound action potential amplitude to be reduced by 80% (p < 0.01) compared to non-diabetic rats. This was partially prevented by omega-6 treatment (29% increase, p < 0.01). Reversal omega-6 treatment had a lesser effect (37% increase, p < 0.05 compared to untreated diabetic rats). omega-3 treatment had no significant effect on conduction failure time. Sciatic endoneurial capillary density increased by 11% with preventive omega-6 treatment (p < 0.05), but was unaffected by reversal omega-6 and by omega-3 treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗