Vascular Responses in Diabetic Peripheral Neuropathy

Moorhouse, J. A.; Carter, S. A.; Doupe, J.

doi:10.1136/bmj.1.5492.883

Cited by 82 publications

(28 citation statements)

References 16 publications

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“…This implies that the differences we have demonstrated are due to changes at the %-adrenoceptor. These findings are in keeping with previous work [15][16][17], including a recent study [17] which assessed vascular responses using a similar technique. This latter study compared hand vein reactivity with postural drop in blood pressure in IDDM patients with symptomatic autonomic neuropathy, and found a positive correlation with responses to NA but not to PE.…”

Section: Discussionsupporting

confidence: 90%

Asymptomatic peripheral nerve dysfunction and vascular reactivity in IDDM patients with and without microalbuminuria

et al. 1994

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SummaryAbnormal vascular reactivity has been implicated in the aetiology of diabetic microvascular disease and we have previously demonstrated enhanced contractility of hand veins to noradrenaline in insulin-dependent diabetic (IDDM) patients with microalbuminuria. We have now assessed the possible contribution of subclinical peripheral nerve dysfunction to exaggerated vascular reactivity in microalbuminuric patients. Twenty-five IDDM patients (15 with microalbuminuria), none of whom had symptomatic neuropathy, and 10 control subjects were studied. Vasoconstrictor responses were measured in dorsal hand veins using noradrenaline and phenylephrine. Conduction in median, peroneal and sural nerves was assessed using electrophysiology, and autonomic function using standard cardiovascular reflex tests. The noradrenaline dose causing 50 % vasoconstriction was significantly lower in the microalbuminuric diabetic subjects compared with normoalbuminuric (3.6(1.7) mean (SEM) ng/min vs 20.1(6.0) ng/min, p = 0.0002) and non-diabetic subjects (35.1(5.0) ng/min; p < 0.0001). However, reactivity to phenylephrine did not differ between the groups. Median nerve motor conduction velocity was significantly slower in microalbuminuric (48.4(1.4) m/s) than in normoalbuminuric (52.7(1.2) m/s, p = 0.04) and non-diabetic subjects (56.7(0.9) m/s, p = 0.0001). In the diabetic group overall, there was a strongly positive linear correlation between vascular response to noradrenaline and conduction velocity in both the median nerve (r = 0.62, p = 0.0009) and peroneal nerve (r = 0.53, p = 0.006). There was no correlation between phenylephrine-induced responses and motor conduction velocity in either nerve, nor were indices of autonomic function correlated with vascular reactivity to either agent. Enhanced vascular reactivity to noradrenaline ((x 1-and a2-agonist), but not phenylephrine (ch-agonist only), in subclinical neuropathy is correlated with severity of nerve damage. This suggests that damage to presynaptic inhibitory a2-adrenoceptors is in part responsible for the exaggerated vascular responses found in microalbuminuric subjects. [Diabetologia (1994) Vascular tone is determined by neural and hormonal influences, including noradrenaline (NA) [1], which acts on vascular smooth muscle (x-adrenoceptors to cause vasoconstriction. These receptors can be stimulated by NA released locally from sympathetic nerve endings, and into the circulation from nerve endings and the adrenal medulla. We have previously reported that vascular reactivity to NA is exaggerated in normotensive insulin-dependent diabetic (IDDM) patients with incipient nephropathy [2]. We measured vascular responses in veins on the dorsum of

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Section: Discussionsupporting

confidence: 90%

Asymptomatic peripheral nerve dysfunction and vascular reactivity in IDDM patients with and without microalbuminuria

et al. 1994

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“…Autonomic neuropathy causes a reduction in response both to reflexlyinduced thermoregulatory stimuli [21] and to local increases in venous pressure [22]. The changes we have observed are probably due to local structural or functional disturbances in the arterioles which are independent of autonomic neuropathy.…”

Section: Discussionmentioning

confidence: 57%

Impaired autoregulation of blood flow in skeletal muscle and subcutaneous tissue in long-term type 1 (insulin-dependent) diabetic patients with microangiopathy

et al. 1983

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Summary.Autoregulation of blood flow was studied in skeletal muscle and subcutaneous tissue in seven Type 1 (insulindependent) diabetic patients (median age: 36 years) with nephropathy and retinopathy and in eight normal subjects of the same age. Blood flow was measured by the local 133Xe washout technique. Reduction in arterial perfusion pressure was produced by elevating the limb 20 and 40 cm above heart level. Blood flow remained within 10% of control values when the limb was elevated in normal subjects. In five of the seven diabetic subjects blood flow fell significantly in both tissues when the limb was elevated 40 cm indicating impaired autoregulation. The results suggest that intrinsic vascular (arteriolar) mechanisms (myogenic and/or metabolic) underlying the normal autoregulatory response are defective in some diabetic patients with microangiopathy.Key words: Autoregulation, blood flow, 133Xe washout, postural change, diabetic microangiopathy.Autoregulation of blood flow, i.e. the maintenance of blood flow within narrow limits during changes in perfusion pressure induced by changing arterial pressure, has been demonstrated in many tissues and organs. Much attention has been paid to autoregulation in the brain [1] and the kidney [2] but it has also been demonstrated in human subcutaneous tissue [3] and skeletal muscle. The mechanisms underlying the compensatory changes in vascular (arteriolar) tone during changes in arterial pressure are unknown. The autoregulatory response is unaffected by chronic sympathetic denervation [4] indicating that intrinsic vascular mechanisms are responsible. The major theories invoke changes in myogenic activity [5] or local metabolic factors [6]. Arteriolar tone is influenced by local changes in concentrations of various metabolites including adenosine [7], pyrophosphate [8] and potassium [9]. Furthermore, local changes in oxygen [10] and carbon dioxide tensions [11] may play an important role.In diabetic subjects cerebral blood flow is less rigidly controlled than in normal subjects, suggesting impaired autoregulation [12,13]. Apart from this no information is available on autoregulation in diabetes. The purpose of our study was to determine whether impaired autoregulation was present in skeletal muscle and subcutaneous tissue in long-standing, Type 1 (insulin-dependent) diabetic patients with microangiopathy.

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“…Long-term diabetics are supersensitive to IV infusion of catecholamines [11,105]. This supersensitivity is probably caused by several different mechanisms.…”

Section: Catecholamines In Long-term Diabeticsmentioning

confidence: 99%