Catecholamines and diabetes mellitus

Summary. Plasma concentrations of adrenaline and noradrenaline were measured radio-enzymatically in nine patients with diabetic autonomic neuropathy, seven diabetic patients without autonomic neuropathy and nine normal subjects, in the recumbent position and after standing. Furthermore, in six patients with autonomic neuropathy and in the normal subjects, plasma noradrenaline and adrenaline concentrations were determined during and after cyclo-ergometer exercise. No differences in plasma adrenaline concentrations were found at any time in the study. Basal plasma noradrenaline levels were significantly lower in diabetic patients with autonomic neuropathy than in the non-neuropathic diabetics or healthy control subjects. After standing, plasma noradrenaline rose to significantly higher levels in both control and diabetic subjects without neuropathy than in the patients with autonomic neuropathy. During exercise (up to 100 W load), plasma noradrenaline rose to similar levels in healthy controls and in patients with diabetic neuropathy. These data indicate that in diabetic autonomic neuropathy there is reduced peripheral neurosympathetic tone at rest but a normal response to moderate exercise. Blunted neurosympathetic responses to standing seem to be a consistent feature of diabetic autonomic neuropathy, particularly in those patients with severe postural hypotension.Key words: Plasma catecholamines, adrenaline, noradrenaline, sympathetic nervous activity, diabetes mellitus, autonomic neuropathy, postural stimulation, orthostatic hypotension, muscular exercise.Autonomic neuropathy in diabetes mellitus produces a variety of different symptoms and signs due to variable involvement of the sympathetic and parasympathetic branches of the autonomic nervous system [6,14,16].Plasma catecholamine levels have been investigated in only a few studies in recent years, as a possible humoral index of sympathetic function in complicated or uncomplicated diabetes. While the results obtained from these studies indicate that plasma catecholamine levels in uncomplicated diabetes are normal, the frequency of sympathetic deficiency, as reflected by subnormal plasma noradrenaline concentrations, in diabetic autonomic neuropathy and its possible importance in relation to symptoms, such as postural hypotension, is less clear [1,9,10,12,19]. This uncertainty could be due, at least in part, to difficulties in the accurate measurement of catecholamine responses and also in the characterization of diabetic autonomic neuropathic syndromes.The present investigation was aimed at evaluating peripheral sympathetic function and reactivity to appropriate stimuli, such as standing and muscular exercise, in diabetic patients with autonomic neuropathy, compared with diabetics without neuropathy and normal subjects. For this purpose, the presence of diabetic autonomic neuropathy was ascertained from a series of clinical and instrumental evaluations. Plasma adrenaline and noradrenaline concentrations, measured by a sensitive and specific radio-enzymatic me...

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confidence: 55%

Plasma adrenaline and noradrenaline concentrations in diabetic patients with and without autonomic neuropathy at rest and during sympathetic stimulation

Caviezel

Picotti

Margonato³

et al. 1982

“…B. Hreidarsson: Reversible Autonomic Nervous System Abnormalities can be found in poorly controlled diabetics, especially during ketoacidosis [5]. Alberti et al [1] found, however, no change in catecholamine concentrations in diabetics who developed ketoacidosis after 41 h of insulin deprivation.…”

Section: Discussionmentioning

confidence: 99%

Acute, reversible autonomic nervous system abnormalities in juvenile insulin-dependent diabetes

Hreiðarsson

1981

Summary. Autonomic nervous function was studied by infrared TV-pupillography in nine insulin-dependent diabetic subjects with 0 to 3 years duration of diabetes, during poor and good metabolic control. During poor control there was no change in the latency time, the maximal contraction velocity or the amplitude of the light response, whereas the redilatation time was prolonged by 28%, from 2.26 _+ 0.27 to 2.90 _+ 0.58 s (mean + SD) (2p = 0.012). The pupil size after adaptation to darkness was unchanged, but the light induced pupillary unrest was reduced by 35% from 1.68 + 0.62 to 1.10 + 0.36 mm 2 (2p = 0.0037), and the degree of miosis in continuous illumination was reduced by 47% from 0.32 _+ 0.13 to 0.17 _+ 0.08 (2p = 0.0011), during metabolic derangement. The study has thus demonstrated reversible changes in autonomic nervous function, which are related to the diabetic metabolic state and thereby analogous to the previously well established reversible functional changes in the somatic nervous system in early diabetes.

“…A spectrum of abnormalities in adrenergic physiology and circulatory control after standing has been described in diabetic patients [5][6][7][8][9][10][11]. Measurement of parasympathetic HR control and testing of the postganglionic neuron in the legs made it possible to classify the different abnormal responses in this study.…”

Section: Discussionmentioning

confidence: 99%

“…The sensitivity of the assay was 32 ng/1 for noradrenaline and 16 ng/1 for adrenaline. To facilitate comparison with other studies [6][7][8][9][10][11], catecholamines are expressed in ng/1. Conversion factors are: for adrenaline, l ng/l=5.46pmol/1, and for noradrenaline, l ng/1 = 5.92 pmol/l.…”

Section: Group 3 (N=36)mentioning

confidence: 99%

“…The initial HR response after standing is also used to assess vagal HR control [1][2][3][4][5]. Orthostatic hypotension and an abnormal plasma catecholamine response after standing in diabetic patients has been reported as a sign of impaired sympathetic control [6][7][8][9][10][11]. However, the interrelationship between abnormal parasympathetic and sympathetic cardiovascular control is not well described.…”

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confidence: 99%

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Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus

Wieling

Borst²,

Torman

et al. 1983

Summary.We have investigated the relationship between vagal and sympathetic lesions in 62 diabetic patients and compared the results with those from 37 healthy subjects. Vagal function was assessed by heart rate changes with forced breathing. Sympathetic control was measured by the heart rate and blood pressure changes after standing and the concomitant plasma catecholamine response. The integrity of the postganglionic sympathetic neuron was evaluated separately by testing sudomotor function. Impaired sympathetic control was found only in 15 diabetic patients with severely impaired or absent vagal heart rate control. In 12 patients the chief abnormalities consisted of a delayed and diminished heart rate increase, an excessive fall in systolic blood pressure (> 20 mmHg) in combination with an abnormally small noradrenaline increment (< 120 ng/1) and a lesion of the postganglionic sympathetic neuron. Three patients with severely impaired parasympathetic heart rate control in combination with an intact postganglionic sympathetic neuron demonstrated a large noradrenaline increase on standing (> 700 ng/1). Measurement of vagal heart rate control and testing of sudomotor function makes it possible to classify a spectrum of abnormal cardiovascular responses to standing in diabetic patients.