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Biomedical subjects

J Fagius

Publications and source records attributed to J Fagius.

At least 37 records · Page 2Linked to original sources
PubMed1989

Changes of sympathetic nerve activity induced by 2-deoxy-D-glucose infusion in humans.

Microelectrode recording of sympathetic signals in the peroneal nerve was performed in 14 healthy volunteers following infusion of 2-deoxy-D-glucose (50 ml/kg body wt). Heart rate, blood pressure, body temperature, hematocrit, and blood levels of glucose, insulin, and catecholamines were monitored. Muscle nerve sympathetic activity (MSA), which is involved in cardiovascular homeostasis, increased significantly from a base-line level of 19.9 +/- 4.5 (mean +/- SE) bursts/min to a peak 30 min after the start of the infusion of 33.1 +/- 5.1 bursts/min. Skin nerve sympathetic activity (SSA), which is a mixture of sudomotor and vasoconstrictor signals, also increased to a peak at 30 min. The impulse pattern of SSA suggested that the increase involved mainly sudomotor activity, with simultaneous inhibition of vasoconstrictor signals. The time courses of MSA and the circulatory responses suggested that the increase in MSA was not a baroreceptor-induced counteraction of the cardiovascular changes during glucopenia. The responses of MSA and SSA were remarkably similar to those observed previously during insulin-induced hypoglycemia. The relationship between changes of sympathetic outflow, glucose levels, and insulin levels in the present study indicates that the effects observed are consequences of central nervous system glucopenia, with insulin playing a minor role. It is concluded that the sympathoadrenal system responds in a markedly differentiated way to glucopenia.

Adult↗
PubMed1989

Muscle sympathetic activity and norepinephrine release during mental challenge in humans.

Muscle sympathetic nerve activity (MSA; peroneal nerve) and arterial and femoral venous plasma norepinephrine (NE) were studied in 10 volunteers at rest, during a relaxation procedure (RELAX), and during two mental challenges, a word identification test (WIT) and a color word test (CWT). [3H]NE infusions were used to assess NE spillover to and clearance from plasma. Net NE overflow from the leg was calculated. RELAX reduced MSA and femoral venous NE concentrations. CWT increased blood pressure, cardiac output (thermodilution), and calf flow and reduced systemic vascular resistance. Responses to WIT were less marked. CWT increased MSA by 25%, femoral venous NE concentrations by 25%, and NE overflow from the leg by 26% at 3 min. Fractional epinephrine and [3H]NE extractions were flow related and decreased during CWT. The arterial contribution to femoral venous NE (about half) increased by 10% during CWT. Arterial NE levels and spillover increased, but NE clearance was unchanged. Femoral venous NE concentrations and NE spillover (not based on flow measurements) and regional NE overflow correlated with MSA. Thus NE concentrations in plasma reflect spillover rather than clearance at rest and during mental challenge. Biochemical and neurophysiological indexes of sympathetic activity correlate when assessed in the same region. Mental stress increases sympathetic activity in leg muscle.

Adrenal Glands↗
PubMed1989

Sympathetic activity and blood pressure increases with bladder distension in humans.

Microneurographic recordings of muscle nerve sympathetic activity, which is governed by baroreceptors and involved in blood pressure regulation, were made in the peroneal nerve in 16 healthy volunteers during physiological bladder distension. When the urge to urinate was pronounced, sympathetic outflow increased from a baseline level of 16.3 +/- 1.7 to 23.2 +/- 1.9 bursts/min (mean +/- SEM, p less than 0.01). There was a concomitant significant rise in both systolic and diastolic blood pressure, from 125 +/- 2/74 +/- 2 to 140 +/- 4/84 +/- 3 mm Hg. After micturition, sympathetic activity and blood pressure returned toward initial values. It is concluded that 1) increased sympathetic outflow contributed to the rise in blood pressure, 2) there is a vesicovascular response mediated by sympathetic vasoconstrictor neurons in humans corresponding to mechanisms observed in animals, and 3) the described functional relation between bladder distension and sympathetic vasoconstrictor activity probably plays a role in clinical conditions such as autonomic dysreflexia in humans with cervical spinal cord lesions and nocturnal micturition syncope.

Adult↗
PubMed1989

Sympathetic response to oral carbohydrate administration. Evidence from microelectrode nerve recordings.

Microneurography was used to measure sympathetic outflow in human muscle nerves (MSA) for up to 90 min after the ingestion of 100 g D-glucose, 75.8 g D-xylose, intravenous D-glucose (0.35 g/kg), and 300 ml water. 19 healthy subjects were examined using a microelectrode positioned in the right peroneal nerve. MSA increased from 21 +/- 0.9 bursts/min at rest to 36.9 +/- 4.3 bursts/min 30 min after ingestion of D-glucose and from 18.9 +/- 2.9 to 26.3 +/- 3.4 bursts/min 30 min after D-xylose. The increase in MSA was already significant by 15 min. MSA had not returned to the basal level after 90 min. Neither intravenous D-glucose nor water intake enhanced MSA. MSA increased in parallel with plasma norepinephrine, and a significant correlation (r = 0.55; P less than 0.001) was observed between the plasma insulin concentration and MSA after D-glucose ingestion. In three subjects the outflow of sympathetic nerve activity to the skin was examined after oral D-glucose and no change was observed, emphasizing the differentiated nature of the sympathetic nerve response to carbohydrate. Multiple factors such as insulin alone, hemodynamic adjustment to splanchnic vasodilation, and gastrointestinal distension are probably involved in the increased muscle nerve sympathetic outflow after carbohydrate ingestion.

Adult↗
PubMed1989

Plasma volume substitution does not inhibit plasma noradrenaline and muscle nerve sympathetic responses to insulin-induced hypoglycaemia in healthy humans.

Microelectrode recordings of muscle nerve sympathetic activity and measurements of venous plasma noradrenaline have indicated increased sympathetic outflow during acute hypoglycaemia. Plasma volume reduction during hypoglycaemia, as evidenced by increasing peripheral venous haematocrit might underly the sympathetic activation. To study the effect of prevention of plasma volume reduction during hypoglycaemia, saline containing albumin was infused intravenously in healthy adult volunteers during hypoglycaemia. Hypoglycaemia was induced by an intravenous injection of soluble insulin in a dose of 0.15 IU/kg body weight. Peripheral venous plasma noradrenaline concentrations were identical in experiments without and with plasma volume substitution. Muscle nerve sympathetic activity increased to the same extent during hypoglycaemia with and without plasma volume substitution. It is concluded that increased plasma noradrenaline concentrations and enhanced muscle nerve sympathetic activity during insulin-induced hypoglycaemia in man are not consequences of plasma volume reduction.

Adult↗
PubMed1988

Serum antibodies to peripheral nerve tissue in acute Guillain-Barré syndrome in relation to outcome of plasma exchange.

Mixed haemagglutination and complement fixation tests were used to detect serum antibodies to peripheral nerve in 36 patients with acute Guillain-Barré syndrome. Twenty patients were treated with plasma exchange, 16 served as controls. A significant antibody titre was found in 19 patients with the haemagglutination test; 30 had complement-fixing antibodies. Patients lacking complement-fixing antibodies were less disabled at entry (P less than 0.01). However, there was no correlation between the course of the disease and any of the antibodies in the two patient groups. The two tests were therefore not able to select patients for treatment by plasma exchange.

Adult↗
PubMed1988

Muscle nerve sympathetic activity following ectopic heart beats--a note on the burst pattern of sympathetic impulses.

Under normal conditions in man, sympathetic activity in muscle nerves occurs in bursts that are synchronized with the cardiac rhythm by inhibitory influence from high-pressure baroreceptors. Analysis of sympathetic outflow following ectopic heart beats indicated that in this situation the activity subsides without being inhibited by a baroreceptor input. It is concluded that the activity has an inherent characteristic of occurring not as a continuous outflow, but in clearly defined bursts.

Cardiac Complexes, Premature↗
PubMed1988

Early relapse of acute inflammatory polyradiculoneuropathy after successful treatment with plasma exchange.

Symptoms reappeared within 2-4 weeks in 6 of 23 patients with acute Guillain-Barré syndrome who had demonstrated significant clinical improvement following plasma exchange therapy; all however improved to full recovery after a second series of plasma exchanges. The procedure appears to be associated with increased risk of early relapse. Our observations suggest that a relationship may exist between rapid removal of large amounts of plasma and the possibility of relapse.

Acute Disease↗
PubMed1987

Variation of sympathetic reflex latency in man.

Microelectrode recordings of muscle nerve sympathetic activity (MSA) in man have shown a reflex relationship between heart beat and corresponding sympathetic burst, the latency of which is stable at rest and independent of heart rate. In peroneal nerve recordings in 35 healthy subjects this latency was reduced during the Valsalva manoeuvre by 120 ms (mean; range 40-245 ms; P less than 0.001) from a mean value at rest of 1300 ms. Slow deep breathing and simulated diving shortened the latency by 60 (P less than 0.001) and 80 ms (P less than 0.05), respectively. When intrinsic heart rate was induced by i.v. administration of atropine and propranolol, the latency was increased by 70 ms (P less than 0.001). A number of other manoeuvres affecting the outflow of MSA did not change the latency. It is suggested that the findings indicate the existence of more than one central pathway involved in the baroreflex regulation of MSA. Alternatively, altered central processing time may follow influence from other receptors in different manoeuvres.

Apnea↗
PubMed1986

Skin nerve sympathetic activity during insulin-induced hypoglycaemia.

Microelectrode recordings of skin nerve sympathetic activity, consisting of sudomotor and vasoconstrictor signals, were performed in the peroneal nerve in seven healthy subjects during insulin-induced hypoglycaemia. The nerve activity was recorded at rest and for 90 min after intravenous injection of 0.15 IU insulin/kg body weight. The net outflow of skin nerve sympathetic activity was increased during hypoglycaemia, with the exception of one subject who exhibited a high initial level of activity. In all subjects a change of the temporal pattern of the outflow was found, suggesting a shift from mixed (sudomotor and vasoconstrictor) to pure sudomotor activity. This change coincided with a sensation of warmth, sweating and varying degrees of cutaneous vasodilatation, and was followed by a fall in body temperature. It is concluded that hypoglycaemia has a differential effect on sympathetic activity in skin nerves, with a strong increase of sudomotor impulses and simultaneous inhibition of vasoconstrictor signals. Thus, neurally mediated thermoregulatory adjustment contributes to heat loss during hypoglycaemia.

Adult↗
PubMed1986

The diving response in man: effects on sympathetic activity in muscle and skin nerve fascicles.

Multi-unit recordings of muscle-nerve sympathetic activity (m.s.a) or skin-nerve sympathetic activity (s.s.a) were made in the left peroneal nerve of sixteen healthy volunteers during simulated diving by immersion of the face in a tub of water. The procedure was varied by the use of different water temperatures, by diving with snorkel breathing, by apnoea without diving, and by apnoea with a stream of air against the face instead of immersion in water. Diving for 12 s elicited a pronounced activation of m.s.a., the mean increase from control periods being 360%. The response was stronger with lower water temperatures. Immersion of the whole face evoked a stronger increase in m.s.a. than immersion of mouth and nose only. Diving without apnoea elicited a significant but weaker increase in m.s.a., whereas apnoea only for 12 s did not influence the sympathetic outflow. Cool air against the face during apnoea for 12 s was associated with a significant increase in m.s.a. The increase in m.s.a. usually occurred before the bradycardia. On emersion, m.s.a. ceased abruptly, whereas the bradycardia persisted for a few seconds. Mental arithmetic during diving did not change the m.s.a. response but reduced the bradycardia. M.s.a. increased despite increasing blood pressure levels. On emersion, m.s.a. did not reappear until the pre-diving blood pressure level was attained. S.s.a was inhibited on diving, with concomitant vasodilatation in the skin as recorded in the big toe. It is concluded that the response of m.s.a. to diving is initiated by a central 'pattern recognition' of an input from facial receptors, that this input and the effects of apnoea, acting by mutual reinforcement, maintain the strong sympathetic outflow, and that the mechanism releasing m.s.a. on diving overrides the normal blood pressure regulatory function of m.s.a. Diving exerts differentiated influence on different parts of the sympathetic nervous system, as illustrated by the inhibition of s.s.a.

Adult↗
PubMed1986

Sympathetic outflow in human muscle nerves increases during hypoglycemia.

The normal response to insulin-induced hypoglycemia bears many characteristics of activation of the sympathetic nervous system. In this study, the impulse pattern of muscle nerve sympathetic activity (MSA) involved in cardiovascular homeostasis was identified by microneurography in the peroneal nerve of seven healthy and two adrenalectomized subjects. After recordings at rest and an intravenous injection of 0.15 IU insulin/kg body wt (0.10 IU insulin/kg body wt in adrenalectomized subjects), MSA was followed for 90 min. Nadir of hypoglycemia (2.0 +/- 0.1 mM) was reached at 30 min. All subjects, including the two adrenalectomized subjects, exhibited an increase of MSA, which peaked at the glucose nadir. The time course of MSA increase was a mirror image of the blood glucose curve. This directly measured increase of MSA may be part of the hemodynamic adjustment to the fall in plasma volume known to occur in hypoglycemia. Another possible cause is direct stimulation of central sympathetic motoneurons.

Adrenalectomy↗
PubMed1985

Limited benefit of treatment of diabetic polyneuropathy with an aldose reductase inhibitor: a 24-week controlled trial.

The effects of the aldose reductase inhibitor, sorbinil, on symptomatic symmetrical diabetic polyneuropathy were studied during a 6-month period in a double-blind parallel group placebo-controlled trial. Twenty-seven patients received sorbinil and 28 placebo. The patients were assessed by clinical examination, neurophysiological measurements, sensory threshold determinations and tests of autonomic nerve function. No major clinical benefit was seen in the sorbinil-treated patients and no differences in sensory thresholds were observed. In three out of nine neurophysiological tests (motor nerve conduction velocity of the posterior tibial nerve, F-wave latency and sensory distal latency of the ulnar nerve) and one out of five tests of autonomic nerve function (heart rate variation during deep breathing) significant differences between the patient groups evolved in favour of sorbinil treatment. An overall evaluation of the temporal development of these and remaining neurophysiological and autonomic variables suggested a small but significant benefit from sorbinil treatment. There was no evidence of continuing improvement throughout the treatment period and beneficial effects observed were no greater than those seen in previous trials of considerably shorter treatment periods. It is concluded that sorbinil treatment results in some improvement in peripheral nerve function in symptomatic diabetic polyneuropathy, but that the long-term effect may be of limited value.

Adult↗
PubMed1985

Muscle nerve sympathetic activity in migraine. Lack of abnormality.

Microelectrode recordings of muscle nerve sympathetic activity (MSA) in the peroneal nerve were performed in eight patients with common migraine, when they were free of headache and during a spontaneously occurring attack of migraine. During the migraine headache all subjects remained on the same level of MSA as in the control situation and the responses to manoeuvres (slow deep breathing, the Valsalva manoeuvre, sustained hand grip, immersion of one hand into ice water) showed no qualitative or quantitative change. Assessment of vagal influence on the heart showed no change from control situation to attack of migraine. The study provides direct evidence against the existence of any abnormality of MSA during ongoing migraine headache and does not support the assumption that migraine is a generalized vasomotor disorder. No conclusions about possible dysfunction in other parts of the sympathetic nervous system can be drawn.

Adult↗