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Biomedical subjects

B Lynn

Publications and source records attributed to B Lynn.

At least 37 records · Page 2Linked to original sources
PubMed1996

Collateral sprouting of cutaneous nerves in man.

Cutaneous nerve collateral sprouting was studied in 20 adults in whom a forearm cutaneous nerve had been resected from the upper arm, such that any recovery of cutaneous nerve function could not be accounted for by nerve regeneration. Ten patients entered the study immediately following surgery and the remainder at intervals thereafter, permitting a longitudinal study covering a 27-month period. Modality-specific stimuli were used to study light touch, sharp pain, cooling, warming and heat pain sensation. Efferent sympathetic C fibre function was determined by measuring sweating in response to total body heating. Though the patients described considerable subjective reduction in the sensory defect within 2 months, by 10-15 months the objective sensory tests showed encroachment at the margin by only 6 mm (P < 0.05) for light touch, 7 mm (P < 0.01) for sharp pain and 11.5 mm (P < 0.001) for heat pain, with no significant change for warming or cooling. By 24 months, recovery of sweating was evident within the zone of persistent sensory loss, for > or = 3 cm beyond the initial light touch margin (P < 0.005). This finding has important clinical implications as it calls into question the reliance placed on the recovery of sweating as evidence of nerve regeneration.

Adolescent↗
PubMed1995

The classification and properties of nociceptive afferent units from the skin of the anaesthetized pig.

The afferent properties of nerve fibres innervating the hairy skin of the pig hind limb were investigated by recording from 142 single units from the saphenous nerve. Identified single units were isolated using maximal electrical stimulation of the nerve trunk. Afferent units were classified on the basis of their responses to a range of stimuli, both thermal (heating to 60 degrees C and cooling to 10 degrees C) and mechanical (air jet, von Frey type filaments with forces of 0.1-250 mN, and strong pressure with a blunt needle). A-fibre units (conduction velocity 6.3-64 m/s, n = 60) fell into categories that have been described in hairy skin in other mammalian species. Most were mechanoreceptors, although seven typical A-fibre mechanical nociceptors with large, multipoint fields were also isolated. No cutaneous receptive field could be found for 15% of A-fibre units. Out of 62 C-fibre units (conduction velocity 0.49-2 m/s) 40% had no cutaneous field for pressure, heat or cold. Of the C-fibre units with cutaneous fields, 42% were polymodal nociceptors, 38% were mechanoreceptors with a variety of properties, including some excited by noxious heat, and 19% were heat-only nociceptors. C-polymodal nociceptors had large receptive fields up to 12.5 mm across and did not sensitize following strong heating. Twenty units conducted at 2-6.3 m/s, between the main C- and A-fibre bands, and were varied in their responses. Some had properties identical to C-fibre mechanoreceptors whilst four were sensitive cold thermoreceptors and one was a polymodal nociceptor. Two units were mechanical nociceptors with small receptive fields.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Defective platelet aggregation in uremia is transiently worsened by hemodialysis.

Bleeding is a prominent feature of uremia and remains a significant cause of morbidity in hemodialysis (HD)-dependent patients. To measure the impact of the HD procedure, we performed a prospective cross-over study in eight patients placed consecutively for 2-week periods each on low-flux biocompatible polymethylmethacrylate, low-flux complement-activating cuprophane, and high-flux biocompatible polysulfone membranes. The primary measure of platelet function studied was shear-induced platelet aggregation (SIPA), which has been shown to be a physiologically relevant marker of platelet function and involves the interaction of von Willebrand factor (vWf) with platelet membrane glycoproteins (GP) Ib and IIb-IIIa. Flow-cytometric analysis of the surface expression of platelet membrane GP Ib and GP IIb-IIIa was performed using fluorescein isothiocyanate (FITC)-conjugated monoclonal antibodies CD42b and CD41a, respectively. Multivariate analysis did not demonstrate a statistically significant effect of the type of dialysis membrane on platelet aggregation, calcium flux, or thromboxane B2 production. There was a marked decrease of SIPA in HD patients (pre-HD, mean +/- SEM, 19% +/- 3%) compared with normal controls (43% +/- 3%, P < 0.001), with a further decrease after the HD procedure (post-HD, 12% +/- 2%, P = 0.015 compared with pre-HD). This intradialytic decrease in SIPA correlated with a decrease in GP Ib (pre-HD, 385 +/- 21 mean fluorescence intensity [MFI]; post-HD, 285 +/- 21 MFI, P = 0.0001). GP IIb-IIIa was also significantly decreased post-HD (pre-HD, 1,022 +/- 70 MFI; post-HD, 881 +/- 64 MFI, P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1993

Morphine inhibits antidromic vasodilatation without affecting the excitability of C-polymodal nociceptors in the skin of the rat.

The effect of morphine was examined under identical conditions on (a) antidromic vasodilatation, an 'efferent' function of C-nociceptors in the skin, and (b) afferent responses to heat and pressure of C-polymodal nociceptors. Morphine caused a large, naloxone-reversible, fall in peak antidromic vasodilatation (ADV). However it caused no significant change in heat or mechanical excitability of C-polymodal nociceptors in normal or mildly inflamed skin. The mechanisms by which morphine might affect efferent, but not afferent, functions of C-nociceptors are discussed.

Action Potentials↗
PubMed1992

Blood flow increases in the skin of the anaesthetized rat that follow antidromic sensory nerve stimulation and strong mechanical stimulation.

In anaesthetized rats, punctate pressure using forces greater than or equal to 20 mN caused small transient rises in skin blood flow that were similar in normally innervated and chronically denervated skin. A force of 11 mN, sufficient to excite most C-fibres of the polymodal nociceptor class, failed to cause vasodilatation. Following short periods of low frequency electrical stimulation of the saphenous nerve at C-fibre strength, larger increases in blood flow ('antidromic vasodilatation') were seen. Antidromic vasodilation was unaffected by high frequency stimulation of A alpha beta axons or by simultaneous innocuous mechanical stimulation. The failure of pressure at levels suprathreshold for C-fibre nociceptors to cause neurogenic vasodilatation may mean that antidromic vasodilation in rat skin is due to activity restricted to a mechanically insensitive sub-population of C-fibres.

Anesthesia↗
PubMed1992

The actions of capsaicin applied topically to the skin of the rat on C-fibre afferents, antidromic vasodilatation and substance P levels.

1. Single applications of solutions of capsaicin were made to the intact skin of anaesthetized rats and the effects on cutaneous blood flow and the firing of C-nociceptor afferents determined. Blood flow was measured by laser-Doppler flowmetry. C-fibre activity was recorded from filaments dissected from the saphenous nerve. 2. Following the application of a capsaicin solution (concentration > or = 1 mM) to rat saphenous skin, low frequency firing occurred in C-polymodal nociceptors that sometimes continued for > 10 min. At the some time, large increases in skin blood flow occurred exceeding 300% in some instances. 3. After the initial excitation, some C-polymodal nociceptors lost their sensitivity to pressure whilst their sensitivity to heat was lost or enhanced depending on the vehicle used. 4. Sensitivity of C-polymodal nociceptors to heat recovered in < 1 day following a single application of 33 mM capsaicin. Thresholds to mechanical pressure, however, were still significantly elevated by 123% on day 1, but had recovered on day 2. 5. Vasodilatation in response to saphenous nerve stimulation ('antidromic vasodilatation') was significantly reduced by 35%, 2 days after a single application of 33 mM capsaicin, but was normal at 4 days. 6. Following a single application of 33 mM capsaicin, skin substance P levels fell to only half the normal value at day 1 and remained at this level throughout the 4 day period examined. 7. It is suggested that the ability of relatively low concentrations of capsaicin to desensitize C-fibre nociceptors may underlie the analgesic action of topical capsaicin in man.

Administration, Topical↗
PubMed1992

An investigation into the extent to which flare in human skin crosses the mid-line.

We investigated whether flare crossed the mid-line in various positions in humans using laser Doppler flowmetry to confirm visual observations. On the back and forehead, flare crossed the mid-line. However, on the posterior part of the neck, flare did not cross the mid-line, an observation that may be related to the elongated shape of flare in this region.

Adult↗
PubMed1992

Capsaicin: actions on C fibre afferents that may be involved in itch.

Capsaicin selectively excites C-polymodal nociceptors in mammalian skin. In the rat, the only species so far studied in detail, a long-term desensitization of a subpopulation of C-polymodal nociceptors occurs after the initial excitation. After nerve treatment, permanent loss of some C-polymodal nociceptors is found in the rat. It is argued that capsaicin must act primarily on C fibres involved in signalling about pain and not itch, although there may be overlap between the C afferents involved in these two nociceptive sensations. The possibility is raised that C mechanoreceptors, with their good histamine sensitivity, are also involved in itch.

Animals↗
PubMed1991

The delay in onset of vasodilator flare in human skin at increasing distances from a localized noxious stimulus.

Flare was measured on the arm of human subjects at 8, 16, and 24 mm from localized areas of skin heating, using laser-Doppler flowmetry. Vasodilatation started after a delay that averaged 3.2 sec at 8 mm and increased significantly by 0.4 sec at 16 mm and by 1.1 sec at 24 mm. In contrast, there were no significant changes in onset delay associated with changes in the amplitude of the heat stimulus. Flare appears to spread more slowly than would be expected if rate of spread were determined only by conduction delays in unmyelinated nerve terminals. This finding is discussed in relation to models of flare that involve coupling between adjacent nerve terminals.

Adult↗
PubMed1988

Properties of A delta high threshold mechanoreceptors in the rat hairy and glabrous skin and their response to heat.

Forty-three high threshold mechanoreceptors (HTMs) with myelinated fibres were characterized in hairy and glabrous skin of the hind limb of the rat. Mechanical thresholds and conduction velocities were similar in both skin areas. The behaviour of 15 hairy and 14 glabrous skin HTMs were studied in response to repeated heating to 55-60 degrees C. Responses to heating were either very weak or absent, except for two units, one from each group, that fired on second and subsequent heat trials. A delta-HTMs in rat skin, either hairy or glabrous, are thus much less easily excited by heat than are similar units in rabbit, cat or monkey skin. C-fibres in rat skin are known to respond well to heating, and therefore provide the only significant input about noxious heat in this species.

Action Potentials↗
PubMed1988

Neurogenic inflammation in the skin of the rabbit.

A flare-like spread of vasodilatation can be demonstrated in the limb skin of the anaesthetised rabbit using laser doppler flowmetry. Spread of dilatation from a small mechanical injury (nicking the skin) extends 5-10 mm. The size and time course of the dilatation are as expected from the low frequency C-nociceptor firing that occurs in response to similar nearby injury. Since C-nociceptors cause significant vasodilator responses at frequencies less than 1 Hz, it is proposed that they may often have a pro-inflammatory action without producing any reflex or sensory effects.

Animals↗
PubMed1988

Substance P content of the skin, neurogenic inflammation and numbers of C-fibres following capsaicin application to a cutaneous nerve in the rabbit.

The long-term effects of applying capsaicin briefly to a cutaneous nerve in the rabbit have been assessed 10 days after treatment. No changes in C-fibre numbers were seen in treated saphenous nerves and the average ratio of C-fibres to A-fibres was close to 7 in both control and treated nerves. However, the substance P content of the skin innervated by the saphenous nerve fell by 46% after capsaicin treatment compared with a fall of 65% after nerve section. Plasma extravasation in response to 7.5% mustard oil applied to the skin was also reduced following capsaicin treatment (by 43%) and following denervation (by 47%), although the response to 25% mustard oil was unaffected by previous capsaicin treatment. Thus, as in other species that have been examined (notably the rat), brief capsaicin treatment of rabbit skin nerves leads to a reduction in a neurogenic inflammatory response and in substance P content of the skin. However, unlike the rat, there is no degeneration of C-fibres. In the rabbit it is therefore possible to separate the neurotoxic, degenerative action of capsaicin from its ability to deplete substance P. The question of whether a similar dissociation between neurotoxic and other actions could be achieved in the rat by using lower capsaicin concentrations remains to be answered.

Animals↗
PubMed1988

Neurogenic inflammation.

The main elements of neurogenic inflammation in the skin--antidromic vasodilatation, axon reflex flare and neurogenic plasma extravasation--are briefly described. New evidence is presented for a contribution from small myelinated fibres, as well as unmyelinated fibres, to antidromic vasodilatation. The mechanisms underlying flare are discussed and it is argued that weak coupling between C-fibre terminals must be important in determining the extent of spread of vasodilatation. The extent to which neurogenic factors contribute to a range of inflammatory models and to inflammatory disease states is discussed; it is argued that the importance of neurogenic mechanisms may have been underestimated.

Animals↗
PubMed1987

The immediate and long-term effects of applying capsaicin to cutaneous nerves.

Capsaicin has now been shown to have a neurotoxic action on C-fibres in adult rodents and several other mammalian species. In the adult the effect is preferentially on nociceptive C-fibres. The hypoalgesia and loss of neurogenic inflammation that follow capsaicin treatment are likely to be a direct consequence of the C-fibre loss. In addition to its long-term toxic action, capsaicin also has an immediate effect on conduction in nociceptive C-fibres. This action probably produces the short-term hypoalgesia and loss of antidromic plasma extravasation that follow application of capsaicin to peripheral nerves.

Action Potentials↗