Biomedical subjects

P Hansson

Publications and source records attributed to P Hansson.

At least 37 records · Page 2Linked to original sources

PubMed1998

Cerebrospinal fluid mononuclear cell counts influence CSF HIV-1 RNA levels.

This study evaluated the relation between cerebrospinal fluid (CSF) mononuclear cells (MNC) and CSF HIV-1 RNA levels. HIV-1 RNA levels in plasma and CSF were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) in 58 consecutive patients with neurologic symptoms and late HIV-1 infection. The majority of the patients had no central nervous system (CNS) complication (n = 36), 11 had AIDS dementia complex (ADC) and 11 had CNS opportunistic infection (CNS OI). CSF cell counts were analyzed using a method that also evaluated hypocellular CSF (i.e., from 0.1 x 10(6) cells/L). A strong correlation was found between CSF MNC and CD4+ lymphocyte counts in blood (r = 0.58; p < .0001). HIV-1 RNA was detected in all plasma samples and in 38 of 58 (66%) of the cell-free CSF samples. CSF HIV-1 RNA was less frequently detected in patients with hypocellular CSF than in patients with normocellular or pleocytic CSF (13 of 28 patients [46%] versus 10 of 14 patients [71%] versus 15 of 16 patients [94%], respectively). The levels of CSF HIV-1 RNA correlated with the CSF MNC count (r = 0.61; p < .0001). The correlation also remained strong within the clinical subgroups of CNS asymptomatic patients (r = 0.55; p < .001) and ADC patients (r = 0.79; p < .001), but not among CNS OI patients (r = 0.19). Patients with CNS OI were found to have higher CSF HIV-1 RNA levels than the patients without evidence of CNS complication. Thus, a close relation was found between CSF HIV-1 RNA levels and CSF MNC counts. These data support the hypothesis that a substantial part of the virus in the CSF of HIV-1-infected patients is locally produced by CSF MNC.

AIDS Dementia Complex↗

PubMed1998

Determination of phosphatidylethanol in blood from alcoholic males using high-performance liquid chromatography and evaporative light scattering or electrospray mass spectrometric detection.

The 'pathologic' phospholipid, phosphatidylethanol (PEth), formed only in the presence of ethanol, was determined in extracts of human blood using high-performance liquid chromatography with evaporative light scattering detection (ELSD) or electrospray (ES) mass spectrometry. Separation was performed using a diol column and a normal-phase binary gradient system. Decreasing concentrations of PEth (15 to 1 nmol/ml blood) could be detected by ELSD in three male alcoholics, up to 3 weeks after the beginning of an alcohol-free period. Using ES, levels down to 100 pmol/ml blood was detected. The molecular species of PEth were similar to those of phosphatidylcholine found in the same blood sample. The method provides a rapid quantitative and qualitative determination of PEth in blood. The limits of detection were 200 pmol (approximately 125 ng) using ELSD and 140 fmol (approximately 100 pg) using ES, total amounts injected. ON

Alcoholism↗

PubMed1998

Opioids modulate the calcitonin gene-related peptide8-37-mediated hindpaw withdrawal latency increase in thermally injured rats.

The present study was performed to explore the modulatory potential of different endogenous opioid systems on transmission of presumed nociceptive information at the spinal cord level in thermally injured rats. Thermal injury was performed by dipping the left paw into water 60 degrees C for 20 s. This induced a significant bilateral decrease in hindpaw withdrawal latency HWL to pressure. Intrathecal administration of 10 nmol of CGRP8-37 induced a significant bilateral increase in HWL in the thermally injured group and in the intact controls. The effect of different opioid receptor antagonists on the increased latency to withdrawal response induced by intrathecal injection of 10 nmol of CGRP8-37 was explored in the thermally injured rats. The effect was reversed by intrathecal injection of 40 and 80 nmol of: b-funaltrexamine (mu opioid receptor antagonist) and naltrindole (delta opioid receptor antagonist), but not by norbinaltorphimine (kappa opioid receptor antagonist). The results of the present study show that intrathecal CGRP8-37 increases hindpaw withdrawal latency in thermally injured rats, an effect reduced by a mu as well as by a delta opioid receptor antagonist.

Animals↗

PubMed1998

[Pain analysis is vital in rheumatic diseases. Pain often causes much worry to patients].

The article consists of a synthesis of a rheumatic pain symposium held at the annual meeting of the Swedish Medical Association in 1996. Various aspects of pain in rheumatic diseases were discussed, such as physiological, neurohumoral and neurogenic mechanisms, sensory stimulation treatment, differentiation of mechanical and inflammatory pain, quality enhancement by improved co-operation between primary and tertiary care facilities, pharmacological treatment with (centrally and peripherally acting) opioids, selective cyclo-oxygenase inhibitors, and NMDA (N-methyl-D-aspartate) receptor antagonists. For patients with rheumatic disorders exacerbated by pain problems, as for other patients, a pain diagnosis is of fundamental importance. This can be achieved by analysis of the social, psychological, physiological and medical factors contributing to the cause and degree of pain and to pain behaviour, and of the extent to which the pain may be nociceptive (i.e., inflammatory, mechanical, or ischaemic in origin), neurogenic or idiopathic. Pain analysis should be followed by individualised treatment focused on the patient's most crucial problems, thus enhancing the prospect of optimal treatment outcome.

Analgesics↗

PubMed1998

Phosphatidylethanol in blood as a marker of ethanol consumption in healthy volunteers: comparison with other markers.

Phosphatidylethanol is a "pathological" phospholipid, formed via the action of phospholipase D only in the presence of ethanol. The present study was made to elucidate how different levels and patterns of alcohol intake affect blood levels of phosphatidylethanol in comparison with other markers of abuse. We used a new HPLC-evaporative light-scattering detection technique for phosphatidylethanol quantitation. This method had a total coefficient of variation of <20% at the detection limit of 0.2 nmol, equaling 0.8 micromol/liter of whole blood. Two groups were studied. (a) Five healthy volunteers were given 32 to 47 g of ethanol in a single dose, to give blood ethanol levels of approximately 25 mmol/liter after 30 to 60 min. Phosphatidylethanol, carbohydrate-deficient transferrin (CDT), and blood ethanol were measured before and after the intake. (b) Twelve student volunteers were studied during a 3 week period of prolonged alcohol consumption (total estimated intake: 1334 +/- 488 g, mean +/- SD) and phosphatidylethanol, serum-CDT, gamma-glutamyltransferase, and blood ethanol were measured at the start of the period (day 1) and twice at the end of the period (days 18 and 21). In group (a), no phosphatidylethanol was detected at any time after ethanol dosage/intake. In group (b), no blood phosphatidylethanol or blood ethanol could be demonstrated at the start, and serum-CDT was below the discrimination limit (1.3%) in all persons. No phosphatidylethanol was detected in those four persons with the lowest intake (742 +/- 150 g). However, the remaining eight persons had detectable levels of phosphatidylethanol (1.0 to 2.1 micromol/liter), and these had a higher total intake (1630 +/- 389 g). There was a statistically significant (p = 0.02) increase in serum CDT for 3 weeks. However, only 3 of 12 persons increased above the discrimination limit. The present results indicate that a substantial alcohol intake is needed to elevate blood phosphatidylethanol. In comparison with serum-CDT, blood phosphatidylethanol appears more sensitive.

Adult↗

PubMed1997

Intrathecal CGRP(8-37) results in a bilateral increase in hindpaw withdrawal latency in rats with a unilateral thermal injury.

The present study was performed to explore the effects of intrathecal administration of calcitonin gene-related peptide8-37 (CGRP(8-37)) on the hindpaw withdrawal latency (HWL) to pressure in rats with one thermally injured hindpaw. Furthermore, the interaction of CGRP(8-37)and naloxone was studied. Thermal injury was performed by dipping the left paw into 60 degrees C for 20 s. This induced a significant increase in the volume of the left hindpaw (P<0.001) and significant bilateral decreases of the latency of hindpaw withdrawal response to mechanical stimulation (Left: P<0.001; right: P<0.05). Intrathecal administration of 10, 20 and 40 nmol of CGRP(8-37), but not of 1 or 5 nmol, induced a significant bilateral increase in HWLs (P<0.001). The effect of CGRP(8-37) was partly reversed by intrathecal injection of naloxone at a dose of 32 and 64 microg respectively. Using radioimmunoassay, we found a significant bilateral increase in the concentration of CGRP-like immunoreactivity in the perfusate of both hindpaws 24 h after unilateral thermal injury (left: P< 0.001; right: P< 0.05). There was also an increase in the amount of CGRP-like immunoreactivity in the cerebrospinal fluid (P< 0.001), but not in plasma. The results indicate that CGRP plays a role in the transmission of nociceptive information in the spinal cord of thermally injured rats. Furthermore, our findings suggest that opioids can modulate CGRP-related effects in the spinal cord.

Animals↗

PubMed1997

Peripheral alpha-adrenoreceptors are involved in the development of capsaicin induced ongoing and stimulus evoked pain in humans.

While the sympathetic nervous system seems to be involved in some pain states, the mechanisms linking the sensory and sympathetic nervous system are unclear. In this study the possible involvement of peripheral alpha-adrenoreceptors in the development of capsaicin induced ongoing pain and mechanical hypersensitivity was examined in humans. Intradermal capsaicin injections in the volar aspect of the arm gave rise to ongoing burning pain and dysesthesia as well as mechanical hypersensitivity. Ongoing pain and pain evoked by von Frey filament stimulation was rated on a numerical rating scale after intradermal capsaicin injection. The area of skin in which von Frey filament stimulation evoked pain was measured. A subcutaneous injection of phentolamine (alpha-adrenoreceptor antagonist) on one side and saline on the other side prior to the capsaicin injection was done to evaluate the role of the peripheral alpha-adrenoreceptors in development of capsaicin induced sensory symptoms and signs. Significantly less ongoing and evoked pain developed on the phentolamine injected side compared to the saline side, the latter in the area adjacent to the capsaicin injection (primary zone) and well outside the area of flare (secondary zone). The area in which pain could be evoked on the phentolamine injected side was restricted to the area of flare and was significantly smaller than on the saline injected side. Mechanical stimulation gave rise to aftersensation and radiation of pain on the saline injected side in all subjects but only in one case on the phentolamine injected side. Peripheral alpha-adrenoreceptors thus seem to be involved in functional changes of primary afferents which contribute to ongoing pain and mechanical stimulus evoked pain.

Adrenergic alpha-Antagonists↗

PubMed1997

Modulatory influence on somatosensory perception from vibration and heterotopic noxious conditioning stimulation (HNCS) in fibromyalgia patients and healthy subjects.

In order to assess the function of endogenous mechanisms modulating somatosensory input in fibromyalgia (FM), the effect of vibratory stimulation (VS) and heterotopic noxious conditioning stimulation (HNCS) on perception of various somatosensory modalities was assessed. Ten female FM patients and 10 healthy, age-matched, females participated. VS (100 Hz) was applied to the left forearm for 45 min and quantitative sensory testing (QST) was performed within the vibrated area and in the right thigh before, during and 45 min following vibration. Pressure pain thresholds (PPTs) were assessed by pressure algometry. Perception thresholds to non-painful cold (CT) and warmth (WT), heat pain thresholds (HPTs), cold pain thresholds (CPTs) and stimulus-response curves of pain intensity as a function of graded nociceptive heat stimulation were assessed using a Peltier element based thermal stimulator. The effects of HNCS were tested using the upper extremity submaximal effort tourniquet test. Subjects rated tourniquet induced pain intensity on a visual analogue scale (VAS). QST was performed in the right thigh before, during and 60 min following the tourniquet. FM patients did not differ from controls in the response to VS. There was a local increase of PPTs during vibration (P < 0.001) and of WTs following vibration (P < 0.001). HPTs increased in the forearm and in the thigh (P < 0.009) during vibration. CTs and sensitivity to suprathreshold heat pain were not influenced by VS. The intensity of pain induced by the tourniquet did not differ between groups. PPTs increased during the tourniquet in controls (P < 0.001) but not in FM patients (difference between groups P < 0.001). Decreased sensitivity to non-painful cold (P < 0.001) and non-painful warmth (P < 0.001) was seen during and following (P < 0.001; P < 0.05, respectively) the tourniquet in both groups alike. HPTs and perception of suprathreshold heat pain remained unaffected in both groups. In conclusion, FM patients did not differ from healthy controls in their response to vibration, but no modulation of pressure pain was induced by HNCS, as opposed to controls, suggesting a dysfunction in systems subserving 'diffuse noxious inhibitory controls' (DNIC).

Adult↗

PubMed1997

Effects of dextromethorphan in clinical doses on capsaicin-induced ongoing pain and mechanical hypersensitivity.

The analgesic properties of the noncompetitive N-methyl-D-aspartate (NMDA)-receptor antagonist dextromethorphan, available for clinical use as an antitussive, have been studied in the human capsaicin pain model to determine a possible clinical effect on pain due to central sensitization. Ninety milligrams dextromethorphan or vehicle was given orally to ten volunteers, each at two different occasions in a double-blind fashion, prior to an intradermal injection of 300 micrograms capsaicin. Ongoing pain, pain evoked by von Frey filament stimulation, and pressure pain thresholds were assessed before and after the capsaicin injection. The area in which von Frey filament stimulation evoked pain was mapped after the capsaicin injection. There were no significant group effects on ongoing pain, or on von Frey or pressure hypersensitivity. There was also no significant effect on the area of mechanical hypersensitivity. These results show that clinical doses of dextromethorphan do not effect ongoing or mechanically evoked pain after capsaicin injection.

Adult↗

PubMed1997

Peripherally administrated morphine attenuates capsaicin-induced mechanical hypersensitivity in humans.

We examined the hypothesis that peripheral morphine can modulate pain and hyperalgesia/allodynia in the human capsaicin model. Subcutaneous injections of 1 mL morphine (1 mg/mL) in one arm and of 1 mL 0.9% saline in the other arm were made prior to bilateral intradermal injections of 50 microL (6 mg/mL) capsaicin. All injections were made on the volar aspect of the arm. Before and after the capsaicin injections, spontaneous pain and pain evoked by repetitive von Frey filament stimulation was rated on a numerical rating scale; furthermore, pressure pain thresholds were determined. The area in which von Frey filament stimulation evoked pain and the area of visible flare were mapped after the capsaicin injection. Capsaicin injection resulted in spontaneous pain on the saline-injected side not significantly different from that on the morphine-injected side. However, capsaicin injections gave rise to significantly less pain evoked by mechanical stimuli, as well as to a significantly smaller area of mechanical hypersensitivity, on the morphine-injected side compared with the saline-injected side. These results suggest that morphine can modulate sensitization mechanisms involved in the development of capsaicin-induced mechanical hypersensitivity.

Adult↗

PubMed1997

Blood phosphatidylethanol as a marker of alcohol abuse: levels in alcoholic males during withdrawal.

Phosphatidylethanol (PEth) is formed only in the presence of ethanol, via the action of phospholipase D. We studied PEth in blood as a possible marker of alcohol abuse in 15 male alcoholics admitted for detoxification. Blood was drawn on the first day after admission and up to 28 days thereafter. PEth in whole blood was 13.2 +/- 2.2 mumol liter-1 (mean +/- SE) at first sampling and remained detectable up to 14 days after admission. Blood ethanol was 0 on the morning after admission. The time courses of PEth disappearance varied among individuals. No PEth could be found in blood of control persons who had abstained from ethanol for 4 days. Levels of PEth and carbohydrate-deficient transferrin or gamma-glutamyltranspeptidase did not correlate. Its high specificity and prolonged detectability suggest PEth in blood as a marker of recent alcohol abuse.

Adult↗

PubMed1996

Intrathecal and systemic R-phenylisopropyl-adenosine reduces scratching behaviour in a rat mononeuropathy model.

The aim of the present study was to investigate the effect of intravenous or intrathecal (i.t.) administration of R-phenylisopropyladenosine (R-PIA), a selective A1 adenosine receptor agonist, on spontaneous scratching behaviour, a phenomenon presumably related to pain in a mononeuropathy model (sciatic nerve ligation) in rats. The acute effect of daily i.t. R-PIA injections was studied up to 21 days following nerve ligation. The results demonstrate that both i.v. (30 nmol) and i.t. (3 nmol) R-PIA, in doses not producing any motor impairment, significantly reduces scratching behaviour in this animal model. The mechanism of action for this presumed antinociceptive effect is suggested to occur at the spinal cord level.

Adenosine↗

PubMed1996

The calcitonin gene-related peptide antagonist CGRP8-37 increases the latency to withdrawal responses bilaterally in rats with unilateral experimental mononeuropathy, an effect reversed by naloxone.

The present study was performed in rats with experimental mononeuropathy after left common sciatic nerve constriction. A bilateral decrease in hindpaw withdrawal latency to thermal and mechanical stimulation was observed after unilateral ligation of the left common sciatic nerve; however, it was more pronounced on the lesioned side. Compared with sham-operated rats, the content of calcitonin gene-related peptide-like immunoreactivity was significantly decreased in the left dorsal horn of the spinal cord and left dorsal root ganglia in rats with mononeuropathy. Blocking the receptor of calcitonin gene-related peptide, by intrathecal injection of 5 or 10 nmol of calcitonin gene-related peptide (8-37), induced a significant bilateral increase in hindpaw withdrawal latency to both thermal and mechanical stimulation which, however, was significantly less pronounced in mononeuropathic rats than in intact rats. The effect of calcitonin gene-related peptide (8-37) was reversed by intrathecal administration of the opioid antagonist naloxone. The contribution of calcitonin gene-related peptide and its receptors to transmission of presumed nociceptive information appears to be reduced in the sciatic nerve constriction model. The decrease in reflex responsiveness induced by calcitonin gene-related peptide (8-37) was counteracted by naloxone, indicating that opioids control the net effect of excitation in the spinal cord circuitry induced by calcitonin gene-related peptide and possibly other co-released neurotransmitters.

Animals↗

PubMed1996

Sensory dysfunction in fibromyalgia patients with implications for pathogenic mechanisms.

This study, addressing etiologic and pathogenic aspects of fibromyalgia (FM), aimed at examining whether sensory abnormalities in FM patients are generalized or confined to areas with spontaneous pain. Ten female FM patients and 10 healthy, age-matched females participated. The patients were asked to rate the intensity of ongoing pain using a visual analogue scale (VAS) at the site of maximal pain, the homologous contralateral site and two homologous sites with no or minimal pain. Quantitative sensory testing was performed for assessment of perception thresholds in these four sites. Von Frey filaments were used to test low-threshold mechanoreceptive function. Pressure pain sensitivity was assessed with a pressure algometer and thermal sensitivity with a Thermotest. In addition the stimulus-response curve of pain intensity as a function of graded nociceptive heat stimulation was studied at the site of maximal pain and at the homologous contralateral site. FM patients had increased sensitivity to non-painful warmth (P < 0.01) over painful sites and a tendency to increased sensitivity to non-painful cold (P < 0.06) at all sites compared to controls, but there was no difference between groups regarding tactile perception thresholds. Compared to controls, patients demonstrated increased sensitivity to pressure pain (P < 0.001), cold pain (P < 0.001) and heat pain (P < 0.02) over all tested sites. The stimulus-response curve was parallely shifted to the left of the curve obtained from controls (P < 0.003). Intragroup comparisons showed that patients had increased sensitivity to pressure pain (P < 0.01) and light touch (P < 0.05) in the site of maximal pain compared to the homologous contralateral site. These findings could be explained in terms of sensitization of primary afferent pathways or as a dysfunction of endogenous systems modulating afferent activity. However, the generalized increase in sensitivity found in FM patients was unrelated to spontaneous pain and thus most likely due to a central nervous system (CNS) dysfunction. The additional hyperphenomena related to spontaneous pain are probably dependent on disinhibition/facilitation of nociceptive afferent input from normal (or ischemic) muscles.

Adult↗

PubMed1996

Intrathecal CGRP8-37-induced bilateral increase in hindpaw withdrawal latency in rats with unilateral inflammation.

1. Recent work in our laboratory has demonstrated that intrathecal administration of a selective antagonist of calcitonin gene-related peptide (CGRP), CGRP8-37, increased the hindpaw withdrawal latency (HWL) to thermal stimulation and hindpaw withdrawal threshold (HWT) to pressure in normal rats, and that these effects were more pronounced than in rats with mononeuropathy. 2. The present study was performed to investigate the effects of intrathecal administration of CGRP8-37 on the HWL and HWT in rats with unilateral hindpaw inflammation induced by subcutaneous injection of carrageenin. The effect of naloxone was also studied. 3. Subcutaneous injection of 0.1 ml of carrageenin into the plantar region of the left hindpaw induced a significant increase in the volume of the ipsilateral hindpaw (P < 0.001), and significant bilateral decreases of the HWL to thermal stimulation (ipsilateral: P < 0.001; contralateral: P < 0.01) and HWT to pressure (ipsilateral: P < 0.001; contralateral: P < 0.01). 4. Intrathecal administration of 10 nmol of CGRP8-37, but not of 1 or 5 nmol, induced a significant bilateral increase in the HWL and HWT in rats with experimentally induced inflammation (thermal test: P < 0.001; mechanical test: P < 0.001). 5. The effect of intrathecal administration of 10 nmol CGRP8-37 on HWL and HWT was significantly more pronounced in intact rats than in rats with experimentally induced inflammation (ipsilateral: P < 0.001; contralateral: P < 0.001). 6. The effect of CGRP8-37 on withdrawal responses in the inflamed paw was partly reversed by intrathecal injection of naloxone at a dose of 88 nmol in the thermal (ipsilateral: P < 0.01; contralateral: P = 0.14) and mechanical tests (ipsilateral: P < 0.05; contralateral: P = 0.60). 7. A significant bilateral increase in the concentration of CGRP-like immunoreactivity in the perfusate of both hindpaws was demonstrated 24 h after unilateral injection of carrageenin (ipsilateral: P < 0.001; contralateral: P < 0.05). There was also an increase in the amount of CGRP-like immunoreactivity in the cerebrospinal fluid (P < 0.001), but not in plasma (P = 0.75). 8. The present study demonstrates that acute experimentally-induced unilateral hindpaw inflammation, induces bilateral increases in the amount of CGRP-like immunoreactivity in hindpaw perfusates. Intrathecal administration of CGRP8-37 increased the HWL to thermal stimulation and HWT to pressure bilaterally. 9. The results indicate that CGRP plays a role in the transmission of presumed nociceptive information in the spinal cord of rats with experimentally induced inflammation. Furthermore, our findings suggest that opioids can modulate CGRP-related effects in the spinal cord.

Animals↗

PubMed1995

Opioid antagonists naloxone, beta-funaltrexamine and naltrindole, but not nor-binaltorphimine, reverse the increased hindpaw withdrawal latency in rats induced by intrathecal administration of the calcitonin gene-related peptide antagonist CGRP8-37.

We recently demonstrated that intrathecal administration of calcitonin gene-related peptide 8-37 (CGRP8-37), a selective antagonist of calcitonin gene-related peptide receptors, dose-dependently increased the latency to hindpaw withdrawal responses induced by both thermal and mechanical stimulation in intact rats, indicating a role for CGRP and its receptors in the transmission of presumed nociceptive information in the spinal cord. The present study was performed to explore the interaction between CGRP and opioids in the spinal cord of rats. The effects of naloxone, a non-selective opioid receptor antagonist, and three different selective opioid receptor antagonists on the increased latency to withdrawal response induced by intrathecal injection of CGRP8-37 were explored. Intrathecal administration of 10 nmol of CGRP8-37 induced a significant bilateral increase in hindpaw withdrawal latency to both thermal and mechanical stimulation. The effect was partly reversed by intrathecal injection of 4 or 8 micrograms of naloxone, 10 nmol of either the mu opioid receptor antagonist beta-funaltrexamine or the delta opioid receptor antagonist naltrindole, but not by 10 nmol of the kappa opioid receptor antagonist nor-binaltorphimine. These results indicate that mu and delta, but not kappa, opioid receptors are involved in the modulation of post-synaptic effects and/or release of CGRP and other neurotransmitters.

Animals↗

PubMed1995

Changes of neuropeptide concentrations in the brain following experimentally induced mononeuropathy in Wistar Kyoto and spontaneously hypertensive rats.

The effect of unilateral, experimentally induced, mononeuropathy on concentrations of neuropeptide Y (NPY), neurokinin A (NKA), substance P (SP), calcitonin gene-related peptide CGRP) and galanin- (GAL-) like immunoreactivities (-LI) was studied in Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rat brains. Two weeks following ligation of the sciatic nerve, significantly higher concentrations of NPY-LI were found in the hippocampus, striatum and occipital cortex of both rat strains. CGRP-LI and GAL-LI were increased in the hippocampus of WKY rats. NKA-LI and SP-LI were decreased to different degrees in the pituitary of the WKY and SHR rats, indicating that the changes of the tachykinins, CGRP and GAL were selectively associated with the basal level of sympathetic tone. The increased concentrations of NPY-LI in the brain, not influenced by sympathetic tone, may be part of a general defense reaction in response to trauma.

Animals↗

PubMed1995

Systemic adenosine infusion alleviates spontaneous and stimulus evoked pain in patients with peripheral neuropathic pain.

In seven patients with peripheral neuropathic pain, the effect of systemic adenosine infusion on pain symptoms was evaluated in a double-blind, placebo controlled, cross-over study. The study infusions, adenosine (50 micrograms.kg-1.min-1) or placebo, were given intravenously (IV) during 45-60 min at two separate occasions. Before and during infusions, bedside examination of sensibility and quantitative sensory testing (QST), i.e., assessments of perception thresholds for touch, touch-evoked pain, cold, warmth, painful heat, and cold, were performed. In the neuropathic area, sensation magnitude was rated by a visual analog scale (100 mm VAS) using a pin and at perception threshold for touch-evoked pain using von Frey filaments. Adenosine infusion reduced spontaneous pain (P < 0.05), and caused an increase of the touch-evoked pain threshold from 10.8 +/- 5.3 to 22.2 +/- 6.9 g (P < 0.05), whereas placebo had no effect. Pain intensity at perception threshold for touch-evoked pain was, however, unaltered. Pinprick-evoked pain in the neuropathic areas was reduced from 53 +/- 11 to 29 +/- 10 mm (P < 0.05). No other sensory modality was consistently changed during adenosine infusion. In conclusion, the present study demonstrates that adenosine infusion alleviates spontaneous neuropathic pain, tactile allodynia, and pinprick hyperalgesia in patients with peripheral neuropathic disorders, probably by a central mechanism of action.

Adenosine↗