Anesthesiology 2001 Aug;95(2):565; discussion 566-7
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PMID: 11506140, UI: 21396939
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PMID: 11506139, UI: 21396938
Anesthesiology 2001 Aug;95(2):565-7
PMID: 11506138, UI: 21396940
Anesthesiology 2001 Aug;95(2):500-8
Klinik fur Anaesthesiologie und operative Intensivmedizin, Universitatsklinikum Benjamin Franklin, Freie Universitat Berlin, Germany. rittner@medizin.fu-berlin.de
BACKGROUND: Inflammatory pain can be effectively controlled by an interaction of opioid receptors on peripheral sensory nerve terminals with opioid peptides released from immune cells upon stressful stimulation. To define the source of opioid peptide production, we sought to identify and quantify populations of opioid-containing cells during the course of Freund's complete adjuvant-induced hind paw inflammation in the rat. In parallel, we examined the development of stress-induced local analgesia in the paw. METHODS: At 2, 6, and 96 h after Freund's complete adjuvant inoculation, cells were characterized by flow cytometry using a monoclonal pan-opioid antibody (3E7) and antibodies against cell surface antigens and by immunohistochemistry using a polyclonal antibody to beta-endorphin. After magnetic cell sorting, the beta-endorphin content was quantified by radioimmunoassay. Pain responses before and after cold water swim stress were evaluated by paw pressure thresholds. RESULTS: In early inflammation, 66% of opioid peptide-producing (3E7+) leukocytes were HIS48+ granulocytes. In contrast, at later stages (96 h), the majority of 3E7+ immune cells were ED1+ monocytes or macrophages (73%). During the 4 days after Freund's complete adjuvant inoculation, the number of 3E7+ cells increased 5.6-fold (P < 0.001, Kruskal-Wallis test) and the beta-endorphin content in the paw multiplied 3.9-fold (P < 0.05, Kruskal-Wallis test). In parallel, cold water swim stress-induced analgesia increased by 160% (P < 0.01, analysis of variance). CONCLUSIONS: The degree of endogenous pain inhibition is proportional to the number of opioid peptide-producing cells, and distinct leukocyte lineages contribute to this function at different stages of inflammation. These mechanisms may be important for understanding pain in immunosuppressed states such as cancer, diabetes, or AIDS and for the design of novel therapeutic strategies in inflammatory diseases.
PMID: 11506126, UI: 21396926
Anesthesiology 2001 Aug;95(2):416-20
Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1009, USA.
BACKGROUND: Adenosine and adenosine agonists reduce hypersensitivity following inflammation and peripheral nerve injury models of chronic pain. Because inhibitors of adenosine reuptake or metabolism are also effective at reducing hypersensitivity, it is likely that there is a tonic release of spinal adenosine in these models. One approach to avoid adverse effects from direct agonists is to enhance the effect of the endogenous ligand by administering a positive allosteric modulator of its receptor. METHODS: Rats with mechanical hypersensitivity after spinal nerve ligation received intrathecal injections of adenosine, the allosteric adenosine receptor modulator T62, or their combination, or received systemic T62 alone or with intrathecal injection of a specific A1 adenosine antagonist. RESULTS: Both adenosine and T62 reduced hypersensitivity alone, with 50% maximal doses (ED50) of 14+/-5.9 and 3.7+/-0.8 microg, respectively. They interacted in an additive manner as determined by isobolography. T62 also reduced mechanical hypersensitivity after systemic administration (15 mg/kg), and this effect was blocked by intrathecal injection of 9 microg of the A1-specific adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine. CONCLUSIONS: These results add to previous studies that suggest ongoing spinal release of adenosine, which is antiallodynic, in this animal model of neuropathic pain. Positive allosteric modulation of the adenosine receptor reduces hypersensitivity by a spinal mechanism involving A1 adenosine receptor stimulation. Although obvious adverse effects were not observed in this investigation, further study is required to determine the feasibility of the use of such modulators in the treatment of chronic pain associated with hyperalgesia and allodynia.
PMID: 11506115, UI: 21396915
Anesthesiology 2001 Aug;95(2):390-4
Department of Anesthesiology, Baystate Medical Center, The Tufts University School of Medicine, Springfield, Massachusetts 01199, USA. scott.reuben@bhs.org
BACKGROUND: Harvesting autogenous bone grafts from the ilium may cause considerable pain and may represent a significant source of postoperative morbidity. The local application of morphine can reduce pain in a rat model of bone damage. We evaluated the analgesic efficacy of administering morphine to the donor bone graft site for spinal fusionsurgery. METHODS: Sixty patients undergoing cervical spinal fusion surgery using autogenous bone harvested from the ilium were randomly assigned to one of three groups: Group 1 was given saline infiltrated into the harvest site, group 2 was given 5 mg intramuscular morphine; group 3 was given 5 mg morphine infiltrated into the harvest site. After surgery, all patients were given morphine through a patient-controlled analgesia pump. Pain scores both from the harvest and the incision sites, as well as morphine use, were recorded at 2, 4, 6, 8, 12, and 24 h after surgery. At 1 yr after surgery the presence and subjective characteristics of donor site pain were recorded. RESULTS: Total 24-h morphine use (milligrams) was significantly lower (P < 0.0001) in group 3 (33.7+/-8.3 mg, mean +/- SD), compared with either group 1 (64.3+/-6.6 mg) or group 2 (59.6+/-9.3 mg). Pain from the graft site was scored the same at 2 h but remained significantly lower (P < 0.0001) for group 3 at all later time intervals. Pain scores from the incision site were similar among the three study groups. One year after surgery, 25% of patients reported having chronic donor site pain. The association of chronic donor site pain was significantly higher (P < 0.05) in groups 1 (33%) and 2 (37%) compared with group 3 (5%). CONCLUSION: Low-dose morphine applied to the harvest graft site can reduce local pain, morphine use, and chronic donor site pain after cervical spine fusion surgery.
PMID: 11506111, UI: 21396911
Anesthesiology 2001 Aug;95(2):334-9
Department of Emergency Medicine and Surgery, Groupe Hospitalier Pitie-Salpetriere, Universite Pierre et Marie Curie, Paris, France. valerie.safa@psl.ap-hop-paris.fr
BACKGROUND: Lumbar epidural blood patch (EBP) is a common treatment of post-dural puncture headache, but its effectiveness and mode of action remain a matter of debate. The aim of this study was to assess both the effectiveness and the predictive factors of failure of EBP on severe post-dural puncture headache. METHODS: This prospective observational study includes all patients treated in the authors' hospital with EBP for incapacitating post-dural puncture headache, from 1988 to 2000. The EBP effect was classified into complete relief (disappearance of all symptoms), incomplete relief of symptoms (clinically improved patients who recovered sufficiently to perform normal daily activity), and failure (persistence of severe symptoms). The following data were analyzed using a logistic regression to identify predictive factors of failure of EBP: (1) patient characteristics; (2) circumstances of dural puncture; (3) delay between dural puncture and EBP; and (4) the volume of blood injected for EBP. RESULTS: A total of 504 patients were analyzed. The frequency rates of complete relief, incomplete relief of symptoms, and failure after EBP were 75% (n = 377), 18% (n = 93), and 7% (n = 34), respectively. In a multivariate analysis, only the diameter of the needle used to perform dura mater puncture (odds ratio = 5.96; 95% confidence interval, 2.63-13.47; P < 0.001) and a delay in EBP less than 4 days (odds ratio = 2.63; 95% confidence interval, 1.06-6.51; P = 0.037) were independent significant risk factors for a failure of EBP. CONCLUSIONS: Epidural blood patch is an effective treatment of severe post-dural puncture headache. Its effectiveness is decreased if dura mater puncture is caused by a large bore needle.
PMID: 11506102, UI: 21396902
Cephalalgia 2001 Apr;21(3):216-23
Unidad de Neurologia, Hospital Ntra. Sra. de Sonsoles, Avila, Spain. acaminero@hnss.insalud.es
A series of 18 patients suffering from supraorbital neuralgia have been studied through a seven year period. Appropriate investigations ruled out other headaches. There was a female (67%) preponderance. Mean age at onset was 51.6 years. The mean headache duration was 5.9 years. Five patients had a history of ipsilateral forehead trauma. The main areas of pain were the forehead and orbit. The pain was dull with short sharp or burning exacerbations. The temporal pattern was either remitting (n = 7) or chronic continuous (n = 11). Autonomic accompaniments were generally lacking. Neurological assessment was normal in all but 4 patients who were found to have signs/symptoms of sensory dysfunction in the forehead of the symptomatic side. Trials of different drugs, including migraine and anti-neuralgic drugs, only provided slight relief. Anaesthetic nerve blocks of the supraorbital nerve provided an absolute but transitory relief of pain. Although aetiology and pathogenesis of supraorbital neuralgia is largely unknown, entrapment of the supraorbital nerve at its outlet and successful decompressive surgery have been previously reported. This and other pathogenic hypotheses are discussed.
PMID: 11442557, UI: 21336118
Eur J Pharmacol 2001 Jun 29;423(1):85-92
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160 014, India.
The leukotrienes are potent inflammatory mediators, which may have a role in inflammatory diseases such as allergic rhinitis, inflammatory bowl disease and asthma. Zafirlukast, a cysteinyl leukotriene receptor antagonist, is claimed to be effective in asthma. However, it is not known whether these leukotrienes are involved in nociceptive and peripheral inflammation. The present study aimed to assess the role of cysteinyl leukotrienes in nociceptive and inflammatory conditions in experimental animals. Central nociception was assessed with tail-flick and hot-plate methods and peripheral nociception was assessed by acetic acid-induced chemonociception in mice. Local administration (intraplantar) of carrageenan-induced hyperalgesia and inflammation, measured by paw withdrawal latency and paw volumes, respectively. Zafirlukast (2.5--20 mg/kg, p.o.) produced a significant and dose-dependent antinociceptive and antiinflammatory effect against acetic acid-induced chemonociception in mice and carrageenan-induced paw oedema in rats, respectively. Zafirlukast (2.5 and 5.0 mg/kg, p.o.) also attenuated the carrageenan-provoked hyperalgesia but did not alter the pain threshold in central nociception up to 20 mg/kg. Zafirlukast (5 and 10 mg/kg ) significantly inhibited exudate formation and migration of polymorphonuclear leukocytes in carrageenan-induced pleurisy. Further, zafirlukast (5 mg/kg) also reduced myeloperoxidase activity in carrageenan-treated paw. When nimesulide (2 mg/kg, p.o.) was co-administered with zafirlukast, the antinociceptive, antihyperalgesic and antiinflammatory effects of nimesulide were significantly increased as compared to the per se effect. The results indicate that cysteinyl leukotrienes are involved in nociceptive/inflammatory conditions. It is expected that combination of cysteinyl leukotriene receptor antagonist with cyclooxygenase inhibitor would prove to be a novel approach to treat complex inflammatory conditions.
PMID: 11438310, UI: 21331553
Eur J Pharmacol 2001 Jun 29;423(1):17-26
Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343, Krakow, Poland. kozela@if-pan.krakow.pl
We investigated the effects of pretreatment with low-affinity, uncompetitive NMDA receptor antagonists on morphine-induced antinociception in rats using the same intensity of thermal stimulus applied to the tail and the paws. Similar baseline responses to thermal stimuli of the same intensity were recorded from tails and hind paws. However, morphine produced equal antinociception from the tail and hind paw when used at doses of 2.5 and 6 mg/kg, respectively. These doses were used in further experiments. Thirty minutes before morphine, rats were administered the NMDA receptor antagonists dextromethorphan (2.5--30 mg/kg), memantine (2.5--15 mg/kg) and MRZ 2/579 (1-amino-1,3,3,5,5-pentamethyl-cyclohexane HCl) (1.25--10 mg/kg). All three compounds significantly and dose-dependently potentiated morphine-induced antinociception recorded from the tail. However, none of these NMDA receptor antagonists affected morphine antinociception recorded from the paw. These findings suggest that low-affinity NMDA receptor antagonists modulate differently morphine antinociceptive activity recorded from the tail and hind paws.
PMID: 11438302, UI: 21331545
Lancet 2001 Aug 25;358(9282):636
Department of Internal Medicine, University of California Davis Medical Center, 95817, Sacramento CA, USA
[Medline record in process]
PMID: 11530152, UI: 21421383
Lancet 2001 Jul 28;358(9278):302
PMID: 11498223, UI: 21389475
Pain 2001 Jun;92(3):373-80
Department of Anesthesiology, University of Louvain, St. Luc Hospital, Avenue Hippocrate 10-1821, 1200, Brussels, Belgium. dekock@anes.ucl.ac.be
We investigated whether intraoperative 'subanesthetic doses' of ketamine have a postoperative anti-hyperalgesic and an analgesic effect and which is the preferential route of administration, either systemic (intravenous, i.v.) or epidural. One hundred patients scheduled for rectal adenocarcinoma surgery under combined epidural/general anesthesia were included. Before skin incision all the patients received an epidural bolus followed by an infusion of continuous bupivacaine/sufentanil/clonidine mixture. They were randomly assigned to receive no ketamine (group 1), i.v. ketamine at the bolus dose of 0.25 mg/kg followed by an infusion of 0.125 mg/kg per h (group 2), 0.5 mg/kg and 0.25 mg/kg per h (group 3), epidural ketamine 0.25 mg/kg and 0.125 mg/kg per h (group 4), or 0.5 mg/kg and 0.25 mg/kg per h (group 5). All i.v. and epidural analgesics were stopped at the end of surgery and patients were connected to an i.v. morphine patient-controlled analgesia (PCA) device. Short-term postoperative analgesia (72 h) was assessed by pain visual analog scale scores at rest, cough, and movements as well as by PCA requirements. Wound mechanical hyperalgesia was evaluated and residual pain was assessed by asking the patients at 2 weeks, and 1, 6, and 12 months. The area of hyperalgesia and morphine PCA requirements were significantly reduced in group 3. These patients reported significantly less residual pain until the sixth postoperative month. These observations support the theory that subanesthetic doses of i.v. ketamine (0.5 mg/kg bolus followed by 0.25 mg/kg per h) given during anesthesia reduce wound hyperalgesia and are a useful adjuvant in perioperative balanced analgesia. Moreover, they show that the systemic route clearly is the preferential route.
PMID: 11376910, UI: 21273357
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