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At least 937 records · Page 52Linked to original sources
PubMed1994

Effect of oral clonidine and intrathecal fentanyl on tetracaine spinal block.

We studied the effect of oral clonidine and intrathecal (IT) fentanyl on the onset and duration of a hyperbaric tetracaine-induced spinal block. Forty adult males undergoing elective surgery were studied according to a randomized, double-blind, placebo-controlled protocol involving four treatment regimens: Group I, placebo per os (PO) + tetracaine 12 mg IT; Group II, placebo PO+tetracaine 12 mg IT+fentanyl 10 micrograms IT; Group III, clonidine 200 micrograms PO+tetracaine 12 mg IT; Group IV, clonidine 200 micrograms PO+tetracaine 12 mg IT+fentanyl 10 micrograms IT. Onset time to highest sensory level was 8.5 +/- 3.1, 8.2 +/- 2.3, 6.1 +/- 1.6, and 6.8 +/- 1.4 min in Groups I, II, III, and IV, respectively. The time required for sensory regression to the L1 dermatome level was 153 +/- 34, 151 +/- 51, 183 +/- 63, and 209 +/- 39 min in Groups I, II, III, and IV, respectively. Similarly, the duration of Grade III motor block was 132 +/- 37, 140 +/- 55, 160 +/- 51, and 189 +/- 52 min in Groups I, II, III, and IV, respectively. IT fentanyl 10 micrograms did not change the onset or duration of tetracaine-induced spinal block. Furthermore, there was no significant interaction between clonidine and fentanyl in Group IV. Episodes of bradycardia and hypotension were more frequent in the clonidine-treated patients (40%-50% vs 10%). We conclude that oral clonidine (200 micrograms) shortened the onset time of tetracaine's sensory block and prolonged the duration of sensory and motor block. However, clonidine premedication increased the risk of hypotension and bradycardia.

Administration, Oral↗
PubMed2004

Interaction between intrathecal gabapentin and adenosine in the formalin test of rats.

Spinal gabapentin and adenosine have been known to display an antinociceptive effect. We evaluated the nature of the interaction between gabapentin and adenosine in formalin-induced nociception at the spinal level. Male Sprague-Dawley rats were prepared for intrathecal catheterization. Pain was evoked by injection of formalin solution (5%, 50 microL) into the hindpaw. After examination of the effects of gabapentin and adenosine, the resulting interaction was investigated with isobolographic and fractional analyses. Neither gabapentin nor adenosine affected motor function. Gabapentin or adenosine decreased the sum of the number of flinches during phase 2, but not during phase 1 in the formalin test. Isobolographic analysis, in phase 2, revealed an additive interaction between gabapentin and adenosine. Taken together, intrathecal gabapentin and adenosine attenuated the facilitated state and interacted additively with each other.

Adenosine↗
PubMed1999

Characterization of antiallodynic actions of ALE-0540, a novel nerve growth factor receptor antagonist, in the rat.

There is growing evidence that nerve growth factor (NGF) may function as a mediator of persistent pain states. We have identified a novel nonpeptidic molecule, ALE-0540, that inhibits the binding of NGF to tyrosine kinase (Trk) A or both p75 and TrkA (IC50 5.88 +/- 1. 87 microM, 3.72 +/- 1.3 microM, respectively), as well as signal transduction and biological responses mediated by TrkA receptors. ALE-0540 was tested in models of neuropathic pain and thermally-induced inflammatory pain, using two routes of administration, a systemic i.p. and a spinal intrathecal (i.th.) route. Morphine was also tested for comparison in the antiallodynia model using mechanical stimuli. We show that either i.p. or i.th. administration of ALE-0540 in rats produced antiallodynia in the L5/L6 ligation model of neuropathic pain. The calculated A50 values (and 95% confidence intervals) for ALE-0540 administered i.p. and i. th. were 38 (17.5-83) mg/kg and 34.6 (17.3-69.4) microgram, respectively. ALE-0540 given i.th., at doses of 30 and 60 microgram, also blocked tactile allodynia in the thermal sensitization model. Although morphine displayed greater potency [A50 value of 7.1 (5.6-8. 8) mg/kg] than ALE-0540 in anti-allodynic effect when given i.p. to L5/L6-ligated rats, it was not active when administered i.th. These data suggest that a blockade of NGF bioactivity using a NGF receptor antagonist is capable of blocking neuropathic and inflammatory pain and further support the hypothesis that NGF is involved in signaling pathways associated with these pain states. ALE-0540 represents a nonpeptidic small molecule which can be used to examine mechanisms leading to the development of agents for the treatment of pain.

Analgesics↗
PubMed2000

Regeneration of lesioned corticospinal tract fibers in the adult rat induced by a recombinant, humanized IN-1 antibody fragment.

Axons in the CNS of higher vertebrates generally fail to regenerate after injury. This lack of regeneration is crucially influenced by neurite growth inhibitory protein constituents of CNS myelin. We have shown previously that a monoclonal antibody (mAb IN-1) capable of binding and neutralizing Nogo-A, a myelin-associated inhibitor of neurite growth, can induce long-distance axonal regeneration and increased structural plasticity with improved functional recovery in rat models of CNS injury. In this paper we demonstrate that a partially humanized, recombinant Fab fragment (rIN-1 Fab) derived from the original mAb IN-1, was able to promote long-distance regeneration of injured axons in the spinal cord of adult rats. When infused into a spinal cord injury site, regrowth of corticospinal fibers in 11 of 18 animals was observed after a survival time of 2 weeks. Regenerating fibers grew for >9 mm beyond the lesion site and arborized profusely in the distal cord. Regenerated fibers formed terminal arbors with varicosities in the spinal cord gray matter, strongly resembling synaptic points of contact to neurons in the spinal cord distal to the lesion. In animals that had received a bovine serum albumin solution or a recombinant IN-1 fragment that had been mutated in the antigen binding site (mutIN-1 Fab), no significant growth beyond normal lesion-induced sprouting was observed. Neutralization of endogenous nerve growth inhibitors represents a novel use of recombinant antibody technology with potential therapeutic applications after traumatic CNS lesions.

3T3 Cells↗
PubMed1994

[Value of vertebroplasty combined with surgical decompression in the treatment of aggressive spinal angioma. Apropos of 3 cases].

Vertebral hemangiomas can cause difficult-to-treat neurological complications. We report our experience with three such cases. Patients no. 1 and 2 were females aged 64 and 71 years, respectively; patient no. 1 had a two-year history of weakness in the lower limbs and patient no. 2 had a five-month history of back pain. Both these patients had a pyramidal syndrome in the lower limbs. Patient no. 3 was a 61 year old male with a one-year history of left sciatica. Roentgenograms were suggestive of a hemangioma occupying the entire T8 (cases 1 and 2) or L5 (case 3) vertebra. Computed tomography and magnetic resonance imaging confirmed this diagnosis and showed that patients 1 and 2 had an anterior epidural hemangioma opposite T8 impinging on the spinal cord. In patients 1 and 2, treatment consisted in embolization of T8 followed by transpedicular injection of 6 cc of methylmethacrylate into the body of T8. One cubic centimeter of histoacryl was also injected in each lamina. The third patient had a similar vertebroplasty procedure without prior embolization since he had no epidural hemangioma. One patient (no. 1) developed intercostal neuralgia of several hours duration after the procedure. All three patients subsequently underwent laminectomy (T7-T8 with removal of the epidural hemangioma in cases 1 and 2, L5 in case 3). The pyramidal syndrome resolved within 15 days in patients 1 and 2; the nerve root pain resolved within 48 hours in patient 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Intrathecal cholinergic agonists lessen bupivacaine spinal-block-induced hypotension in rats.

Hypotension is an important side effect of spinal anesthesia. Intrathecal (IT) cholinergic agonists, including neostigmine (NEO), increase arterial blood pressure by stimulating spinal sympathetic neurons. Therefore, we tested the ability of IT cholinergic agonists to prevent the hypotensive effect of IT bupivacaine (BUP) (430 nmol) in rats instrumented with IT and arterial catheters. The mean arterial pressure (MAP) decreased 35 +/- 4 mm Hg (n = 10) after IT-BUP alone. In contrast, MAP did not significantly change after IT-BUP + IT-NEO (12.5 and 25 nmol; n = 5 for each dose). Intramuscular (IM) NEO was not effective, and MAP decreased 38 +/- 4 mm Hg after IT-BUP + IM-NEO (25 nmol; n = 5). Three additional cholinesterase inhibitors, physostigmine, edrophonium, and ambenonium, as well as the direct-acting cholinergic agonists carbachol, oxotremorine, and arecoline, each lessened the hypotension seen after IT-BUP. Furthermore, the nonselective muscarinic antagonist, atropine, as well as the M2 receptor selective antagonist, methoctramine, prevented the vasopressor effect of IT-NEO in our model. Finally, the nicotinic antagonist, mecamylamine, and the M1 selective antagonist, pirenzepine, did not affect the pressor effects of NEO in our model. In conclusion, IT cholinergic agonists lessen BUP spinal-block-induced hypotension in rats by a muscarinic dependent pathway.

Anesthesia, Spinal↗
PubMed1997

Nerve growth factor treatment increases brain-derived neurotrophic factor selectively in TrkA-expressing dorsal root ganglion cells and in their central terminations within the spinal cord.

Using immunocytochemistry and in situ hybridization, we have examined the expression of brain-derived neurotrophic factor (BDNF) and of neurotrophin receptors in dorsal root ganglion cells. In the adult rat, BDNF mRNA and protein were found mainly in the subpopulation of cells that express the nerve growth factor (NGF) receptor trkA and the neuropeptide calcitonin gene-related peptide (CGRP). NGF increased BDNF within the trkA/CGRP cells to the extent that almost 90% of trkA cells contained BDNF mRNA after intrathecal NGF treatment, and 80-90% of BDNF-expressing cells contained trkA. Non-trkA cells that expressed BDNF included some trkC cells and some small cells that labeled with the lectin Griffonia simplicifolia IB4, a marker for cells that do not express trks. However, very few trkB cells expressed either BDNF mRNA or protein, and NGF did not increase BDNF expression in non-trkA cells. BDNF protein was anterogradely transported both peripherally and centrally. The central transport resulted in BDNF immunoreactivity in CGRP containing terminal arbors in the dorsal horn of the spinal cord, and this immunoreactivity was increased by NGF treatment. Electron microscopic analysis revealed that the BDNF immunoreactivity was present in finely myelinated and unmyelinated axons and in axon terminals, where it was most concentrated over dense-cored vesicles. Our data do not support an autocrine or paracrine role for BDNF within normal dorsal root ganglia, but indicate that BDNF may act as an anterograde trophic messenger. NGF levels in the periphery could influence dorsal horn neurons via release of BDNF from primary afferents.

Afferent Pathways↗
PubMed1997

[Spinal analgesia and perioperative low molecular weight heparin (LMWH) prophylaxis of thrombosis. Safety aspect].

For many gynecological surgery patients belonging to deep vein thrombosis (DVT) high-risk group the analgesia of choice is regional spinal analgesia. Perioperatively LMWH--Fraxiparine was administered to 426 gynecological surgery patients and to 113 caesarean section patients. The first dose 7500 ICU s.c. was administered 2 hours before operation and consecutive ones every 24 hours for 5 to 7 days. The drug didn't cause any anaesthesia complications like enhanced bleeding after lumbar punction. It was emphasised in the discussion that in choosing this kind of prophylaxis certain conditions should be fulfilled in order to avoid spinal hematoma.

Adult↗
PubMed1993

Regulation of sigma activity by the amino-terminus of substance P in the mouse spinal cord: involvement of phencyclidine (PCP) sites not linked to N-methyl-D-aspartate (NMDA) activity.

Behavioral responses to kainic acid (KA) injected intrathecally in mice are enhanced by N-but not C-terminal fragments of substance P (SP). Repeated injections of KA result in sensitization to KA-induced activity, an effect that appears to be mediated by SP N-terminal activity and inhibited by PCP ligands. The present study was initiated to determine whether the ability of SP N-terminal fragments to enhance KA activity is also sensitive to PCP ligands. We compared the effect of a PCP ligand, dizocilpine (MK-801), to that of haloperidol, a sigma ligand and dopamine antagonist. MK-801 (1 nmol) failed to alter the enhancement of behavioral responses to KA (25 pmol) produced by SP(1-7) (22.5 pmol, 30 min). However, pretreatment with 1 nmol of either haloperidol or the N-terminal SP antagonist, [D-Pro2-D-Phe7]SP(1-7) [D-SP(1-7)], prevented potentiation of KA by SP(1-7). Like SP(1-7), 5 nmol of the sigma ligand 1,3-di(2-tolyl)guanidine (DTG) also enhanced behaviors elicited by KA, and this effect was also blocked by haloperidol or D-SP(1-7), but not spiperone (2.5 nmol), a dopamine antagonist. Together these data suggest that sigma receptors are involved in the potentiation of KA. A large dose of SP(1-7) (10 nmol) or DTG (20 nmol) did not alter the response to KA 24 hr later, yet further potentiated responses to KA 30 min after SP(1-7) (22.5 pmol) or DTG (5 nmol), suggesting sensitization to the effects of these compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Dynorphin-A-(1-13) antagonizes morphine analgesia in the brain and potentiates morphine analgesia in the spinal cord.

Intrathecal injection of subanalgesic doses of morphine (7.5 nmol) and dynorphin-A-(1-13) (1.25 nmol) in combination resulted in a marked analgesic effect as assessed by tail flick latency in the rat. The analgesic effect of the composite dynorphin/morphine was dose-dependent in serial dilutions so that a composition of 1/8 of the analgesic dose of dynorphin and 1/3 that of morphine produced an analgesic effect equipotent to full dose of either drug applied separately. The analgesic effect induced by dynorphin/morphine mixture was not accompanied by motor dysfunction and was easily reversed by a small dose (0.5 mg/kg) of naloxone. Contrary to the augmentatory effect of dynorphin on morphine analgesia in the spinal cord, intracerevroventricular (ICV) injection of 20 nmol of dynorphin-A-(1-13) exhibited a marked antagonistic effect on the analgesia produced by morphine (120 nmol, ICV). The theoretical considerations and practical implications of the differential interactions between dynorphin-A-(1-13) and morphine in the brain versus spinal cord are discussed.

Analgesia↗
PubMed2000

Effects of ketamine on formalin-induced activity in the spinal dorsal horn of spinal cord-transected cats: differences in response to intravenous ketamine administered before and after formalin.

BACKGROUND: Although formalin has been widely used as an algesic substance in rodent studies, the unique biphasic effect seen in rats is not present in humans. Humans, like cats, have a monophasic behavioral response to formalin injection. Electrophysiologically, spinal dorsal horn neurons in cats also have what could be considered a monophasic response after the initial burst of activity following formalin injection. Although several studies of the effects of ketamine on formalin responses have been carried out in rodents, we are unaware of similar studies in cats. We hypothesize that such species differences may explain observed differences in preemptive analgesic effects. Therefore, we examined the effects of ketamine on activity of spinal wide dynamic range (WDR) neurons evoked by formalin injection in cats. METHODS: We investigated in cats the effect of ketamine on the activity of WDR neurons in the spinal dorsal horn that was evoked by formalin. In addition, we studied the effects of pre- and post-administration of ketamine on the maintained phase of the formalin response. Each dose was a subanesthetic, anesthetic or high anesthetic dose (3.0 mg x kg(-1), 10 mg x kg(-1), and 30 mg x kg(-1)). RESULTS: Intravenously administered ketamine produced a dose-dependent depression of evoked activity that was significantly greater when the drug was administered before formalin. CONCLUSION: In spite of the species differences in responses to formalin, there still appears to be a clear preemptive effect of ketamine in the cat. Species differences may not explain apparent differences between human and animal preemptive analgesia.

Anesthetics, Dissociative↗
PubMedDate not supplied

Differential motor and blood pressure effects of intrathecal oxytocin and TRH in the rat.

While previous reports have immunocytochemically localized oxytocin and TRH in the spinal cord, the functional significance of these peptides is unclear. The present paper examined this issue and tested the effects of these peptides upon intrathecal administration. We found both peptides produced lasting motor and blood pressure changes. Oxytocin elicited prolonged jerks of the hindlimbs and the tail, while TRH produced an increase of hindlimb muscle tone and tail tremor. TRH in larger doses (5, 10 micrograms) also caused tail erections and whipping. The motor effects of both peptides were dose-dependent. Intrathecal oxytocin (0.75 or 1.5 IU) caused a transient drop in blood pressure followed by a rise, in 4 out of 7 rats. The other 3 only showed a hypertensive effect. In contrast, intrathecal TRH produced a rise in blood pressure in all the animals tested. These findings suggest that both oxytocin and TRH may play a role in the regulation of motor and automatic functioning at the spinal level.

Animals↗
PubMed1996

Effect of spinal infusion of L-NAME, a nitric oxide synthase inhibitor, on spinal tolerance and dependence induced by chronic intrathecal morphine in the rat.

Systemic L-NG-nitroarginine methyl ester or L-NAME (LN), a nitric oxide synthase inhibitor, has been reported to attenuate systemic opioid tolerance and withdrawal. Intrathecal co-administration of LN (100 and 500 nmol/microliter per h) with spinal morphine produced only a small diminishing attenuation of tolerance and attenuated only one of seven signs of withdrawal. These results show that LN has little effect on morphine tolerance and withdrawal at spinal sites.

Animals↗
PubMed1987

Spinal opiates: a review of their effect on spinal function with emphasis on pain processing.

Several opiate receptor systems have been identified in the spinal cord. They produce a powerful analgesia when opioid agonists are administered intrathecally in the intact, unanesthetized animal. These effects appear mediated by an action on opioid receptors which are located presynaptically, in the terminals of primary afferents, and postsynaptically on certain dorsal horn neurons. Based on structure-activity relationships in different tests, quantitative studies of naloxone antagonism and selective cross tolerance, it appears that, in the spinal cord, there are three distinguishable populations of opioid receptors: mu, delta and kappa. Aside from the effects on nociception, these receptors are also associated with a variety of spinal mechanisms related to other aspects of sensory, autonomic and motor functions. Though in some cases these represent important side-effects (e.g. inhibition of the micturition reflex), in others, the subtle effects may have important therapeutic benefits (e.g. relieving spasticity in spinal injured patients).

Animals↗
PubMed1985

Intrathecal morphine induces myoclonic seizures in the rat.

The development of myoclonic activity as a toxic effect of morphine application into the intrathecal space in rats is described. This syndrome resembled the human syndrome of action myoclonus by its spontaneous onset and its augmentation by initiation of movement or by an acoustic stimulus. It was not reversed or prevented by naloxone. This effect of morphine was associated with an increase in serotonergic activity in the spinal cord and was reduced by pretreatment with parachlorophenylalanine in doses which reduced spinal 5-HT by approximately 60%. The dose which produced this syndrome was about ten times higher than the analgesic dose applied by the same route. Other commonly used opiates such as: methadone (0.5-2 mg/kg), pethidine (2-10 mg/kg), fentanyl (2-10 micrograms/kg) and ketamine (2-10 mg/kg) did not produce myoclonic-like activity, but methadone and pethidine at the highest doses caused respiratory arrest. Fentanyl appeared to be the safest of the drugs tested since a relatively high dose, administered into the intrathecal space did not cause any side effects, while morphine was least safe of the five drugs since it produced myoclonic activity in addition to the widely documented respiratory depression. We suggest that the production of the myoclonic activity is mediated by spinal serotonergic systems.

Analgesics↗