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PubMed1988

Neurological dysfunction after intrathecal injection of dynorphin A (1-13) in the rat. I. Injection procedures modify pharmacological responses.

In rats, the spinal subarachnoid injection of the kappa opioid agonist Dynorphin A (Dyn A)(1-13) and the delta opioid receptor antagonist ICI 174864 produced dose-related flaccid paralysis of hindlimbs and tail that were influenced appreciably by injection procedures. When injected through indwelling intrathecal (i.t.) catheters terminating at L1 to L2, both peptides were significantly more potent producing paralysis 1 day, rather than 10 to 14 days, after i.t. catheterization. Other rats received direct subarachnoid injections of these peptides through 30-gauge needles placed in the L4 to L5 intervertebral space. In naive, uncatheterized and acutely catheterized rats, direct intervertebral injection of these peptides, as well as D-Ala2-Dyn A (1-13) amide (a metabolically stable analog of Dyn A (1-13), produced hindlimb paralysis with potencies comparable to those recorded after injections through acutely implanted catheters. In contrast, chronically catheterized rats showed significantly reduced responsivity to direct intervertebral injections of all three of these peptides. Loss of hindlimb motor function was associated with loss of nociceptive responsiveness. Elevations in tail-flick latencies were only seen with doses of Dyn A (1-13) which produced motor dysfunction, and were not blocked or reversed by high doses of the opioid antagonist naloxone. These results indicate that: 1) indwelling i.t. catheters induce spinal cord alterations which complicate their experimental usefulness, 2) Dyn A (1-13) does not alter responsiveness to thermal nociceptive stimuli through opioid mechanism and 3) Dyn A (1-13) causes parallel disruptions of spinal cord motor and nociceptive function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

The role of nitric oxide in the phosphorylation of cyclic adenosine monophosphate-responsive element-binding protein in the spinal cord after intradermal injection of capsaicin.

We investigated the involvement of nitric oxide (NO) in the phosphorylation of cyclic adenosine monophosphate-responsive element-binding protein (CREB) in the spinal cord of rats during central sensitization after intradermal capsaicin injection. CREB and phosphorylated CREB (p-CREB) were measured by immunoblotting. The level of p-CREB increased by 20 minutes, peaked between 20 and 60 minutes after capsaicin injection, and started to decrease after 150 minutes. CREB itself did not show an obvious change after capsaicin injection. The p-CREB expression on the ipsilateral side of the spinal dorsal horn, but not on the contralateral side, increased significantly after capsaicin injection. The increase in p-CREB induced by capsaicin injection was partially blocked by pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, administered through a microdialysis fiber placed across the spinal cord. D-NAME, an inactive form of L-NAME, had no effect. CREB phosphorylation, not the level of CREB, was induced within 20 minutes by microdialysis administration of SIN-1, an NO donor. These results indicate that CREB phosphorylation in the spinal cord results from both endogenous and exogenous NO release and that p-CREB may play a role in central sensitization or in longer-term changes in gene expression induced by strong peripheral noxious stimulation.

Journal Article↗
PubMed1987

Neuropeptide Y-like immunoreactive C1 neurons in the rostral ventrolateral medulla of the rabbit project to sympathetic preganglionic neurons in the spinal cord.

After injection into the thoracic spinal cord of the rabbit, gold particles coupled to concanavalin A were found in the rostral ventrolateral medulla in neurons which contained neuropeptide Y-like immunoreactivity. These cells have previously been shown to belong to the C1 catecholamine (presumably adrenaline)- synthesizing group. Nerve terminals in the intermediolateral column contained both tyrosine hydroxylase and neuropeptide Y-like immunoreactivity. When fast blue was injected into the adrenal gland the retrogradely labeled preganglionic neurons were shown to be surrounded by nerve terminals containing neuropeptide Y-like immunoreactivity. Our results indicate that at least some of these terminals derive from C1 neurons which also synthesize neuropeptide Y.

Animals↗
PubMed1990

Spinal effects of four injectable anaesthetics on nociceptive reflexes in rats: a comparison of electrophysiological and behavioural measurements.

1. To assess the direct spinal contributions to the depression of reflexes caused by general anaesthetics, the intravenous potency of four injectable anaesthetics has been compared in two preparations: in decerebrate, spinalised rats, using a novel preparation requiring little surgical intervention, and in intact rats with chronically implanted i.v. cannulae. 2. Methohexitone (1-8 mg kg-1 i.v.), alphaxalone/alphadolone (0.5-8 mg kg-1 i.v.), alpha-chloralose (20-80 mg kg-1 i.v.) and ketamine (0.5-16 mg kg-1 i.v.) all produced a dose-dependent depression of single motor unit activity evoked by controlled noxious mechanical stimuli in decerebrate, spinalised animals. 3. The sedative and motor effects brought about by equivalent doses to those used in the electrophysiological experiments were assessed in intact rats. Methohexitone, alphaxalone/alphadolone and alpha-chloralose all caused similar levels of behavioural sedation at the doses that caused depression of spinal reflexes. Ketamine required relatively much higher doses to cause sedation. 4. To determine whether background anaesthesia modulated the potency with which these compounds affected spinal reflex activity, depressant effects in decerebrate, unanaesthetized rats were compared with those in animals maintained under anaesthesia with either alpha-chloralose or the steroid mixture of alphaxalone/alphadolone. The presence of either of these two agents as maintenance anaesthetics did not influence the effectiveness with which other compounds depressed nociceptive responses. However, additional doses of the maintenance anaesthetics were less effective than the same doses tested in decerebrate animals. 5. All the anaesthetics tested produced a significant depression of spinal reflex responses to noxious stimuli at doses well below those required for anaesthesia. Whilst the presence of maintenance anaesthetics appears not to distort pharmacological tests of other agents, there may nonetheless be a biasing of the samples of cells recorded.

Anesthetics↗
PubMed2000

A novel injectable bioactive bone cement for spinal surgery: a developmental and preclinical study.

The injection of bone cement by minimally invasive techniques for the treatment of vertebral body fractures or for stabilization of an osteoporotic vertebral body is regarded as promising in spinal surgery. The purpose of this study was to develop a novel injectable bioactive bone cement to address such concerns. The cement was composed mainly of strontium-containing hydroxyapatite (Sr-HA) filler and Bisphenol A Diglycidylether Dimethacrylate (D-GMA) resin. The Sr-HA filler was prepared by precipitation and calcination, then analyzed with Fourier transform infrared (FTIR) spectra and X-ray diffraction (XRD) patterns. Samples of strontium-containing hydroxyapatite cement (SrHAC) were formed by a combination of powder filler and resin matrix, with the setting time and peak temperature recorded. Cell relative growth rate (RGR), Tetrazolium bromide (MTT), and haemolysis tests were used to detect initial in vitro biocompatibility of the new cement. In vitro spinal biomechanical testing and morphological observation after bone cement injection were performed on pig spines. Results indicate that the setting time and peak temperature of the cement was 15 min and 55 degrees C, respectively. Cytotoxicity of the cement was class 1 (no cytotoxicity) and haemolysis was 1% (no haemolysis). Stiffness after cement injection and fatigue loading were 112% and 95% of the intact bone, respectively, which is similar to that of natural bone. Radiopacity of SrHAC allowed easy radiographic imaging. The use of SrHAC cement is, thus, promising in spinal surgery.

Animals↗
PubMed1994

Spinal cholinergic alpha-2 adrenergic interactions in analgesia and hemodynamic control: role of muscarinic receptor subtypes and nitric oxide.

Intrathecal injection of neostigmine enhances antinociception from clonidine while it counteracts clonidine-induced hypotension. This study further examined the pharmacology of neostigmine-clonidine interactions in the spinal cord and focused on the roles of muscarinic receptor subtypes and local nitric oxide synthesis. Spinal neostigmine counteracted clonidine-induced decreases in blood pressure and heart rate in conscious sheep and this effect was blocked by spinal injection of the M2 muscarinic antagonist, AFDX-116, but not by the M1 muscarinic antagonist, pirenzepine. Carbamylcholine injected spinally alone increased blood pressure and heart rate and these effects and neostigmine's hemodynamic interaction with clonidine were blocked by spinal injection of the nitric oxide synthase inhibitor, N-methyl-L-arginine. The authors also investigated antinociceptive interactions by using a mechanical pressure stimulus on the forelimb of conscious sheep. Spinal clonidine produced dose-dependent antinociception, which was enhanced by neostigmine and antagonized by N-methyl-L-arginine. NADPH diaphorase staining of sheep spinal cord revealed dense localization to the superficial dorsal horn and the intermediolateral cell column. These results suggest that counteraction of spinal clonidine-induced hypotension by neostigmine is due to stimulation of spinal M2 muscarinic receptors and synthesis of nitric oxide. Nitric oxide synthesis is also necessary for clonidine-induced antinociception in sheep.

Analgesia↗
PubMed2004

Spinal cord effects from lumbar myelographic injection technique in the dog.

To characterize spinal cord effects of needle placement using lumbar puncture myelography technique, lumbar puncture was performed in 5 dogs and computed tomography images of the spinal column were acquired in the transverse plane at the level of the puncture site after contrast injection and both before and after needle removal. The spinal cords were punctured during needle placement and parenchymal contrast enhancement was present in 4 of 5 dogs. Although no dogs exhibited overt neurological abnormalities following computed tomographic imaging, hemorrhage, gliosis and axonal degeneration were confirmed microscopically in all subjects. These results suggest that spinal cord morbidity is induced when lumbar myelography is performed using currently accepted technique.

Animals↗
PubMed1981

Transplantation of rat Schwann cells grown in tissue culture into the mouse spinal cord.

Injections of lysolecithin were used to produce acute focal demyelination in the dorsal columns of 2 strains of mice, the myelin mutant quaking and the normal C57BL/6J. A small collection of rat Schwann cells grown in tissue culture was transplanted with their collagen substrate into this demyelinated area. The host mice were immune-suppressed to prevent graft rejection. Evidence of remyelination by Schwann cells was seen in the dorsal columns from 2-18 weeks after implantation. Proof that these Schwann cells were foreign to the host was derived from their rejection after the recipient mice were allowed to recover immunological competence by discontinuation of the immune suppression and by transferring immune cells sensitized against the donor tissue. It was concluded that Schwann cells grown in vitro retain their potential to produce myelin when returned to an in vivo situation and can myelinate central axons of a xenogenic host.

Animals↗
PubMed1980

Rapid effect of nerve injury upon axonal transport of phospholipids.

1. Axonal transport of phospholipids labelled by lumbosacral spinal cord injection of [3H]choline has been studied in normal and injured sciatic nerves of the rat. 2. The appearance of labelled material in progressively increasing amounts in the sciatic nerve following spinal cord injection was consistent with a maximum velocity of axonal transport of about 20 mm/hr. There was also evidence of substantial amounts of labelled phospholipids being transported at much slower velocities. 3. In sciatic nerves injured by crushing there was an accumulation of labelled phospholipid immediately proximal to the crush. The accumulation was progressive with time. There was also an increase of labelled phospholipid in all the more proximal segments of the crushed nerves; this reached a maximum of about twice that in uncrushed nerves at 10 hr. after spinal cord injection. 4. The labelled phospholipid was shown to be about 80-90% phosphatidylcholine both in uncrushed and crushed nerves. 5. The nature of the mechanism of this very rapid response of neurones to peripheral injury did not appear to be due to loss of 'information' from the periphery or action potentials initiated at the site of injury. The phenomenon has been further investigated by injection of drugs into the injured or control nerves. KCl injected at (but not proximal to) the site of injury was effective in blocking the injury response providing it was injected between a few minutes before or up to 30 min after the time of injury. Injection of either tetrodotoxin or local anaesthetic was as effective as injury in increasing the amount of labelled phospholipid transport. 6. These results suggest that the occurrence of an injury in a distant process of a neuron can be signalled retrogradely to the cell body by a mechanism involving a signal velocity of at least 140 mm/hr.

Animals↗
PubMed1978

Direct administration of methotrexate into the central nervous system of primates. Part 2: Distribution of 3H methotrexate after intrathecal lumbar injection.

The kinetics of distribution of 3H methotrexate (3HMTX) in the central nervous system, plasma, and urine after intraventricular, lumbar percutaneous puncture, and spinal catheter injections were compared. Levels of 3HMTX in whole brain after lumbar percutaneous injection were 40 times less than after intraventricular injection. Injection of 3HMTX via a spinal catheter increased the level of 3HMTX in whole brain but this was still tenfold less than after direct intraventricular instillation. Also, it was found that a disproportionately high amount of 3HMTX was in the brain-stem-cerebellum region which would further reduce the concentration of methotrexate in the cerebral hemispheres. Both intraventricular and lumbar spinal catheter administration of 3HMTX produced 3HMTX levels greater than 10(-6)M (moles/kg wet weight) in spinal cord tissue as measured by 3H specific activity between 2 to 8 hours after injection. Administration by lumbar percutaneous puncture, however, rarely resulted in this suggested therapeutic level of 10(-6)M. Initial 3HMTX levels in plasma after lumbar percutaneous instillation was 24 times greater than after intraventricular or lumbar spinal catheter injections. This indicated significant and unavoidable extradural leakage after lumbar percutaneous puncture, which may account for the substantially lower levels of 3HMTX in the brain and spinal cord tissue. It is concluded that intraventricular instillation of methotrexate is the best route of administering the drug to achieve therapeutic levels of methotrexate in both whole brain and throughout the spinal cord.

Animals↗
PubMed1993

The mechanosensitivity of spinal sensory neurons following intraspinal injections of quisqualic acid in the rat.

The mechanoreceptive properties of rat spinal sensory neurons were evaluated in segments adjacent to those injected with the excitatory amino acid agonist quisqualic acid. Following survival periods of 7-36 days cells recorded in quisqualate injected animals had an increased level of background activity, increased sensitivity to mechanical stimuli, and an increase in the duration of afterdischarge responses. It is suggested that a central mechanism that alters the functional state of neurons may be responsible for the sensory abnormalities, e.g. allodynia and hyperalgesia, that occur following excitotoxic induced cell death associated with ischemic and traumatic spinal cord injury.

Animals↗
PubMed1986

Activation of inhibition from the periaqueductal grey matter mediates central analgesic effect of metamizol (dipyrone).

The pyrazolone derivative, metamizol (dipyrone), possesses analgesic, antipyretic, anti-inflammatory and spasmolytic properties. It is often classified as peripherally acting. To test the possibility that a central action of the drug contributes to its antinociceptive and analgesic effects, experiments were carried out in which the tail-flick response to radiant heat, flexor reflex activity in the tibialis anterior muscle and activity in ascending spinal axons evoked by stimulation of afferent C fibres in the sural nerve, and activity of neurones in the periaqueductal grey matter and the substantia nigra were assessed in rats. Metamizol administered by intraperitoneal (i.p.; 10, 20 and 40 mg/kg) or intrathecal (i.t.; 50 to 400 micrograms) injection to intact rats dose-dependently prolonged the tail-flick latency. Administration by i.t. injection to spinal rats was without effect. Intravenous (i.v.) injection of metamizol (140 mg/kg) reduced flexor reflex activity in intact animals, while an i.t. injection to spinal rats was ineffective at a low dose (100 micrograms) or enhanced the reflex activity at a higher dose (400 micrograms). Activity in ascending axons responding to afferent C fibre stimulation was mostly depressed by i.t. injection of metamizol (40, 80 and 140 mg/kg) in rats with an intact spinal cord. Ascending activity was increased by i.t. injection of the drug (100 and 200 micrograms) to spinal rats. Metamizol (140 mg/kg) i.v. increased the activity of neurones in the PAG and reduced that of neurones in the substantia nigra. Metamizol administered by microinjection into the PAG prolonged the tail-flick latency (15-100 micrograms) and depressed C fibre-evoked activity in ascending axons (100 micrograms). The results suggest that a central action is involved in the analgesic effect of metamizol and that this central action manifests itself by an activation of inhibition originating in the PAG.

Action Potentials↗
PubMed1999

Dilution of spinal lidocaine does not alter the incidence of transient neurologic symptoms.

BACKGROUND: Although it has been suggested that the dilution of 5% hyperbaric lidocaine before injection for spinal anesthesia may decrease the incidence of transient neurologic symptoms, previous studies have not noted a decreased incidence between 5% and 2% lidocaine. The aim of the current study was to determine whether the incidence of transient neurologic symptoms could be altered by further diluting spinal lidocaine from 2.0% to 0.5%. METHODS: One hundred nine patients with American Society of Anesthesiologists physical status 1 or 2 undergoing outpatient knee arthroscopy were randomized in a double-blind fashion to receive 50 mg hyperbaric spinal lidocaine as a 2.0%, 1.0%, or 0.5% concentration. On the third postoperative day, patients were contacted by a blinded investigator and questioned regarding the incidence of postoperative complications, including transient neurologic symptoms, defined as pain or dysthesia in one or both buttocks or legs occurring within 24 h of surgery. RESULTS: The incidence of transient neurologic symptoms did not differ among patients receiving 2.0% (incidence of 15.8%), 1.0% (incidence of 22.2%), and 0.5% (incidence of 17.1%) lidocaine (P = 0.756). CONCLUSIONS: For ambulatory patients undergoing arthroscopy, the incidence of transient neurologic symptoms is not reduced by decreasing spinal lidocaine concentrations from 2.0% to 1.0% or 0.5%. The incidences of transient neurologic symptoms with the 0.5%, 1.0%, and 2.0% solutions are similar to previously reported incidences for 5.0% lidocaine, suggesting that dilution of lidocaine from 5.0% to 0.5% does not change the incidence of these symptoms.

Adult↗
PubMed1990

Spinal cord thromboplastin-induced coagulopathy in a rabbit model.

Coagulopathy results from many diverse events, including several neurogenic causes. Using a rabbit model, we produced coagulopathy by injecting autologous spinal cord and extracted thromboplastin intravenously. Serial coagulation panels were performed to evaluate the activation of the thrombotic and fibrinolytic pathways. Group 1 animals (n = 4) received intravenous injections of homogenized spinal cord tissue. Coagulopathy was not produced with 36 mg of homogenized spinal cord tissue, but 50 mg or more resulted in death. Group 2 animals (n = 12) received intravenous injections of extracted rabbit cord thromboplastin, which contained approximately 60% activity of a commercially purified rabbit brain thromboplastin. Five animals receiving 2.5 to 5.5 mg of thromboplastin per kilogram of body weight survived with evidence of coagulopathy. Seven animals receiving 2.5 to 100 mg of thromboplastin per kilogram of body weight died. Group 3 (4 control animals) received normal saline injections without changes in clinical or laboratory status. The thrombotic pathway was activated in all animals as evidenced by decreased platelet counts and fibrinogen levels. Activation of the fibrinolytic system was demonstrated by increased concentrations of protamine sulfate and abnormal euglobulin clot lysis times. The most sensitive parameters were the platelet count, protamine sulfate concentration, and white cell count (margination), which became abnormal within 15 minutes after the injections and returned to normal within 1 hour.

Animals↗