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PubMed1989

[Intrathecal clonidine--how does it work in spinal fentanyl analgesia in rats?].

The effects of intrathecal clonidine on spinal fentanyl analgesia were studied by the hot-plate test (52.0 degrees C) in rats. Clonidine (5 micrograms) and/or fentanyl (5 micrograms) were administered alone or combined in volume of 10 microliters through a chronically-implanted polyethylene catheter (PE-10) whose tip was near the lumbar enlargement of the spinal cord. Injections were done repeatedly every two or three days to determine the time course of thermal analgesia. Results were as follows; 1) Intrathecal clonidine (n = 5) produced no thermal analgesia. 2) Intrathecal fentanyl (n = 10) produced a profound thermal analgesia which was attenuated markedly by the repeated injections in six rats before the 9th injection. 3) Two out of six fentanyl tolerated rats responded with remarkable increases in thermal thresholds following the intrathecal clonidine with fentanyl. 4) Rats which were administered with both clonidine and fentanyl from the 1st injection (n = 9) responded with a extended prolongation of the escape latency, compared with the rats which received fentanyl only. In this group, the tolerance developed in only three animals by the 9th injection. In conclusion, combined intrathecal administration of clonidine with fentanyl potentiated the analgesic effect of fentanyl and then definitely suppressed the tolerance formation even if a small dose of clonidine which produces no analgesic effect was used. These results suggest that intrathecal or epidural administration of clonidine with narcotics might be useful in managing intractable pain.

Adaptation, Physiological↗
PubMed1988

Prostaglandins inhibit endogenous pain control mechanisms by blocking transmission at spinal noradrenergic synapses.

Spinal intrathecal injections of the nonsteroidal antiinflammatory analgesics (NSAIAs) indomethacin and acetylsalicylic acid, which inhibit prostaglandin synthesis, cause dose-dependent hypoalgesia in the rat. Intrathecal injections of prostaglandin-E2 (PGE2) produce dose-dependent hyperalgesia. To determine whether this action of prostaglandins on the central nervous system is mediated through pain-generating or analgesia pathways, we studied the effect of intrathecal PGE2 on endogenous opioid-induced analgesia. Intrathecal PGE2 antagonized the analgesia produced by both brain stimulation and intracerebroventricular morphine. In contrast, the NSAIAs synergized with brain stimulation and morphine-induced analgesia. The alpha-adrenergic antagonist phentolamine and the catecholaminergic selective neurotoxin 6-hydroxydopamine, used to block tonic catecholamine activity in endogenous opioid-mediated analgesia systems, prevented the hyperalgesia induced by intrathecal PGE2. Phentolamine did not, however, block the hyperalgesia caused by intradermal PGE2. These findings suggest that prostaglandins can block endogenous opioid-mediated analgesia systems by inhibiting the bulbospinal noradrenergic component of this analgesia pathway.

Animals↗
PubMed1984

Pulmonary fate of [3H]bleomycin A2 in mice.

The pulmonary fate of radiolabeled bleomycin [S-methyl-3H]bleomycin A2 ( [3H]BLM A2) was studied in mice after intratracheal (i.t.) or s.c. injection. The loss of radioactivity from the lungs followed apparent first-order kinetics during the first 3 hr after i.t. drug instillation with a half-time of removal of 32 min. In addition, the initial pulmonary removal was linear with instilled doses ranging from 0.02 to 2.2 mg/kg. Radioactivity was detected in liver, kidneys, spleen and serum 1 hr after i.t. administration. Approximately 1% of the i.t. administered dose was detected in the lungs after 24 hr, indicating that the rate of removal of radioactivity slowed between 3 and 24 hr after i.t. drug instillation. Eighty percent of the radioactivity found in the lungs 1 hr after i.t. instillation was unmetabolized [3H]BLM A2, but by 24 hr less than 25% was unmetabolized drug and almost 40% was the nonfibrogenic metabolite, desamidobleomycin A2. After s.c. administration of 10 mg/kg of [3H]BLM A2, peak pulmonary levels were observed between 45 and 60 min and were less than 1% of the injected dose. Pulmonary levels comparable to those seen with a single fibrogenic i.t. dose (2.2 mg/kg) could not be obtained after a s.c. injection even with a toxic dose of the drug (100 mg/kg). In addition, twice weekly s.c. injections of unlabeled BLM A2 (10 mg/kg) for 5 weeks did not alter the amount of radioactivity seen in the lungs after a s.c. injection of [3H]BLM A2. Thus, the pulmonary fibrosis seen with i.t. BLM administration may reflect the high initial content of unmetabolized drug achieved in the lungs.

Animals↗
PubMed1994

Thermal hyperalgesia in association with the development of morphine tolerance in rats: roles of excitatory amino acid receptors and protein kinase C.

In a rat model of morphine tolerance, we examined the hypotheses that thermal hyperalgesia to radiant heat develops in association with the development of morphine tolerance and that both the development and expression of thermal hyperalgesia in morphine-tolerant rats are mediated by central NMDA and non-NMDA receptors and subsequent protein kinase C (PKC) activation. Tolerance to the analgesic effect of morphine was developed in rats utilizing an intrathecal repeated treatment regimen. The development of morphine tolerance and thermal hyperalgesia was examined by employing the tail-flick test and paw-withdrawal test, respectively. Intrathecal MK 801 (an NMDA receptor antagonist), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; a non-NMDA receptor antagonist), or GM1 ganglioside (an intracellular PKC inhibitor) treatment was given to examine the effects of these agents on the development and expression of thermal hyperalgesia in morphine-tolerant rats. Tolerance to the analgesic effect of morphine was reliably developed in rats following once daily intrathecal (onto the lumbosacral spinal cord) injection of 10 micrograms of morphine sulfate for 8 consecutive days as demonstrated by the decreased analgesia following morphine administration on day 8 as compared to that on day 1. In association with the development of morphine tolerance, thermal hyperalgesia to radiant heat developed in these same rats. Paw-withdrawal latencies were reliably decreased in morphine-tolerant rats as compared to nontolerant (saline) controls when tested on day 8 before the last morphine treatment and on day 10 (i.e., 48 hr after the last morphine treatment). The coincident development of morphine tolerance and thermal hyperalgesia was potently prevented by intrathecal coadministration of morphine with MK 801 (10 nmol) or GM1 (160 nmol), and partially by CNQX (80 nmol). MK 801 (5, 10 nmol, not 2.5 nmol) and CNQX (80, 160 nmol, not 40 nmol), but not GM1 (160 nmol), also reliably reversed thermal hyperalgesia in rats rendered tolerant to morphine when tested 30 min after each drug treatment on day 10 (48 hr after the last morphine treatment). The data indicate that thermal hyperalgesia develops in association with the development of morphine tolerance and that the coactivation of central NMDA and non-NMDA receptors is crucial for both the development and expression of thermal hyperalgesia in morphine-tolerant rats. Furthermore, intracellular PKC activation plays a critical role in the development of thermal hyperalgesia in morphine-tolerant rats.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1994

Antinociception produced by oral, subcutaneous or intrathecal administration of SC-39566, an opioid dipeptide arylalkylamide, in the rodent.

This study characterized the prototypic "minimum structure" enkephalin SC-39566 [2,6-dimethyl-L-tyrosinyl-D-alanine-(3-phenyl-1-propyl)-amide hydrochloride]. SC-39566 bound with highest affinity to mu opioid receptors (Ki, 0.13 nM), as well as to delta (Ki, 4.0 nM) opioid receptors in the rat brain, and with much lower affinity to kappa opioid receptors (Ki, 83.8 nM) in the guinea pig brain. In the mouse, SC-39566 inhibited phenylbenzoquinone-induced writhing and increased tail-flick and hot-plate latencies in a dose-dependent manner after either s.c. or p.o. (i.g.; intragastrical) administration. This antinociception was antagonized by the opioid antagonist naloxone, but not by alpha adrenergic, serotonergic, histaminergic, muscarinic cholinergic or dopaminergic receptor antagonists. In the rat, SC-39566 dose-dependently inhibited acetic-acid-induced writhing after s.c. or i.g. administration and increased response latencies in the tail-flick and hot-plate test after s.c. or intrathecal (i.t.) administration. The increase in tail-flick latency produced by s.c. SC-39566 in the rat was antagonized by s.c. naloxone with an apparent pA2 value of 7.9. Pretreatment with naltrindole, a delta opioid receptor antagonist, increased the ED50 of SC-39566 by only 1.7-fold. In addition, the increase in tail-flick latency produced by i.t. SC-39566 was not antagonized by i.t. administration of naltrindole or nor-binaltorphimine, a kappa receptor antagonist. These data suggest that the antinociceptive activity of SC-39566 is mediated predominantly by mu opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1997

Current status of patient-controlled analgesia in cancer patients.

Patient-controlled analgesia (PCA) is a relatively new technique in which patients are able to self-administer small doses of opioid analgesics when needed. Many different devices are available for opioid infusion, including a syringe pump, disposable plastic cylinder, and battery-operated computer-driven pump. These devices allow patients to choose an intermittent (demand) bolus, continuous infusion, or both modes of administration. Parameters, such as route, drug concentration dose, frequency, and maximum daily or hourly dose, are programmed by the physician. The patient decides whether or not to take a dose. Devices can be used to deliver the drug into a running intravenous infusion, the epidural space, or subcutaneously. Controlled trials indicate that PCA is probably superior to regular opioid administration in postoperative pain. Reported advantages include greater patient satisfaction, decreased sedation and anxiety, and reduced nursing time and hospitalization. Preliminary experience suggests that PCA is also useful and safe for cancer pain, but further research is greatly needed.

Administration, Oral↗
PubMed1997

[Clinical study on action of artificial respiration produced by pressing in massage under anesthesia for lumbar intervertebral disc prolapse].

OBJECTIVE: To observe whether the gas exchange is sufficient for the requirement of body when the patient was prone in position and pressed in the course of massage under intravenous anesthesia with sodium pentothal (SP) for the treatment of lumbar intervertebral disc prolapse. METHODS: The oxygen would not be given to the patients whose heart and lung functions were good during the course of anesthesia and massage, respiratory function and blood gas analysis were studied on 20 patients selected randomly. RESULTS: Tidal volume was smaller and respiratory rate was faster than normal respiration. Saturation pulse oxygen was still normal in all patients. There were no significant changes in blood gas analysis before spinal injection and after massage (P > 0.05). CONCLUSION: The pressing could attain the action of artificial respiration. The respiration pattern was similar to high frequency positive pressure ventilation. The action of vibration and diffusion had normal respiratory effect.

Adult↗
PubMed2005

Diagnostic utility of facet (zygapophysial) joint injections in chronic spinal pain: a systematic review of evidence.

BACKGROUND: Chronic refractory spinal pain poses a peculiar diagnostic challenge because of multiple putative pain sources, overlapping clinical features, and nonspecific radiologic findings. Diagnostic injection techniques are employed to isolate the source(s) of pain. Facet or zygapophysial joint pain is an example of spinal pain diagnosed by local anesthetic injections of the facet joint or its nerve supply. Diagnostic facet joint injections are expected to meet the cardinal features of a diagnostic test (i.e., accuracy, safety and reproducibility). Accuracy must be compared with a "gold" or criterion standard that can confirm presence or absence of a disease. There is, however, no available gold standard, such as biopsy, to measure presence or absence of pain. Hence, there is a degree of uncertainty concerning the accuracy of diagnostic facet joint injections. OBJECTIVES: To evaluate accuracy, safety and reproducibility of facet or zygapophysial joint injections in diagnosing chronic spinal pain of facet joint origin. STUDY DESIGN: A systematic review of the literature for clinical studies on efficacy and utility of facet joint/nerve injections in diagnosing spinal pain from facet joints. METHODS: Relevant literature on diagnostic facet injections was identified through database searches. Excluded were abstracts, reviews, book chapters, case reports and studies based on single blocks or blocks without radiologic control. Prospective studies with placebo control, or controlled comparative local anesthetic blocks, were given priority over retrospective studies. Each study was graded using AHRQ and QUADAS criteria. The level of evidence was classified as conclusive, strong, moderate, limited, or inconclusive. RESULTS: Available literature pointed to strong evidence for controlled comparative local anesthetic facet joint medial branch blocks in the diagnosis of neck and low back pain. There was moderate evidence in the diagnosis of pain arising from thoracic facet joints. CONCLUSION: The evidence obtained from literature review suggests that controlled comparative local anesthetic blocks of facet joint nerves (medial branch or dorsal ramus) are reproducible, reasonably accurate, and safe. The sensitivity, specificity, false-positive rates, and predictive values of these diagnostic tests for neck and low back pain have been validated and reproduced in multiple studies.

Journal Article↗
PubMed2000

Reinforcement of spinal anesthesia by epidural injection of saline: a comparison of hyperbaric and isobaric tetracaine.

PURPOSE: An epidural injection of saline was reported to extend spinal anesthesia because of a volume effect. The aim of this study was to evaluate the influence of the baricity of spinal local anesthetics upon the extension of spinal anesthesia by epidural injection of saline. METHODS: Forty patients undergoing elective lower-limb surgery were randomly allocated to four groups of 10 patients each. Group A received no epidural injection after the spinal administration of hyperbaric tetracaine (dissolved in 10% glucose). Group B received an epidural injection of 8 ml of physiological saline 20 min after spinal hyperbaric tetracaine. Group C received no epidural injection after spinal isobaric tetracaine (dissolved in physiological saline). Group D received an epidural injection of 8 ml of saline 20 min after spinal isobaric tetracaine. The level of analgesia was examined by the pinprick method at 5-min intervals. RESULTS: The levels of analgesia 20 min after spinal anesthesia were significantly higher in hyperbaric groups than in isobaric groups [T5 (T2-L2) vs. T7 (T3-12)]. After epidural injection of saline, the levels of analgesia in groups B and D were significantly higher than in groups A and C. The segmental increases after epidural saline injection were 2 (0-3) in group B and 2 (1-7) in group D. Sensation in the sacral area remained 20 min after spinal block in one patient in group D; however, it disappeared after epidural saline injection. CONCLUSION: In this study, 8 ml of epidural saline extended spinal analgesia. However, there was no difference between the augmenting effect in isobaric and hyperbaric spinal anesthesia. We conclude that the reinforcement of spinal anesthesia by epidural injection of saline is not affected by the baricity of the spinal anesthetic solution used.

Clinical Trial↗
PubMedDate not supplied

Paralysis after transforaminal epidural injection and previous spinal surgery.

OBJECTIVE: This case discusses a rare but devastating complication of transforaminal epidural injection. Elements in the patient's history that may be risk factors are discussed. CASE REPORT: A 64-year-old man was evaluated for chronic low-back pain after multiple spine surgeries. After the most recent surgery, he suffered transient cauda equina symptoms. Because conservative therapy was not helpful for spinal stenosis and neuroclaudication, a left L2 transforaminal epidural injection was attempted, but a posterolateral fusion mass made this procedure impossible. A left L1 transforaminal approach was successful, and 1 mL of iopamidol (Isovue) contrast was injected, followed by 5 mL of a solution of 0.125% bupivacaine and 40 mg of triamcinolone. Approximately 1 to 2 minutes after injection, the patient described discomfort in the lower abdomen, and 1 minute later, he was unable to move his lower extremities. An MRI showed T2 signal change in the conus medullaris gray matter at T11-12, consistent with an acute vascular infarct. Spinal shock protocol with high-dose methylprednisolone was begun without change. More than 4 years later, the patient continues to be troubled by persistent paraparesis and chronic pain. CONCLUSIONS: This case report is part of a new and growing body of literature that demonstrates the potential risk of transforaminal injection. Further study is necessary to ensure that spinal vascular injuries can be kept to an acceptably rare level.

Anesthetics, Local↗
PubMed2003

Effects of spinally and supraspinally injected 3-isobutyl-1-methylxanthine, cholera toxin, and pertussis toxin on immobilization stress-induced antinociception in the mouse.

The effects of intracerebroventricular (i.c.v.) and intrathecal (i.t.) 3-isobutyl-1-methylxanthine (IBMX), cholera toxin (CTX) and pertussis toxin (PTX) administration on immobilization-induced antinociception were studied in ICR mice. Antinociception was assessed by the tail-flick assay. Immobilization of the mouse increased inhibition of the tail-flick response for at least 1 h. The pretreatment with i.t. IBMX (0.01-1 ng), but not i.c.v. IBMX, significantly attenuated immobilization-induced inhibition of the tail-flick response. The pretreatments with i.c.v. PTX (0.05-0.5 microg) as well as i.t. CTX, but neither i.c.v. CTX (0.05-0.5 microg) nor i.t. PTX, potentiated the inhibition of the tail-flick response induced by immobilization stress. Our results suggest that spinally located phosphodiesterase appears to be involved in the production of immobilization stress-induced antinociception. In addition, inactivation of supraspinally located PTX-sensitive G-proteins and spinally located CTX-sensitive G-proteins may modulate immobilization stress-induced antinociception.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Influence of obesity on the spread of spinal analgesia after injection of plain 0.5% bupivacaine at the L3-4 or L4-5 interspace.

Spinal anaesthesia was compared in 40 obese patients (increased body mass index (BMI] and 40 patients with normal BMI when 3 ml of plain 0.5% bupivacaine was injected at either the L3-4 or L4-5 interspace. More extensive cephalad spread of sensory block was achieved in patients with increased BMI compared with patients with normal BMI after injection at both L3-4 and L4-5 (P less than 0.05). The use of the L3-4 interspace instead of L4-5 resulted in a higher mean spread of block in patients with both increased (T4 vs T8) or normal (T9 vs T11) BMI (P less than 0.05). The interindividual variability of the blocks was relatively small in patients with normal BMI injected at L4-5, compared with the three other groups (normal BMI injected at L3-4, increased BMI injected at L3-4 and L4-5). Good anaesthesia was produced in all patients for orthopaedic surgery of the lower extremity. In an obese patient it is recommended that plain bupivacaine be administered at L4-5 instead of L3-4 when extensive spread of the block is to be avoided.

Adult↗