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PubMed1982

Neural blockade and pharmacokinetics following subarachnoid lidocaine in the rhesus monkey. I. Effects of epinephrine.

A sensitive and reliable animal model for the objective physiologic and pharmacokinetic evaluation of spinal anesthesia has been developed. Using this model, spinal anesthesia using lidocaine (30 mg) in 7.5% dextrose with and without epinephrine was compared. Epinephrine did not alter the degree or duration of time to achieve maximum motor block. However, epinephrine did significantly increase the time for complete motor recovery. A significantly higher dermatome level of sensory block was achieved in the epinephrine-containing solutions, as well as a significantly longer time for complete recovery. This reflects a latent effect of epinephrine, as the time for two-segment regression was independent of epinephrine. Pharmacokinetic analysis showed no effect of epinephrine on absorption and elimination constants. The maximum plasma concentration and time to reach maximum plasma concentration were equal with and without epinephrine.

Anesthesia, Spinal↗

PubMed1993

Scyliorhinin-I and -II induce reciprocal hindlimb scratching in mice: differentiation of spinal and supraspinal neurokinin receptors in vivo.

Scyliorhinin-I amide (SCY-I) (selective for NK-1 and NK-2 receptors) or scyliorhinin-II amide (SCY-II) (selective for NK-3 receptors) were injected either spinally (i.t.; intrathecally) or supraspinally (i.c.v.; intracerebroventricularly) to mice. Following i.c.v. administration, SCI-I and SCY-II produced potent, dose-related reciprocal hindlimb scratching about equipotently (ED50 = 0.05 and 0.08 nmol, respectively). However, following i.t. administration, only SCY-I elicited greater than 50% response (ED50 = 0.07 nmol). Reciprocal hindlimb scratching is a behavioral response that has not been associated previously with neurokinins. These results might provide the first functional in vivo correlate for the differential localization of neurokinin receptor types within the mammalian central nervous system.

Amino Acid Sequence↗

PubMed1985

Morphine concentration in brain and spinal cord after subarachnoid morphine injection in baboons.

Tritium-labeled morphine was injected into the lumbar (L4-5) subarachnoid space of three baboons. The animals were sacrificed 3, 6, and 24 hr thereafter. Morphine concentrations were measured at five predetermined positions within the spinal cord, medulla oblongata, and frontal lobes of the brain by scintillation-count assay. The results revealed that morphine ascends in the subarachnoid space and is absorbed into the spinal cord and medulla oblongata in a time-dependent fashion. Ventilation was most depressed and maximal concentrations of morphine were detected in the medulla six hours after injection. Delayed respiratory depression, occasionally reported after intraspinal morphine injection, may therefore be caused as a result of the affinity of morphine for binding sites, possibly opiate receptors, situated within the vital respiratory and cardiovascular neuronal complexes of the medulla.

Animals↗

PubMed1990

Direct injection of cytokines into the spinal cord causes autoimmune encephalomyelitis-like inflammation.

A single micro-injection of Tumour Necrosis Factor alpha (TNF) or gamma Interferon (IFN-gamma) into the lumbosacral spinal cord of the rat produced meningitis and mononuclear cuffs within the cord, an inflammatory response remarkably similar in pattern to that observed during experimental autoimmune encephalomyelitis (EAE), a research analog of multiple sclerosis. Rats injected with saline or heat-inactivated cytokine exhibited no such inflammatory response. In other experiments, the accumulation of radiolabeled spleen cells into spinal cord was measured after the injection of various doses of TNF and IFN-gamma, results indicated that both cytokines elicited accumulation of spleen cells in an additive but not synergistic manner. Potentially, the direct injection model offers a new and simplified way of examining mechanisms of early inflammation in the central nervous system, without the need for immunisation with neuroantigen or passive transfer of sensitised cells.

Animals↗

PubMed1986

Changes in micturition volume thresholds in conscious dogs following spinal opiate administration.

Micturition difficulties appear as an often-reported side effect of the clinical use of opiates for spinal analgesia. Only a few experimental studies have focused specifically on this problem, especially in an unanesthetized animal model where chronic pharmacological studies can be carried out. The changes in micturition volume thresholds that occurred following spinal intrathecal injections of 1 mg of morphine sulphate were measured in 11 conscious dogs and compared with threshold changes produced in these same dogs by i.v. injections of various doses of morphine sulphate and by intrathecal and i.v. injections of naloxone HCl. In all cases, intrathecal or systemic morphine at doses of 1.0 mg or greater significantly (P less than 0.05) increased the bladder volume at which micturition took place. Naloxone, injected intrathecally to reverse the effects of intrathecal morphine, significantly reduced the micturition volume threshold, in most cases to below control volumes. A 400 microgram dose of naloxone, injected intrathecally without prior injection of morphine, significantly lowered the volume threshold in 9 dogs, even though two of these dogs had elevated thresholds following naloxone injection. The reduction in volume thresholds by i.v. naloxone not preceded by morphine injection was not statistically significant over that of control. These results are interpreted in light of recent findings concerning localization of endogenous opiate receptors within the micturition reflex pathway.

Anesthesia, Spinal↗

PubMed1993

Systemic or intracerebroventricular injection of NMDA receptor antagonists attenuates the antinociceptive activity of intrathecally administered NMDA receptor antagonists.

We have previously reported that the response latency in the mouse hot-plate test is affected differently by spinal intrathecal (i.t.) injection of competitive and non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists, in that only the former produces an antinociceptive effect. Since the lipophilic non-competitive antagonists will redistribute rapidly from the spinal injection site, it is conceivable that they reach sites where they counteract the spinal antinociceptive effect. In the present study, we have tested this hypothesis by comparing the antinociceptive effect of the competitive NMDA receptor antagonist CGS 19755 and the non-competitive NMDA receptor antagonist MK-801 after i.t., intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration as well as after combinations thereof. CGS 19755 injected i.p. or i.c.v. and MK-801 injected i.p. or i.t. attenuated the antinociceptive effect of i.t. injected CGS 19755. Both i.p. and i.c.v. administration of either CGS 19755 or MK-801 dose-dependently impaired motor function without producing antinociceptive effects. Thus, the effect of CGS 19755 and MK-801 on the motor system was found to be separate from their antinociceptive effect. In a separate experiment, changes in hind-paw skin temperature were excluded as a possible confounding factor. These findings demonstrate that supraspinal systems can limit the spinal antinociceptive effect of NMDA receptor antagonists.

Animals↗

PubMed1983

Antinociceptive actions of morphine and buprenorphine given intrathecally in the conscious rat.

1 The antinociceptive effects of morphine and buprenorphine given intrathecally and subcutaneously have been compared in the conscious rat. 2 In the paw pressure test, when given subcutaneously buprenorphine 0.001-0.1 mg/kg s.c., was approximately 100 times more potent than morphine 0.1-3 mg/kg s.c., but in the hot plate test, buprenorphine 0.03-3.0 mg/kg s.c., produced a bell-shaped dose-response curve of low maximum effect and was about equipotent with morphine 0.03-3 mg/kg s.c. 3 When given intrathecally buprenorphine 10 micrograms and morphine, 10-60 micrograms, were approximately equipotent in both paw pressure and hot plate tests. Furthermore, morphine produced these effects at 1/25th of the minimum effective parenteral dose while the dose of buprenorphine exceeded the parenteral dose. 4 It is concluded that the predominant site of the analgesic action of buprenorphine is supraspinal. The significance of these findings in relation to the role of spinal opiate receptors is discussed.

Analgesics↗

PubMed2003

Gene expression and functional characterization of melatonin receptors in the spinal cord of the rat: implications for pain modulation.

Recently, a species-dependent distribution of melatonin binding sites have been found in lamina I-V and lamina X of the spinal cord. In order to learn more about the function of spinal melatonin receptors, we investigated (i) the gene expression for melatonin receptor subtypes in lumbar and thoracal spinal cord tissue by means of the reverse-transcriptase polymerase chain reaction (RT-PCR) technique, and (ii) the electrophysiological and pharmacological properties of melatonin receptors heterologously expressed in Xenopus oocytes after injection of spinal cord mRNA by means of the voltage clamp technique. Because ample evidence indicates an antinociceptive effect of melatonin, (iii) the role of spinal melatonin receptors for maintaining mechanical and thermal hyperalgesia was studied in a rat model for postoperative pain. The RT-PCR data revealed that transcripts for MT1 and MT2 melatonin receptors are present in the dorsal and ventral horn of lumbar and thoracal spinal cord tissue. Injection of mRNA from lumbar spinal cord tissue into Xenopus oocytes led to the functional reconstitution of melatonin receptors which activate calcium-dependent chloride inward currents. Melatonin responses were abolished by simultaneous administration of the antagonists, 2-phenylmelatonin and luzindole and were unaffected by the MT2 antagonist 4-phenyl-2-propionamidotetralin. Intrathecal administration of different melatonin doses (10-100 nmol) did not inhibit mechanical or thermal hyperalgesia. However, intrathecal application of a low dose of morphine together with melatonin caused a brief antinociceptive effect suggesting an enhanced morphine analgesia by melatonin. In conclusion, the present study demonstrated for the first time the presence of transcripts of MT1 and MT2 receptors located in the dorsal and ventral horn of the spinal cord. Furthermore, spinal melatonin enhanced the antinociceptive effect of morphine indicating that melatonin acts as a neuromodulator in the spinal cord.

Animals↗

PubMed1995

Intracavernous injection of prostaglandin E1 in spinal cord injured patients with erectile dysfunction. A preliminary report.

Our experience with intracavernous injection of prostaglandin E1 in spinal cord injured patients with neurogenic erectile dysfunction included 15 men. They received testing dosage starting from 5 micrograms with increasing dosage (maximum 20 micrograms) to achieve a rigid erection of Schramek's grade 5 and lasting for at least 20 min. All of them had achieved functional erection adequate for coitus after treatment except one patient who had been proved to have venogenic impotence. We found that intracavernous injection of prostaglandin E1 had significantly improved the erectile condition. No systemic side effect or any other complication was noted except that pain at the injection site was complained of in two patients with incomplete lesion.

Adult↗

PubMed1996

Spinal anaesthesia with 0.5% hyperbaric bupivacaine in elderly patients: effect of site of injection on spread of analgesia.

In this randomized, observer-blind study, we have examined, in elderly patients, the effect of site of injection on analgesia levels after spinal injection of 0.5% hyperbaric bupivacaine solution. Thirty male patients, aged 68-87 yr, undergoing minor urological surgery during spinal anaesthesia received 3 ml of a 0.5% hyperbaric bupivacaine solution at either the L3-4 (n = 15) or L4-5 (n = 15) interspace. The solution was injected with the patient in the sitting position. The patient remained sitting for 2 min and was then placed in the supine horizontal position. Analgesia levels were assessed bilaterally using pin-prick. The highest analgesia levels did not differ between groups (medians were approximately T7). There were no significant differences in the time to maximum cephalad spread of analgesia, maximum degree of motor block or haemodynamic changes. We conclude that injection at the L4-5 interspace has no advantage compared with injection at the L3-4 interspace.

Aged↗

PubMed1994

Is ST segment depression of the electrocardiogram during cesarean section merely due to cardiac sympathetic block?

ST segment depression frequently is observed in women undergoing cesarean section with regional anesthesia, yet myocardial ischemia as a cause of such depression seems unlikely in this healthy population. To test whether ST segment depression in this setting is due to decreased sympathetic outflow to the heart, we monitored electrocardiograph (ECG) leads II and V5 in 15 healthy women undergoing cesarean section with spinal anesthesia. We estimated cardiac sympathetic tone by spectral analysis of heart rate variability, measuring the area under the power frequency curve of the fast Fourier transform of heart beat intervals. The area under this curve in the low frequency range (0.02-0.15 Hz) has been described recently and validated in humans and animals as a semiquantitative measure of cardiac sympathetic tone. Significant, > 1 mm horizontal or downsloping depression of the ST segment occurred in five women (33%), beginning 5-30 min after spinal bupivacaine injection. Those with ST segment depression had increased heart rate (117 +/- 7 beats/min) compared to those without (94 +/- 6 beats/min; P < 0.05), and had received more ephedrine (25 +/- 3 mg vs 7 +/- 3 mg; P < 0.05). Before spinal bupivacaine injection and after block resolution the area in the low frequency range of the heart rate power spectrum was similar in all women. During spinal anesthesia, those with ST segment depression had less power in this low frequency range (0.0018 +/- 0.0010 ms2/Hz) than those without ST depression (0.0028 +/- 0.0006 ms2/Hz).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1997

The effect of epidural saline injection on analgesic level during combined spinal and epidural anesthesia assessed clinically and myelographically.

UNLABELLED: An epidural injection of physiological saline solution after spinal anesthesia may produce a higher level of analgesia than spinal anesthesia alone because of a volume effect. The purpose of this study was to clarify the volume effect caused by epidural injection of saline after spinal anesthesia. Twenty patients undergoing combined spinal and epidural anesthesia for elective surgery whose analgesic levels did not reach the surgical regions 10 min after spinal anesthesia at the L4-5 interspace were randomly assigned to two groups. The control group (n = 10) received no epidural saline injection. The saline group (n = 10) received 10 mL of saline through an epidural catheter at the L2-3 or L3-4 interspace 10 min after spinal anesthesia. In the saline group, the levels of analgesia 15 and 20 min after spinal anesthesia were significantly higher than those in the control group (P < 0.05). Next, we examined the volume effect of epidural injection of saline with myelography using two adult volunteers. In both volunteers, the upper level of the contrast medium, which was injected in the lumbar subarachnoid space, began to increase concurrently with lumbar epidural injection of saline, reaching from L3 to L1 and from L2 to T12. The diameter of the subarachnoid space diminished to less than 25% after injection of saline. We conclude that lumbar epidural injection of saline increases the analgesic level 10 min after spinal anesthesia, probably because of a volume effect. IMPLICATIONS: In this study, using surgical patients and volunteers, we determined that a lumbar epidural injection of physiological saline solution 10 min after spinal anesthesia produces a higher analgesic level than spinal anesthesia alone because of a volume effect.

Adult↗

PubMed1994

Spinal cord uptake of lead injected into muscle.

It has been hypothesised that some motor neuron diseases may result from lead (Pb) being retrogradely transported in axons from muscle to spinal cord. To test this hypothesis, we injected mice in the right hindlimb with 0.1 ml of 0.25% or 2.5% Pb. In some animals the sciatic nerve was cut before injection. Pb levels were measured in the lumbar and thoracic spinal cord and the kidney with atomic absorption spectrophotometry (AAS). Four weeks after injection, Pb was found in the spinal cord on AAS, with higher levels in the lumbar than the thoracic cord only in the high-Pb group. Sciatic nerve cut did not inhibit the passage of Pb to the cord. The results suggest that most Pb injected into muscle reaches the spinal cord via the blood or damaged axons, rather than via intact axons. These data do not support the hypothesis of Pb-induced motor neuron disease via retrograde axonal transport from muscle.

Animals↗

PubMed2003

Enhanced thermal antinociceptive potency and anti-allodynic effects of morphine following spinal administration of endotoxin.

Recently, an animal model of central inflammation characterized by widespread cutaneous hyperalgesia and allodynia following intracerebroventricular (i.c.v.) administration of lipopolysaccharide (LPS) was described. In the present study, we demonstrate that central administration of LPS via intrathecal (i.t.) injection produces bilateral tactile allodynia and thermal hyperalgesia in the rat. Also, the effects of morphine-induced antinociception were determined in this model. Here we demonstrate enhanced thermal antinociceptive potency of i.t. morphine in LPS-treated rats compared to controls. Intrathecal morphine was also effective in alleviating the tactile allodynia induced by LPS. Both the antinociceptive and anti-allodynic effects produced by i.t. morphine were completely antagonized by pretreatment with subcutaneous naloxone (1 mg x kg(-1)). This study demonstrates the presence of both heat hyperalgesia and mechanical allodynia following central administration of LPS, and an increased antinociceptive potency of i.t. morphine in this model.

Analgesics, Opioid↗

PubMed1984

Target neurons for [3H]corticosterone in the rat spinal cord.

Rats were injected with [3H]corticosterone and their spinal cords processed for autoradiography. Nuclear concentration of the tritiated steroid was observed in motor neurons in cervical, thoracic, lumbar, and sacral regions. Nuclear concentrations of [3H]corticosterone was also observed in certain neurons of laminae VII and III in all levels of the spinal cord. Injection of unlabeled corticosterone 5 min before the [3H]corticosterone injection abolished the nuclear concentration of the adrenal steroid. These results provide the morphological basis for a direct genomic action of corticosterone in spinal motor neurons and in neurons of laminae III and VII.

Adrenalectomy↗

PubMed1993

Inhibition of naloxone-precipitated withdrawal jumping by i.c.v. and i.t. administration of saline in morphine-dependent mice.

In morphine-dependent mice, s.c. and i.t. administered naloxone produced withdrawal jumping (ED50 values were i.t. = s.c.) but i.c.v. administered naloxone failed to produce dose-dependent jumping. Peak times of jumping were earliest after i.t. administration of naloxone among the three administration routes. These results suggested that the spinal site was more sensitive to naloxone than the supraspinal site. Concomitant administration of naloxone i.c.v. and i.t. did not precipitate jumping. It was found that i.c.v. and i.t. injections of saline inhibited withdrawal jumping precipitated by s.c. administered naloxone and that the i.c.v. effect was more profound than the i.t. effect. I.c.v. injection of saline also delayed the peak time of withdrawal jumping precipitated by s.c. administered naloxone. These inhibitory effects of the injection procedures may explain the difficulty of i.c.v. administered naloxone and concomitant i.c.v. + i.t. administered naloxone to precipitate jumping, and may explain the difference in the ED50 values of naloxone and the time courses of jumping.

Animals↗

PubMed1989

Kainic acid induces early and delayed degenerative neuronal changes in rat spinal cord.

Intrathecal injections of kainic acid and sodium chloride were performed in rats to study the cellular modifications observed in spinal cord. Early neuronal changes (2 and 24 h) associated dark and shrunken or swollen and vacuolated cytoplasms. Delayed (3, 6, 14 days) changes, mainly consisted in degenerative aspect of motoneurons with eccentric and indented nucleus, swollen cytoplasms with proximal neurite enlargements, the presence of 'lipofuscin-like' pigments, disorganized intracytoplasmic organelles and filament accumulations.

Animals↗

PubMedDate not supplied

Pharmacological interaction between neuropeptides and morphine or pentazocine in rat spinal cord.

Male Wistar rats were treated with morphine or pentazocine subcutaneously (sc) and then intrathecally (it) by methionine- or leucine-enkephalin, neurotensin, substance P or cholecystokinin octapeptide 26-33. Then antinociceptive effect was measured during 1 h using tail-immersion test. Leucine-enkephalin potentiated and methionine-enkephalin antagonized morphine or pentazocine analgesia. Neurotensin, substance P and cholecystokinin acted biphasically on morphine induced antinociception. After short elevation, the diminution of antinociceptive effect was seen. Neurotensin diminished but substance P and cholecystokinin elevated analgesic effect elicited by pentazocine. Experimental model employed by us may be useful for preliminary screening of pharmacological interactions between neuropeptides and opioid analgesics on the spinal level. Our data confirm the results of other authors that individual enkephalins have different pharmacological features.

Animals↗