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PubMed1996

Spinal cord blood flow after intrathecal injection of ropivacaine: a screening for neurotoxic effects.

The study of spinal cord blood flow (SCBF) after spinal drug application is an important aspect of preclinical neurotoxicological screening. This investigation was designed to study how a new local anesthetic, ropivacaine, affects SCBF after intrathecal (IT) administration in the rat. SCBF was measured continuously in spontaneously breathing, enflurane/N2O-anesthetized rats, using the laser-Doppler flowmetry technique. The spinal cord was exposed by laminectomy, and a laser-Doppler probe was placed over the dorsal horn, allowing on-line registration of spinal blood flow in a tissue hemisphere of 1-2 mm. Relative changes in spinal blood flow over time were then measured after IT administration of either 0.9% saline, 5 mg/mL ropivacaine, i.e., a concentration within the pharmacological range, or a high, provocative concentration of 20 mg/mL ropivacaine. A minor and transient decrease in SCBF was seen after administration of 5 mg/mL ropivacaine (50 micrograms given IT), but this decrease was not significantly different from that in the saline group. SCBF decreased significantly to approximately 45% of the predrug value after the high concentration of 20 mg/mL ropivacaine (200 micrograms given IT), and this reduction was reversible within a period of 20 - 40 min after the injection. Whereas a high concentration of ropivacaine caused a definite reduction in spinal cord blood flow when administered IT to anesthetized rats, clinically relevant concentrations induced only minor changes. These results suggest that ropivacaine may be used to induce spinal anesthesia without causing clinically relevant effects on SCBF.

Amides↗
PubMed1988

Mini-dose intrathecal morphine for the relief of post-cesarean section pain: safety, efficacy, and ventilatory responses to carbon dioxide.

To determine the safety, efficacy, and the ventilatory responses to carbon dioxide (CO2) of mini-dose intrathecal morphine, 33 healthy women who underwent cesarean section with spinal anesthesia using 0.75% bupivacaine in 8.25% dextrose were studied. Patients were randomly assigned to receive, in a double-blind fashion, either morphine 0.25 mg (group I, n = 11), morphine 0.1 mg (group II, n = 10), or saline (group III, placebo group, n = 12) in 0.5 ml volume mixed with the bupivacaine. In both groups I and II excellent postoperative analgesia with long duration was obtained (27.7 +/- 4.0 and 18.6 +/- 0.9 hours, respectively, X +/- SEM). All patients in group III required an analgesic (8 mg subcutaneous morphine) within 3 hours of spinal anesthesia. Seven patients in group I and four patients in group II developed mild pruritus that did not require treatment. Ventilatory responses to CO2 showed no evidence of depression attributable to either the 0.25 or 0.1 mg of morphine, but significant depression of the CO2 responses was observed in group III patients after administration of subcutaneous morphine. It is concluded that a dose as low as 0.1 mg of intrathecal morphine gives excellent analgesia with minimal to no side effects and that subcutaneous morphine is associated with marked depression of the ventilatory variables.

Adult↗
PubMed1986

Effect of intrathecal and subepineural capsaicin on thermal sensitivity and autotomy in rats.

In 79 Sprague-Dawley rats, we determined the effect of either intrathecal or subepineural capsaicin injection on: latency of withdrawal of the hind foot to a nociceptive thermal stimulus (50 +/- 1 degree C hot plate) and the onset and severity of putative behavioral evidence of chronic pain in the rat (autotomy) which commonly appears following sciatic nerve section. Capsaicin (50 micrograms) was suspended in 5 microliters of vehicle (10% Tween-80 in 0.9% saline) then injected either intrathecally at the level of the L4-5 vertebral interspace or subepineurally in the sciatic nerve at the level of the midfemur. Subepineural capsaicin consistently and efficiently produced thermal analgesia in the rat, while intrathecal capsaicin had no significant analgesic effect. In chronically denervated rats, both subepineural and intrathecal capsaicin decreased the latency to onset of first autotomy, and intrathecal capsaicin increased the severity of this behavior significantly. These data are consistent with the hypothesis that autotomy is the rat's response to abnormal sensations perceived in the denervated hind limb. Deafferentation of dorsal horn neurons appears to be of paramount importance in the production of autotomy while the relevance of peripherally originating spontaneous neuroma discharges to autotomy behavior is questioned.

Afferent Pathways↗
PubMed2000

Sensory thresholds and the antinociceptive effects of GABA receptor agonists in mice lacking the beta3 subunit of the GABA(A) receptor.

A line of mice was recently created in which the gabrb3 gene, which encodes the beta3 subunit of the GABA(A) receptor, was inactivated by gene-targeting. The existence of mice with a significantly reduced population of GABA(A) receptors in the CNS enabled an investigation of the role of GABA and GABA(A) receptors in nociception. The present study examined the sensory thresholds of these mice, as well as the antinociceptive effects of subcutaneously or intrathecally administered GABA(A) and GABA(B) receptor agonists. Homozygous null (beta3-/-) mice displayed enhanced responsiveness to low-intensity thermal stimuli in the tail-flick and hot-plate test compared to C57BL/6J and 129/SvJ progenitor strain mice, and their wild-type (beta3+/+) and heterozygous (beta3+/-) littermates. The beta3-/- mice also exhibited enhanced responsiveness to innocuous tactile stimuli compared to C57BL/6J, 129/SvJ and to their beta3+/+ littermates as assessed by von Frey filaments. The presence of thermal hyperalgesia and tactile allodynia in beta3-/- mice is consistent with a loss of inhibition mediated by presynaptic and postsynaptic GABA(A) receptors in the spinal cord. As expected, subcutaneous administration of the GABA(A) receptor agonist 4,5,6,7-tetrahydroisoxazolo-(5,4-c)pyridin-3-ol did not produce antinociception in beta3-/- mice, whereas it produced a dose-dependent increase in hot-plate latency in C57BL/6J, 129/SvJ, beta3+/+ and beta3+/- mice. However, the antinociceptive effect of the GABA(B) receptor agonist baclofen in the tail-flick and hot-plate tests was also reduced in beta3-/- mice compared to the progenitor strains, beta3+/+ or beta3+/- mice after either subcutaneous or intrathecal administration. This finding was unexpected and suggests that a reduction in GABA(A) receptors can affect the production of antinociception by other analgesic drugs as well.

Animals↗
PubMed1991

Spinal antinociception by dexmedetomidine, a highly selective alpha 2-adrenergic agonist.

The antinociceptive effects of dexmedetomidine, a highly selective new alpha 2-adrenoceptor agonist, were evaluated in rats after intrathecal, intraperitoneal and subcutaneous administration. Antinociception was tested using the tail-flick method. Both 3 and 6 micrograms of intrathecal dexmedetomidine produced maximal antinociception within 10 min. The effect lasted for up to 6 hr. The smaller dose of 1.5 micrograms produced a mean antinociception of 50% (of the maximum possible effect, MPE%) which lasted for about 2 hr. Subcutaneous atipamezole, a specific alpha 2-adrenergic antagonist completely abolished the antinociception produced by intrathecal dexmedetomidine. When given intraperitoneally, dexmedetomidine produced on average a 50% antinociceptive effect with the highest dose of 60 micrograms/kg. The lower doses of 10 and 30 micrograms/kg were ineffective. After subcutaneous administration a maximal effect was achieved with 120 micrograms/kg, a 70% effect, on average, with 60 micrograms/kg and a short lasting effect of 60% with 30 micrograms/kg. In conclusion, dexmedetomidine is a very potent antinociceptive agent when given intrathecally to rats.

Adrenergic alpha-Agonists↗
PubMed2005

Protein kinases mediate increment of the phosphorylation of cyclic AMP-responsive element binding protein in spinal cord of rats following capsaicin injection.

BACKGROUND: Strong noxious stimuli cause plastic changes in spinal nociceptive neurons. Intracellular signal transduction pathways from cellular membrane to nucleus, which may further regulate gene expression by critical transcription factors, convey peripheral stimulation. Cyclic AMP-responsive element binding protein (CREB) is a well-characterized stimulus-induced transcription factor whose activation requires phosphorylation of the Serine-133 residue. Phospho-CREB can further induce gene transcription and strengthen synaptic transmission by the activation of the protein kinase cascades. However, little is known about the mechanisms by which CREB phosphorylation is regulated by protein kinases during nociception. This study was designed to use Western blot analysis to investigate the role of mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase (MEK 1/2), PKA and PKC in regulating the phosphorylation of CREB in the spinal cord of rats following intraplantar capsaicin injection. RESULTS: We found that capsaicin injection significantly increased the phosphorylation level of CREB in the ipsilateral side of the spinal cord. Pharmacological manipulation of MEK 1/2, PKA and PKC with their inhibitors (U0126, H89 and NPC 15473, respectively) significantly blocked this increment of CREB phosphorylation. However, the expression of CREB itself showed no change in any group. CONCLUSION: These findings suggest that the activation of intracellular MAP kinase, PKA and PKC cascades may contribute to the regulation of phospho-CREB in central nociceptive neurons following peripheral painful stimuli.

Animals↗
PubMed2005

Transcriptional and translational regulation of glial activation by morphine in a rodent model of neuropathic pain.

Glial cells function in maintenance of homeostasis as well as in pathophysiology. In this study, we determined the time course of spinal glial cell activation during the development of morphine analgesic tolerance in an L5 spinal nerve transection rodent model of neuropathic pain. We also sought to assess whether the method of morphine administration affected neuroimmune activation at the levels of transcription and translation. Rats received L5 spinal nerve transection or no surgery on day 0. On day 6 post-transection, osmotic minipumps were implanted to deliver saline or morphine s.c. (1 or 10 mg/kg) or i.t. (5 or 20 nmol/h). Mechanical allodynia developed immediately after spinal nerve transection; this hypersensitivity was reversed with both low- and high-dose morphine by either route. Tolerance to antiallodynia developed after 3 days of i.t. morphine and after 6 days of s.c. morphine, indicating hastened tolerance following i.t. delivery. Analysis of mRNA revealed that s.c. morphine treatment did not lead to increases in glial activation markers. In contrast, i.t. morphine caused a biphasic alteration in glial fibrillary acidic protein (GFAP) and integrin alpha M mRNA. Protein levels for GFAP were elevated after s.c. and i.t. administration of morphine; however, induction was further enhanced in the latter group. Here, we show for the first time that there is differential recruitment of transcriptional and translational mechanisms of glial activation by systemic and i.t. morphine. Furthermore, we suggest that enhanced neuroimmune activation after i.t. dosing contributes to the hastened development of analgesic tolerance seen in these animals.

Animals↗
PubMed2005

The influence of lumbosacral cerebrospinal fluid volume on extent and duration of hyperbaric bupivacaine spinal anesthesia: a comparison between seated and lateral decubitus injection positions.

UNLABELLED: We designed the present study to examine the influence of lumbosacral cerebrospinal fluid (CSF) volume on the spread and duration of hyperbaric bupivacaine spinal anesthesia when the injection is made with the patient in the lateral position compared with that when the patient is in a seated position. Seventy-four patients undergoing peripheral orthopedic or urogenital surgery with spinal block were enrolled. Lumbosacral CSF volumes were calculated from axial magnetic resonance images. Patients were randomly assigned to 1 of 2 groups: the lateral (L) and seated (S) groups (n = 37 each). Spinal anesthesia (3 mL hyperbaric 0.5% bupivacaine) was administered using a 25-gauge pencil-type needle with the needle aperture directed cephalad and the patient in the lateral decubitus position with the non-operated side up (L group) or with the patient in a seated position (S group). Patients were turned supine immediately after spinal injection (L group) or after remaining seated for 2 min (S group). Statistical correlation coefficients (rho) were assessed using Spearman's rank correlation. There were negative correlations between CSF volume and peak sensory block level in both the L (rho = -0.69, P < 0.0001) and S groups (rho = -0.68, P < 0.0001). In the S group, but not in the L group, CSF volume significantly correlated with onset time of peak sensory block level (rho = -0.48, P = 0.004), and time required for regression to L1-4 (P < 0.05-0.01). We conclude that CSF volume influences the spread of spinal anesthesia with hyperbaric bupivacaine regardless of patient position when the spinal injection is made. CSF volume influenced the duration of spinal sensory anesthesia when the injection was made with the patient in a seated position, but not in the lateral position. IMPLICATIONS: Patient position during the spinal injection does not alter the influence of cerebrospinal fluid (CSF) volume on the spread of hyperbaric bupivacaine spinal anesthesia. However, CSF volume influences the duration of spinal sensory anesthesia when the injection is made with the patient in a seated position, but not in the lateral position.

Adult↗
PubMed1996

Neural and endocrine circuits mediating inhibition of bradykinin-induced plasma extravasation by subcutaneous and spinal-intrathecal nicotine.

In this study we evaluated the mechanisms underlying s.c. and spinal intrathecal (i.t.) nicotine inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat (J. Pharmacol. Exp. Ther. 262: 889-895, 1992; ibid., 264: 839-844, 1993). The dose-response curve for the inhibitory action of s.c. nicotine on bradykinin-induced plasma extravasation was attenuated by adrenal medullectomy and by intra-articular perfusion of ICI-118,551 (a beta-2 adrenoceptor antagonist). In addition, the dose-response curve of s.c. nicotine was attenuated by acute surgical lumbar sympathectomy and by intra-articular phentolamine (an alpha adrenoceptor antagonist). The dose-response curve for i.t. nicotine (up to 1 mg/kg) was not attenuated by intra-articular ICI-118,551 and was potentiated by adrenal medullectomy. The action of i.t. nicotine was also not affected by intra-articular phentolamine or by acute surgical lumbar sympathectomy. These results suggest that the inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat by s.c., but not i.t., nicotine is mediated through the sympathoadrenal and sympathetic systems.

Animals↗
PubMed2001

Antinociceptive action of amlodipine blocking N-type Ca2+ channels at the primary afferent neurons in mice.

We investigated the antinociceptive action of amlodipine, a dihydropyridine derivative, which acts on both L- and N-type voltage-dependent Ca2+ channels (VDCCs), in mice. Intrathecal injection of amlodipine (300 nmol/kg) significantly shortened the licking time in the late phase of a formalin test, while no effect was found with another dihydropyridine derivative, nicardipine (300 nmol/kg). Cilnidipine and omega-conotoxin GVIA also showed marked analgesic effects under the same experimental conditions. Transcripts of alpha1A, alpha1B, alpha1E, alpha1F, alpha1H, beta3, and beta4 subunits were detected by polymerase-chain reaction (PCR) in the dorsal root ganglion, suggesting the existence of a variety of voltage-dependent Ca2+ channels. Electrophysiological experiments showed that amlodipine and cilnidipine inhibit N-type currents in the dorsal root ganglion cells. These results suggest that amlodipine, cilnidipine, and omega-conotoxin GVIA exert their antinociceptive actions by blocking N-type Ca2+ channels in the primary nociceptive afferent fibers. Blocking of the Ca2+ channels results in attenuation of synaptic transmission of nociceptive neurons. Furthermore, it is suggested that some N-type Ca2+ channel blockers might have therapeutic potential as analgesics when applied directly into the subarachnoidal space.

Amlodipine↗
PubMed1991

XAMI and DCDM, agonists at cAMP-associated octopamine receptors in cockroach nerve cord, produce centrally mediated antinociception in mice.

The ability of XAMI (2,3-xylylaminomethyl-2'-imidazoline), the most potent agonist of cAMP-associated octopamine-sensitive adenylate cyclase in cockroach (Periplaneta americana) nerve cord yet reported, and DCDM (N-demethylchlordimeform), a partial octopamine agonist in this preparation, to produce centrally mediated antinociception in mice was evaluated. The antinociception produced by these compounds was compared to that previously reported for p-octopamine, a phenylethylamine and endogenous mammalian hydroxyphenolic analog of norepinephrine. Consonant with the reported greater agonistic activity of XAMI on octopamine-sensitive adenylate cyclase, XAMI was more potent than p-octopamine by spinal or supraspinal administration in the abdominal constriction test (E50 = 0.013 micrograms i.t., 1.45 micrograms i.c.v.) and in the 48 degrees C hot-plate test (ED50 = 0.06 micrograms i.t., 0.4 micrograms i.c.v.), but was inactive in the tail-flick test (up to 4.0 micrograms i.c.v. or i.t.). Unlike p-octopamine, both XAMI and DCDM were active by peripheral routes of administration. DCDM was orally active in the mouse acetylcholine-induced abdominal constriction test (ED50 = 9.98 mg/kg p.o.) and was active via the s.c. route in this test (ED50 = 2.36 mg/kg), the 48 degrees C hot-plate test (ED50 = 5.40 mg/kg) and the tail-flick test (ED50 between 15 and 30 mg/kg). It appeared to be a full agonist against these endpoints. XAMI produced dose-related antinociception in the abdominal constriction test (ED50 = 0.10 mg/kg s.c.) and in the 48 degrees C hot-plate test (ED50 = 3.71 mg/kg p.o. and 0.46 mg/kg s.c.), where the antinociceptive response persisted for at least 60 min following subcutaneous or oral administration. Both compounds were less potent via peripheral routes than clonidine (as reference) in these tests. Mechanistically, XAMI-induced antinociception was antagonized by yohimbine and idazoxan, but not the opiate antagonist naloxone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclase Inhibitors↗
PubMed1991

Intravenous contrast in spinal computed tomography to identify epidural metastases.

In 16 patients with spinal epidural metastases from various neoplasms the usefulness of intravenous (IV) contrast injection in spinal computed tomography (CT) scanning was analyzed for determining the presence and extent of the epidural lesion. In all cases enhancement of the epidural tumor mass occurred, which effectively showed the outline of the lesion. The extent of the epidural metastases in the spinal canal was equally well visualized as by myelography. Compared to spinal CT scanning without contrast administration, all IV contrast enhanced CT scans were clearly superior in demonstrating epidural metastases. Intravenous contrast in spinal CT-scanning appears to add relevant information and seems a useful and simple method to define the extent of the epidural tumor. It should be considered in patients where myelography is contraindicated and it may be a valuable method when the response of the epidural tumor to treatment must be determined.

Contrast Media↗
PubMed2003

Activation of kappa-opioid receptors inhibits pruritus evoked by subcutaneous or intrathecal administration of morphine in monkeys.

Pruritus (itch sensation) is the most common side effect associated with spinal administration of morphine given to humans for analgesia. A variety of agents have been proposed as antipruritics with poorly understood mechanisms and they are effective with variable success. kappa-Opioid agonists possess several actions that are opposite to micro -opioid agonists. We proposed to investigate the role of kappa-opioid receptors (KORs) in morphine-induced scratching and antinociception in monkeys. Scratching responses were counted by observers blinded to treatment. Antinociception was measured by a warm water (50 degrees C) tail-withdrawal assay. Pretreatment with low doses of trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl)-benzeneacetamide (U-50488H) (0.032-0.18 mg/kg s.c.), a selective KOR agonist, dose dependently suppressed the s.c. morphine dose-effect curve for scratching and potentiated s.c. morphine-induced antinociception. In addition, s.c. U-50488H attenuated i.t. morphine (10 and 32 micro g)-induced scratching while maintaining or enhancing i.t. morphine-induced antinociception. The combination of s.c. or i.t. morphine with low doses of U-50488H did not cause sedation. More importantly, pretreatment with 3.2 mg/kg nor-binaltorphimine, a selective KOR antagonist, blocked the effects of s.c. U-50488H on both s.c. and i.t. morphine-induced scratching. These results indicate that activation of KOR attenuates morphine-induced scratching without interfering with antinociception in monkeys. This mechanism-based finding provides functional evidence in support of the clinical potential of KOR agonists as antipruritics in the presence of MOR agonist-induced pruritus.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

Cardiac effects of injections of epinephrine into the spinal intermediolateral column.

Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.

Animals↗
PubMed1997

Direction of injection does not affect the spread of spinal bupivacaine in parturients.

PURPOSE: One of the factors that can affect the distribution of local anaesthetic solutions in the subarachnoid space is the direction of the spinal needle through which injections are made. This study investigated the effect of the direction of the aperture of the Whitacre needle on the spread of hyperbaric bupivacaine in parturients undergoing elective caesarean section. METHODS: Forty healthy term parturients scheduled for caesarean delivery under spinal anaesthesia with 12 mg hyperbaric bupivacaine + 0.2 mg morphine were randomly assigned to one of two groups: needle orifice cephalad (I) or caudad (II). Spinal blocks were administered in the sitting position with patients being positioned supine immediately after. A blinded observer assessed the dermatome level of analgesia to ice every minute for the first 10 minutes, every three minutes for the following 35 min, then every 15 min until the sensory level regressed to T10. RESULTS: There was no difference between the groups regarding the maximal number of segments blocked cephalad to T11 (11.4 +/- 3.4: group I and 12.0 +/- 3.4: group II), time to highest cephalad spread of sensory block (22 +/- 10: group I and 19 +/- 10 min: group II), or time to regression to T10 (164 +/- 26: group I and 153 +/- 24 min: group II). The maximum decrease in blood pressure (33.9 +/- 9.6: group I and 36.8 +/- 11.8 mmHg: group II) and dosage of ephedrine administered (14.7 +/- 10.7: group I and 16.2 +/- 11.0 mg: group II) did not differ. CONCLUSION: The direction of the aperture of the Whitacre needle does not influence the spread of hyperbaric bupivacaine in the term parturient.

Adult↗
PubMed2007

Prospective evaluation of contrast-enhanced MR imaging after uncomplicated lumbar discography.

OBJECTIVE: Postdiscography infection is an uncommon complication. Magnetic resonance (MR) imaging is often the modality of choice for evaluating spinal infection. Discography entails disc access and fluid injection that could alter the baseline MR imaging appearance of the spine and be confounded for infection. Our purpose was to describe the MR imaging findings of the lumbar spine subsequent to uncomplicated discography and to determine if this may mimic infection. DESIGN AND PATIENTS: In a prospective cohort study of eight adults (age 22-64 years, mean 45 years) with 22 intradiscal injections, all subjects underwent routine unenhanced and contrast-enhanced MR imaging during the 2-3 week interval postdiscography. A subset of four returned for additional MR imaging during the 4-8 week interval postdiscography. MR images were reviewed for intradiscal, endplate, marrow, and epidural findings and then compared with prediscography examinations. Infection was excluded by clinical documentation. RESULTS: Postdiscography MR imaging showed that almost all levels were similar to baseline prediscography examinations. No levels developed new vertebral marrow edema, fluid-like intradiscal signal, endplate irregularity, or epidural abnormality. Two subjects simulated potential discitis, but these findings were unchanged from prediscography and were related to prior surgery. CONCLUSIONS: Uncomplicated lumbar spine discography does not cause MR imaging changes that simulate discitis.

Adult↗
PubMed1984

Substance P, injected intrathecally, antagonizes the spinal antinociceptive effect of morphine, baclofen and noradrenaline.

The effect of substance P on the antinociceptive effect of morphine, baclofen and noradrenaline in the spinal cord was examined in the tail-flick and hot plate tests, after intrathecal administration. Substance P (5-20 micrograms) produced a dose-related antagonism of the effect of all three agents, which persisted for the entire time-course of the antinociceptive effect in each case. The rank order of potency of substance P and related peptides in antagonizing the antinociceptive effect of morphine, was substance P greater than physalaemin greater than eledoisin greater than eledoisin-related peptide. A similar order of potency was observed against noradrenaline, except that physalaemin appeared to be the most potent. The intrathecal administration of these peptides did not alter reaction latencies in the tail-flick test when baseline values were 2-3 sec, but produced a significant decrease in latency (hyperalgesia) when baseline values were 6-8 sec. There was a slight increase in reaction latency in the hot plate test. The specificity of the antagonism was examined by determining the effect of phentolamine on the antinociceptive effect of morphine and baclofen. Although phentolamine (30 micrograms) produced comparable hyperalgesia to substance P, it did not significantly alter the antinociceptive effect of morphine or baclofen. These results suggest that alterations in the function of substance P in the spinal cord may contribute to the spinal antinociceptive effects of morphine, baclofen and noradrenaline. The effects of substance P on nociception in the spinal cord appear to be mediated by substance P type receptors.

Afferent Pathways↗