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At least 505 records · Page 28Linked to original sources
PubMed1984

Supersensitivity of the noradrenergic system in the spinal cord following intracisternal injection of 6-hydroxydopamine.

The intracisternal administration of 6-hydroxydopamine (6-OHDA; 100 micrograms on two consecutive days) resulted in a 90-95% depletion of norepinephrine (NE) in the spinal cord 3-60 days following administration of the drug. At 90 days following injection of 6-OHDA, the depletion was only 60% suggesting the regrowth of NE-containing fibers. Consistent with the depletion of NE, 3-60 days after the injection of 6-OHDA a 50-80% decrease in the uptake NE occurred with only a 25% decrease 90 days after administration of 6-OHDA. Associated with decreases in NE and its uptake was a 100-200% increase in the accumulation of NE-stimulated cyclic AMP in slices of spinal cord tissue from 6-OHDA-treated rats. The increased response was evident at 3-60 days after injection of 6-OHDA decreasing on day 90 to 40% above control. No shift in the EC50 for NE was evident and the specificity of agonists for this response was limited to agents with alpha and/or beta-adrenergic receptor activation properties. Radioligand receptor binding techniques, utilizing [3H]prazosin for alpha1 receptors and [3H]dihydroalprenolol for beta receptors demonstrated that increases in the Bmax of response of alpha1 (30-50%) and beta (15-20%) receptors in spinal cord may mediate the enhanced response of NE-stimulated cyclic AMP following the administration of 6-OHDA. This is indicated by similar time-dependent patterns of onset and termination of increased receptor binding and the accumulation of NE-stimulated cyclic AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1992

Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse.

Intrathecal injection of N-methyl-D-aspartate (NMDA) induces a short duration hyperalgesia in mice. An inhibitor of nitric oxide synthase (NOS), N omega-nitro-L-arginine methyl ester (L-NAME), administered either systemically or intrathecally, blocked the NMDA-induced hyperalgesia. This effect was partially reversed by the NOS substrate, L-arginine. Intrathecal hemoglobin mimicked the effects of L-NAME. Intrathecal injection of the NO-donating compounds, sodium nitroprusside (SNP) and hydroxylamine, resulted in a hyperalgesia that lasted 3 h and was reduced by coadministration of hemoglobin. Thus, nitric oxide production appears to mediate NMDA-induced hypersensitivity and may contribute to other forms of centrally induced hyperalgesia.

Amino Acid Oxidoreductases↗
PubMed1992

Time course of the distribution of morphine in brain regions and spinal cord after intravenous injection to spontaneously hypertensive and normotensive Wistar-Kyoto rats.

Previous studies from this laboratory have demonstrated that the analgesic and hyperthermic effects of morphine were found to be greater in spontaneously hypertensive (SHR) rats than in normotensive Wistar-Kyoto (WKY) rats. The enhanced response to morphine could not be explained on the basis of any of the pharmacokinetic parameters of morphine in the serum. In order to determine the possible contribution of altered distribution of morphine in the central nervous system in the differences in the pharmacological response to morphine in the two strains, the time course of the distribution of morphine was determined in brain regions and spinal cord after its i.v. administration. SHR and WKY rats were injected with morphine (10 mg/kg). At various times (5, 30, 60, 120 and 360 min) after the injection of morphine, brain regions (hypothalamus, cortex, hippocampus, midbrain, pons and medulla, striatum and amygdala) and spinal cord were collected. The level of morphine in the tissues was determined by using a highly sensitive and specific radioimmunoassay method. Five minutes after morphine injection, the concentration of morphine was the highest in the spinal cord. Among the brain regions, the highest concentration of morphine was in the hypothalamus and the lowest in the amygdala. In all the brain regions and spinal cord, the concentration of morphine was significantly higher in the SHR than in the WKY rats. Similar effects were observed at 30, 60 and 120 min after morphine injection. At 360 min, the hypothalamus, cortex and spinal cord of the SHR rats had higher concentrations of morphine than the WKY rats, but the other regions did not show differences in the morphine levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed2004

Spinal flexibility increase after chymopapain injection is dose dependent: a possible alternative to anterior release in scoliosis.

STUDY DESIGN: Experimental animal study. OBJECTIVES: To investigate whether the increase in spinal flexibility after chymopapain injection is dose dependent and determine the "optimal" dosage of chymopapain to increase spinal flexibility in a rabbit model. SUMMARY OF BACKGROUND DATA: Spinal instability after chymopapain injection may result in severe back pain. However, this undesired mechanical effect in treating disc herniation may provide a safe minimally invasive approach for anterior spinal release in scoliosis correction. METHODS: A total of 138 lumbar intervertebral discs from 46 New Zealand white rabbits were randomly injected with chymopapain at 6.25, 12.5, 25, 50, 75, and 100 picokatals (pKats)/0.05 mL/disc. The rabbits were killed 1 week after the injection, and the lateral bending stiffness of the spinal segments without posterior elements was determined. RESULTS: The lateral bending spinal stiffness showed no significant change after injection of 6.25 and 12.5 pKats/0.05 mL/disc but reduced significantly following chymopapain injection of 25, 50, 75, and 100 pKats (all P < 0.05 by post hoc least significant difference tests). While the lateral bending stiffness was lowest at the 100-pKats dose, there were no significant differences between the four higher dosages. CONCLUSION: The reduction in the lateral bending spinal stiffness after chymopapain injection is dose dependent, and an optimal dosage for spinal release existed; doses greater than the optimal dosage did not result in further significant decrease in lateral bending spinal stiffness.

Animals↗
PubMed1992

Pharmacology of intrathecal VP-16-213 in dogs.

VP-16-213 is an anticancer drug that is active against a number of malignancies including small cell lung cancer, lymphoma, and leukemia which are often complicated by the development of leptomeningeal carcinomatosis. To investigate the potential usefulness of VP-16-213 for intrathecal administration, the pharmacology and toxicity of intrathecal VP-16-213 was determined. VP-16-213 at varying doses (0.01-1.0 mg.kg) was instilled intrathecally in dogs. Plasma, CSF, spinal cord, and brain tissue drug concentrations were determined by radiochemical and high performance liquid chromatography technique. Drug concentrations were strikingly higher in spinal cord tissue near the injection site compared to more distal cord sites. CSF concentration of VP-16-213 is 3-4 logs higher compared to concurrent plasma levels. Severe neurotoxicity occurred at the higher doses used. Due to limited diffusion and extremely low doses which could be used without life-threatening neurotoxicity, VP-16-213 does not appear to be a useful agent for intrathecal administration.

Animals↗
PubMed1994

Intrathecal gamma-aminobutyric acidB (GABAB) receptor antagonist CGP 35348 induces hypersensitivity to mechanical stimuli in the rat.

Intrathecal (i.t.) administration of the gamma-aminobutyric acidB (GABAB) receptor antagonist CGP 35348 in the rat resulted in a dose-dependent pain-like response (vocalization) to innocuous mechanical stimuli and touch/pressure). The effect was maximally evoked by stimulation applied to a dermatome corresponding to the spinal levels of the i.t. injections. The paw withdrawal threshold to pressure was also moderately decreased after i.t. CGP 35348. In contrast, i.t. CGP 35348 had no effect on the hot plate test. It is suggested that the input of low threshold afferents innervating mechanoceptors is tonically inhibited by the GABA system through B-type receptors, and blockade of this system results in mechanical hypersensitivity that is similar to mechanical allodynia (painful response to innocuous stimulation) observed in humans.

Animals↗
PubMed1997

Manipulations of zinc in the spinal cord, by intrathecal injection of zinc chloride, disodium-calcium-EDTA, or dipicolinic acid, alter nociceptive activity in mice.

Zinc is concentrated in the dorsal horn of the spinal cord and has been proposed to alter excitability of primary afferent C-fibers, structures believed to be important in nociceptive transmission. Based on the inhibitory effect of zinc on the activity of various other neurotransmitters that play a role in nociception, we tested the hypothesis that zinc modulates pain transmission. To test this, we examined the effect of exogenous zinc, administered intrathecally (i.t.), on nociception in the mouse. We also assessed the impact of decreased concentrations of endogenously occurring zinc in the extracellular fluid brought about by an i.t. injection of either ethylenediaminetetraacetic acid disodium-calcium salt (Ca++EDTA), a calcium-saturated, membrane-impermeable chelator of divalent cations, or of dipicolinic acid, a zinc chelator. Injection of zinc produced a dose-related antinociceptive effect, optimal at 90 min in the writhing assay, but had no effect on tail-flick response latencies. In contrast, injection of either Ca++EDTA or dipicolinic acid produced a dose-related hyperalgesia in the tail-flick assay at 90 min after injection. Responses induced in the writhing assay were unaffected by Ca++EDTA. Although zinc had no effect on thermal nociception, the hyperalgesic effect of Ca++EDTA was antagonized by coadministration of Ca++EDTA with zinc. Similarly, the antinociceptive effect of zinc on writhing responses was attenuated when coadministered with Ca++EDTA. Zinc also inhibited primary afferent C-fiber activity because 10 ng of zinc i.t. inhibited the behavioral response induced by injection i.t. of 1 nmol of capsaicin. Neither zinc nor Ca++EDTA altered writhing or tail-flick latencies, respectively, when injected intracerebroventricularly. These findings support the hypothesis that endogenous zinc, localized in the dorsal horn of the spinal cord, plays a role in the regulation of pain.

Analgesics↗
PubMed2001

Rate of injection through whitacre needles affects distribution of spinal anaesthesia.

A prospective, randomized, double-blind study was performed to investigate whether altering the rate of injection of local anaesthetic through a Whitacre needle had any effect on the spinal block achieved. Twenty patients scheduled for elective urological surgery under spinal anaesthesia received an injection of 3 ml of 0.5% plain bupivacaine either by hand (fast) over 10 s (18 ml min(-1)) or by infusion pump (slow) over 3 min (1 ml min(-1)). All patients were in the sitting position both during insertion of the spinal needle and for 3 min after the start of spinal injection, and they then changed to the supine position. The slow injection group achieved peak sensory block earlier, after a median interval of 20 (95% confidence interval 12.5-30) min vs 30 (22.5-45) min (P<0.05) for the fast group. The level of peak sensory block was similar: T3.5 (T2-T4.5) vs T4 (T1.5-T6.5). The time to lowest mean arterial pressure occurred earlier in the slow group, at 10 (8 to 18) vs 20 (15-31) min (P<0.05). Duration of the motor block was shorter in the slow group: 180 (152-242) vs 270 (225-300). We conclude that a slow spinal injection of plain bupivacaine results in a block of more rapid onset and recovery.

Aged↗
PubMed1989

Antinociceptive effect of intrathecal morphine in tolerant and nontolerant spinal rats.

The antinociceptive effect of intrathecal morphine on the tail-flick (TF) reflex of rats was significantly enhanced within one day after spinal transection (ED50 = 0.125 microgram) relative to the effect obtained in intact rats (ED50 = 5.9 micrograms). By 20-30 days after spinalization the potency of intrathecally administered morphine had substantially declined. Intact rats, made tolerant to the antinociceptive effect of systemic morphine (3.0 mg/kg, SC on each of seven consecutive days), were not tolerant to intrathecal morphine (ED50 = 6.5 micrograms). In contrast, rats that were pretreated with either morphine alone, repeated TF tests alone, or both of these treatments, were tolerant to intrathecal morphine when tested one day after spinal transection. The results suggest first, that the antinociceptive effect of intrathecal morphine in intact rats is tonically inhibited by descending supraspinal input and that removal of this input is responsible for the enhanced antinociceptive effect of intrathecal morphine in spinal rats. Second, the data suggest that tolerance to the antinociceptive effect of intrathecal morphine in intact rats may also be tonically inhibited by supraspinal input, because spinal opiate tolerance is expressed after spinal transection.

Anesthetics↗
PubMed1993

Nitric oxide synthase inhibitor blocks spinal sensitization induced by formalin injection into the rat paw.

This study evaluated the role of nitric oxide (NO) in spinal cord nociceptive transmission during peripheral inflammation evoked by formalin injection into the rat paw, using N omega-nitro-L-arginine (N-Arg), an NO synthase inhibitor. Male rats were prepared with intrathecal (IT) catheters. To quantify the formalin response, the instances of "flinching behavior" were counted at 5-min intervals for 60 min. IT N-Arg depressed the flinching behavior in a dose-dependent manner when N-Arg was administered 10 min before the formalin injection. This N-Arg effect was reversed with L-arginine but not D-arginine. We conclude that NO plays an important role in nociceptive transmission in the spinal cord during the formalin test.

Amino Acid Oxidoreductases↗
PubMed1998

[Effect of epidural pressure gradient on buprenorphine flux through the dural hole after combined spinal-epidural anesthesia--comparison between bolus injection and continuous infusion].

Combined spinal-epidural anesthesia is a useful technique. However, there has been no attempt to investigate the risk of epidural opioid, especially buprenorphine, flux through the dural hole. The purpose of this study was to compare the effect of epidural buprenorphine administered across the dura into subarachnoid space, between two different methods of administration; bolus injection (Group I) and continuous infusion (Group II). Sixty patients for transvaginal hysterectomy were divided into two groups. Group I received buprenorphine 0.1-0.2 mg with 0.25% bupivacaine, and Group II 0.4 mg with 0.25% bupivacaine 40 ml continuously (infusion rate was 1.7 ml.h-1). Pain relief was similar in both groups, but the total buprenorphine requirement was lower in Group I than in Group II. The incidence of nausea and vomiting was significantly higher in Group I than that in Group II, 73% and 16%, respectively. It indicates that the increase of nausea and vomiting is predominantly determined by a high rate of flux into subarachnoid space and only partly determined by blood concentrations. In contrast to continuous infusion, the drug movement through the dural hole may increase by bolus injection due to its higher pressure. We recommend careful injection of epidural buprenorphine such as by continuous infusion with low pressure after combined spinal-epidural anesthesia.

Adult↗