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PubMed1993

Antinociceptive effects of combining low doses of neuroleptic drugs and fentanyl in sheep.

Effects of low doses of the neuroleptic drugs droperidol and zuclopenthixol, combined with a subanalgesic dose of the opioid mu-agonist, fentanyl, on mechanical nociceptive thresholds were evaluated in sheep. Intravenously administered droperidol (5 micrograms/kg of body weight) did not induce any change in the nociceptive thresholds when administered alone, but caused marked increase in threshold responses when combined with a subanalgesic dose of fentanyl (5 micrograms/kg). Similarly, a combination of i.v. administered zuclopenthixol (100 micrograms/kg) and fentanyl induced significant (P < 0.05) antinociceptive effects, whereas zuclopenthixol administered i.v. alone had no effect on the threshold responses. Intrathecal administration of a low dose of droperidol (5-micrograms total dose) combined with i.v. administered fentanyl also increased mechanical thresholds significantly (P < 0.05). These results indicate that interactions exist between dopaminergic and opioid systems in the processing of nociceptive information and that these effects may, at least partially, be mediated spinally.

Animals↗
PubMed1995

Remyelination of mouse spinal cord axons demyelinated by local injection of lysolecithin.

Local injections of lysolecithin are commonly used to produce areas of demyelination in the CNS. For the mouse, the demyelinating initial phase of lesion development has been described previously but the spontaneous repair which follows has not. In this study we describe the morphological sequelae which result from the injection of 2 microliters of 1% lysolecithin into the spinal cord of adult mice. Lesion length was variable, extending 8 mm or more in 33% of lesioned animals. By 7 days after injection very little extracellular myelin debris was detected and remyelination had commenced. Remyelination progressed rapidly so that almost all axons were invested by myelin sheaths by 23 days. Remyelination was accompanied by a prominent astrocytosis. The long lesion length and the rapidity of repair has important implications for studies designed to assess the ability of transplanted myelinogenic cells to migrate towards demyelinating lesions.

Animals↗
PubMed1990

Tolerance to the antinociceptive effect of intrathecal morphine in intact and chronic spinal rats.

The antinociceptive effect of daily acute intrathecal morphine injections on the tail-flick withdrawal response was compared in Intact rats and rats that were spinally transected 3 to 4 weeks prior to morphine administration (Spinal rats). Spinal rats became tolerant to repeated intrathecal injections of 5, 15, or 30 micrograms of morphine within 3 days. Intact rats were not tolerant to these doses after 4 daily injections. Spinal rats, made tolerant to repeated intrathecal morphine injections, were not tolerant to a subcutaneous injection of 6.0 mg/kg of morphine. These data suggest that, in intact animals, tolerance to the antinociceptive effect of spinal morphine is modulated by descending, supraspinal input.

Animals↗
PubMed2002

The integrative role of the rat medullary subnucleus reticularis dorsalis in nociception.

Neurons within the medullary subnucleus reticularis dorsalis (SRD) of the rat convey selectively nociceptive information from all parts of the body. We have sought to define the neuronal networks that convey information from widespread noxious stimuli to the diffuse thalamocortical system and also modulate spinal outflow. The experiments, which were performed in rats, were designed to determine whether efferents from the SRD issue collaterals to the thalamus and spinal cord. Injections of the tracers fluorogold and tetramethylrhodamine-labelled dextran were centred stereotaxically in two areas that receive dense projections from the SRD: the cervical spinal cord and the lateral ventromedial thalamus (VMl), respectively. In other experimental series, SRD neurons were characterized electrophysiologically and individually labelled in a Golgi-like manner following juxtacellular iontophoresis of biotin-dextran. More than half reticulothalamic neurons within the SRD provided monosynaptic connections to the spinal cord. SRD neurons that responded to Adelta- or Adelta- and C-fibre activation from any area of the body had axons that gave both ascending and descending collaterals. Because the SRD innervates several areas involved in motor processing and receives strong, direct influences from several cortical regions, it could provide a structural basis for the processing of nociceptive and motor activities.

Animals↗
PubMed1996

Oral clonidine premedication enhances the quality of postoperative analgesia by intrathecal morphine.

Since clonidine potentiates the analgesia by morphine, the current study was performed to investigate whether oral clonidine premedication would enhance the postoperative analgesia by intrathecal morphine. Twenty-six patients, aged 37-60 yr, schedule for abdominal total hysterectomy under spinal anesthesia, were studied. Patients were randomly allocated to one of two groups; the clonidine group (n = 13) received oral clonidine approximately 5 micrograms/kg, and the control group (n = 13) received no clonidine. All patients received hyperbaric tetracaine 12 mg dissolved in 10% dextrose and morphine 0.2 mg for spinal anesthesia. We measured duration of analgesia (time to the first request for supplemental analgesics) and motor block. We also recorded the total number of injections of supplemental analgesics, and intensity of postoperative visual analog pain scores, nausea, and pruritus for 48 h after intrathecal administration. Duration of analgesia in the clonidine group was longer than the control group (2017 +/- 263 vs 1190 +/- 199 min, mean +/- SEM; P < 0.05). Although there was no difference in the total number of injections of supplemental analgesics (1.1 +/- 0.4 and 2.2 +/- 0.3 in the clonidine and control groups, respectively), the number of patients not requiring supplemental analgesics during the entire study period was larger in the clonidine group than the control group (six patients versus one patient; P < 0.05). There were no differences at any observation point between groups in visual analog pain scores, or the incidence of nausea and pruritus. Oral clonidine preanesthetic medication enhances the postoperative analgesia of intrathecal morphine plus tetracaine without increasing the intensity of side effects from morphine.

Administration, Oral↗
PubMed1997

Does dextrose affect analgesia or the side effects of intrathecal sufentanil?

UNLABELLED: Intrathecal (i.t.) sufentanil provides rapid effective pain relief for early labor, but it also produces undesirable side effects, which may be primarily related to cephalad spread. Although the combination of dextrose and positioning the patient head-up limits the spread of other spinally administered drugs, these factors have not been examined in laboring women receiving i.t. sufentanil. We hypothesized that the addition of dextrose to i.t. sufentanil injected with women in the sitting position would limit cephalad spread and side effects. Sixty-six healthy nulliparous parturients in early labor were randomized to receive 2-mL i.t. injections of sufentanil 10 micrograms plus saline with patients in either the lateral decubitus or sitting position, sufentanil 10 micrograms plus dextrose 7.5% with patients in either the lateral decubitus or sitting positions, or plain dextrose 7.5%. Pain scores using a 10-cm visual analog pain scale, sensory block height, and side effects were recorded. Dextrose 7.5% did not affect cephalad spread, as measured by block height to pin testing, but it did significantly reduce the duration of analgesia and the incidence of pruritus from i.t. sufentanil administered to patients in the sitting position compared with patients in the lateral position. In contrast, patient position had no effect on analgesia or side effects in patients receiving i.t. sufentanil in saline. I.t. dextrose alone had no effect. IMPLICATIONS: The authors conclude that the addition of dextrose to intrathecal sufentanil injected into patients in the sitting position reduces the duration of analgesia without significantly reducing side effects with the exception of pruritus, and therefore does not improve the clinical utility of intrathecal sufentanil.

Adult↗
PubMed1997

Adenosine for pain control.

The antinociceptive actions of adenosine and adenosine analogs in animal models has been known for more than 10 years. The recent development with regard to the pain modulatory effects of adenosine, primarily in clinical studies, has generated a renewed interest in this principle for pain control. This review summarizes the current knowledge in adenosine mediated pain modulation in acute and chronic conditions, with focus on studies in man. The endogenous compound adenosine has various modulatory effects in the peripheral and central nervous system, mediated through specific cell-surface associated receptors. The current view is that adenosine receptors of the A1-subtype are associated with a modulatory effect on pain transmission at spinal cord level. Animal studies have repeatedly demonstrated adenosine- and adenosine analog mediated inhibitory influences on presumed nociceptive reflex responses (1,2). These examinations in rodents have tested acute pain models involving tactile, pressure and heat stimulations. More recently, animal lesion models presumably reflecting chronic pain, has shown that adenosine analogs can suppress nociceptive behaviour both by systemic and intrathecal (i.t.) administration (3,4). Consequently, there is substantial evidence that adenosine can modulate nociceptive input. Further, it has been proposed that endogenous adenosine formation is involved in physiological pain control at the spinal cord level and that its release is involved in the action of opioid antinociception (1). Clinical studies have revealed that adenosine administration by bolus injection or by infusion at doses above 70 micrograms x kg-1 x min-1 is associated with pain symptoms from different parts of the body. This algogenic effect of higher doses of adenosine is probably related to sensitization/activation of peripheral nociceptive afferents (5).

Acute Disease↗