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PubMed1997

Delayed antagonism of AMPA/kainate receptors reduces long-term functional deficits resulting from spinal cord trauma.

Excitatory amino acid (EAA) receptors play a significant role in delayed neuronal death after ischemic and traumatic injury to the CNS. Focal microinjection experiments have demonstrated that 2,3-dihydro-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX), a highly selective and potent antagonist of non-N-methyl-D-aspartate ionotropic EAA receptors, i.e., those preferring alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) or kainate, can reduce histopathology and functional deficits when administered at 15 min after traumatic spinal cord injury (SCI). Similarly, intravenous infusion of NBQX, beginning at 15 min postinjury (p.i.), results in a significant amelioration of the functional deficits produced by experimental SCI. However, if antagonists of AMPA/kainate receptors were to be used therapeutically for patients with SCI, administration would likely be delayed for several hours after injury. We therefore examined the effects of NBQX administered at 4 h after SCI on functional deficits and histopathology in a standardized rat model of contusive SCI. An incomplete SCI was produced in Sprague-Dawley rats at T8 with a weight-drop device (10 g x 2.5 cm). NBQX (15 nmol), or vehicle alone, was microinjected into the injury site 4 h later. Recovery of hind limb reflexes, postural control, and locomotor function was determined by a battery of behavioral tests performed for 8 weeks. Spinal cord tissue was then fixed by perfusion and used for morphometric and immunocytochemical analyses. Previous studies with acute NBQX treatment showed significant functional improvement by 1 week; the effects of delayed NBQX treatment on functional deficits were not discernible until 3-4 weeks after SCI. Thereafter, significant reductions in hindlimb deficits were demonstrated in two independent studies. The nature and magnitude of the reductions in chronic deficits were similar to those observed previously when NBQX was administered acutely at 15 min after SCI. Morphometric analyses showed that delayed treatment with NBQX resulted in sparing of gray matter adjacent to the injury site but no significant effect on the area of white matter at the epicenter. However, serotonin immunoreactivity below the lesion, used as a marker for preservation of one supraspinal pathway, was significantly higher in the NBQX-treated group. These results support a therapeutic potential for NBQX, and presumably other AMPA antagonists, in SCI by demonstrating effectiveness in a clinically relevant time frame. They indicate the importance of assessing chronic functional deficits in evaluating the therapeutic potential of a treatment paradigm. Further, they suggest the intriguing hypothesis that mechanisms underlying early functional recovery after SCI are, at least in part, distinct those from those involved in reducing chronic functional deficits.

Animals↗
PubMed2001

Effects of iloprost on vasospasm after experimental spinal cord injury: an electron and light microscopic study.

It has been increasingly reported that traumatic and ischemic insults to the spinal cord may produce tissue damage through both direct and indirect mechanisms. In spite of many theories about post-traumatic spinal cord injury, there is still no satisfactory account of the exact mechanism. Vasospasm may be related to the trauma and release of vasoconstrictor or vasoactive amines. This study aims at studying the possible protective mechanisms of iloprost, a stable analogue of prostacyclin, after spinal cord injury on the rabbit. Forty-two adult male rabbits (New Zealand albino) were inflicted injuries by epidural application of an aneurysm clip to the spinal cord. Twenty-one rabbits received an i.v. infusion of 25 microg kg(-1) x h(-1) iloprost. The remaining twenty-one rabbits received an i.v. infusion of saline as the control group. Intravenous treatment started immediately after the infliction of the spinal cord injury and lasted for 1 h. Iloprost treatment had no side effects on the general physiological parameters in the rabbits. Control and iloprost treatment groups were divided into three sub-groups. The first group of animals was deeply anesthetized and spinal cords were removed 15 min after treatment. Second and third group animals were sacrificed in the 3rd and 24th hours respectively. All spinal cords were removed for light and electron microscopic examination. The width of anteriolar smooth muscle cells and the ultrastructural analysis of sulcal arterioles and venules in the ventral median fissure of spinal cords treated by iloprost revealed less thickening in all groups especially on the 24th hour group (p < 0.01), but less thickening was observed on the 3rd hour group. Iloprost-treated groups had limited edema and moderate protection of myelin and axons. These results suggest that iloprost treatment after spinal cord injury has a highly protective effect, and the possible protective effect of iloprost is resolution of vasospasm due to spinal cord injury.

Animals↗
PubMed1994

Intrathecal morphine and clonidine in the management of spinal cord injury pain: a case report.

Neuropathic pain following spinal cord injury (SCI) can be difficult to manage using currently available pain management techniques. We describe a case of chronic pain following SCI which failed to respond to a variety of approaches including intrathecal administration of morphine. Use of clonidine in addition to the morphine resulted in a marked decrease in pain. The use of intrathecal clonidine with or without opioids may present an effective alternative in the management of intractable SCI pain and other forms of neuropathic pain.

Adult↗
PubMed1992

Indication, efficiency and complications of intrathecal pump supported baclofen treatment in spinal spasticity.

In 19 patients, who suffered from severe spinal spasticity of different etiologies and did not respond sufficiently to oral antispastic therapy, intrathecal Baclofen test boli were administered. In 11 patients a DAD (Drug Administration Device) [SynchroMedR Model 8611 H, Medtronic Inc. Minneapolis, USA] was implanted. Catheter dislocation or torsion was the most common complication to be observed in these 11 patients. Long term intrathecal Baclofen application was effective in all patients, as reducing spasticity, flexor spasms and spasm induced pain. In some cases the motor performance ameliorated.

Adult↗
PubMed1992

Effect of kynurenate on functional deficits resulting from traumatic spinal cord injury.

The potential role of excitatory amino acid (EAA) receptors in spinal cord trauma was examined in a standardized rat model of contusive injury. EAA antagonists were administered in a split-dose protocol with half given 5 min prior to and the remainder 15 min after contusion produced at the T8 vertebral level. Hindlimb function was assessed using a battery of tests of reflex and more complex behaviors at 1 day after injury and weekly thereafter through 4-8 weeks. Functional deficits were compared for groups administered intravenous MK 801 (1 mg/kg), dextromethorphan (10 mg/kg) and kynurenate (300 mg/kg) or the vehicle, saline, alone. In addition, possible effect of the drugs themselves on hindlimb function were assessed in uninjured controls. None of the drugs produced more than transient effect on uninjured rats. In contused rats, only kynurenate produced significant reductions in functional deficits as compared to saline controls. Significant improvement of hindlimb function was also observed when the thoracic cord was locally perfused with kynurenate via intrathecal cannulas and when kynurenate was directly infused into the contusive injury site by stereotaxic microinjection. Using the latter route of administration, a dose-dependent effect of kynurenate (100, 200 and 400 nmol) on the ability of contused rats to use their hindlimbs in locomotion was demonstrated. The highest dose also resulted in a significant reduction in overall functional deficits from 1 week through 1 month and at 2 months after injury. Our results support the hypothesis that EAA receptors at or near the injury site are involved in producing a proportion of the overall functional deficits stemming from traumatic injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1998

Antinociceptive and morphine modulatory actions of spinal orphanin FQ.

Orphanin FQ (nociceptin, OFQ), a hepatdecapeptide peptide, has been designated as an endogenous ligand at the orphan receptor ORL1, which lacks affinity for opioid receptor ligands. OFQ-like immunoreactivity has been localized in spinal cord areas that are involved in the processing of nociceptive signals. In this study, the effects of spinally administered OFQ on thermal and mechanical nociceptive stimuli were investigated following intrathecal (i.t.) injection in unanesthetized rats bearing chronic indwelling catheters in the subarachnoid space. Intrathecal OFQ produced two distinct acute actions: an opioid-like antinociceptive effect, and antagonism of morphine-induced antinociception. Chronic administration produces tolerance. Acute actions were as follows. First, injection of OFQ alone in the dose range 10-100 nmol produced sustained antinociceptive effects in the tail-flick (baseline latency 1.5-2 s) and paw-pressure tests. These effects peaked at 45-60 min post-injection, were fully reversible, and were observed in absence of discernable motor impairments. Intrathecal naloxone (5 nmol) significantly attenuated the antinociceptive effects of OFQ (50 nmol i.t.) in tail-flick and paw-pressure tests. A 24-h pretreatment with the irreversible opioid receptor antagonist, beta-flunatrexamine (2 nmol i.t.), also attenuated the antinociceptive effects of OFQ (50, 100 nmol i.t.) and of morphine (7.5 nmol i.t.) in both tests. Low doses (1, 5 nmol) of OFQ, which failed to produce antinociception in the tail-flick test involving a baseline latency of 1.5-2 s, produced a strong antinociceptive response when the baseline latency was increased to 5-6 s. Second, intrathecal OFQ, at doses (0.5, 1.0, and 5.0 nmol) that had no antinociceptive activity in the tail-flick (baseline latency 1.5-2 s) and paw-pressure tests, attenuated the antinociceptive effect of morphine (7.5 nmol i.t.) in these tests. However, a threshold OFQ dose (10 nmol) significantly extended the duration of antinociception induced by morphine (7.5 nmol i.t.) or deltorphin (20 nmol i.t.). Chronic actions were as follows. In rats that were rendered tolerant to spinal morphine, by a continuous intrathecal infusion (7.5 nmol/h) of the agonist for 5 days, the OFQ dose-response curves for its antinociceptive effect in the tail-flick and paw-pressure tests were significantly shifted to the right. In separate experiments, repeated intrathecal injection of OFQ (50 nmol) or morphine (7.5 nmol) produced a significant decline in their antinociceptive effects. Thus, intrathecally administered OFQ produces both development of tolerance to its antinociceptive actions and cross-tolerance to the action of morphine.

Analgesia↗
PubMed1984

Etomidate by infusion for neuroanaesthesia. Kinetic and dynamic interactions with nitrous oxide.

An etomidate infusion was used to anaesthetise twelve patients for spinal surgery; six (group I) with 67% nitrous oxide and six (group II) with oxygen enriched air. Anaesthesia was induced with infused etomidate at a rate of 100 micrograms/kg/minute for 10 minutes and maintained at a rate of 10 micrograms/kg/minute. Recovery was assessed as the time to opening eyes on command (t1) and the time to giving correct date of birth (t2). In group I, mean value for t1 was 37.9 minutes and t2 59.1 minutes which is significantly longer than in group II where mean value for t1 was 9.0 minutes and t2 15.1 minutes. Blood was taken for estimation of etomidate levels. In group I the maintenance level was 501 ng/ml and the plasma clearance 20.9 ml/kg/minute. In group II the maintenance level was 367 ng/ml and plasma clearance 27.3 ml/kg/minute. Etomidate infusion appears to be a suitable alternative for neuroanaesthesia when nitrous oxide is contra-indicated.

Adult↗
PubMed1999

Neurotrophins promote regeneration of sensory axons in the adult rat spinal cord.

We have investigated the effects of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) on the intraspinal regeneration of anterogradely labeled axotomized ascending primary sensory fibers in the adult rat. These fibers were allowed to grow across a predegenerated peripheral nerve graft and back into the thoracic spinal cord. In control animals that had been infused with vehicle for two weeks into the dorsal column, 3 mm rostral to the nerve graft, essentially no fibers had extended from the nerve graft back into the spinal cord. The number of sensory fibers in the rostral end of the nerve graft was not significantly different between control and neurotrophin-infused animals. With infusion of NGF, 37+/-2% of the fibers at the rostral end of the graft had grown up to 0.5 mm into the dorsal column white matter, 30+/-2% up to 1 mm, 19+/-3% up to 2 mm and 8+/-2% up to 3 mm, i.e., the infusion site. With infusion of NT-3, sensory fiber outgrowth was similar to that seen with NGF, but with BDNF fewer fibers reached farther distances into the cord. Infusion of a mixture of all three neurotrophins did not increase the number of regenerating sensory fibers above that seen after infusion of the individual neurotrophins. These findings suggest that injured ascending sensory axons are responsive to all three neurotrophins and confirm our previous findings that neurotrophic factors can promote regeneration in the adult central nervous system.

Animals↗
PubMed1994

Calorie sources and recovery from central nervous system ischemia.

OBJECTIVES: Glucose is the primary substrate for the energy requirements of the nervous system. Nevertheless, administration of glucose to critically ill patients with central nervous system trauma may have adverse effects on their neurologic recovery. The purpose of this study was to evaluate the effects of other sources of nonprotein calories on spinal cord lactate accumulation and on electrophysiologic recovery after a period of severe spinal cord ischemia. DESIGN: Two randomized, blinded studies were performed: one of glycolytic energy substrates (fructose, xylitol, sorbitol, glycerol) and one of ketogenic energy substrates (beta-hydroxybutyrate, acetate, butyrate). SETTING: College teaching hospital laboratory. SUBJECTS: New Zealand albino rabbits (weight 3.5 to 4.5 kg). INTERVENTIONS: After infusion of the randomly assigned treatment, temporary ischemia was produced in the lumbosacral spinal cord by occluding the abdominal aorta with a balloon catheter. MEASUREMENTS AND MAIN RESULTS: Blood concentrations of glucose, lactate, pyruvate, and ketone bodies and spinal cord dialysate concentration of lactate were measured before and after infusion of the assigned treatment, and during ischemia and during the first 2 hrs after reperfusion. Spinal somatosensory evoked potentials were recorded during ischemia to assure a similar severity of ischemia in all animals and during the first 2 hrs after reperfusion as a measure of electrophysiologic recovery. Infusion of the glycolytic nutrients xylitol and fructose increased blood glucose and lactate concentrations, and resulted in increased lactate accumulation in the spinal cord during ischemia and resulted in a significantly poorer recovery of the spinal somatosensory evoked potential than infusion of saline. Infusion of sorbitol and glycerol did not have these adverse effects in the doses administered. None of the ketogenic nutrients increased blood glucose concentration or increased lactate accumulation in the spinal cord during ischemia when compared with infusion of saline. Infusion of butyrate and acetate caused arterial hypotension and resulted in a poorer recovery of the spinal somatosensory evoked potential than saline. Infusion of beta-hydroxybutyrate did not have an adverse effect on blood pressure or on evoked potential recovery. CONCLUSIONS: Glycerol, sorbitol, and beta-hydroxybutyrate deserve further evaluation as potential nonprotein calorie sources in patients with neurologic injury. Xylitol and fructose are not suitable since these substrates resulted in hyperglycemia and increased lactate accumulation in the central nervous system, and had detrimental effects on electrophysiologic recovery after ischemia. The short-chain fatty acids (acetate and butyrate) also had adverse effects on electrophysiologic recovery after ischemia, probably because of their hypotensive effects when given intravenously, rather than from the effects of their metabolism.

Analysis of Variance↗
PubMed2005

Posterior cervical approach for intrathecal baclofen pump insertion in children with previous spinal fusions. Technical note.

Intrathecal baclofen pumps for the management of severe spasticity are being used more often in children with cerebral palsy. The intrathecal catheter is traditionally introduced dorsally in the lumbar region. In some children with previous thoracolumbar fusions for scoliosis, the fusion mass obviates the introduction of the intrathecal catheter. The authors describe their experience with a posterior cervical approach for intrathecal baclofen pump insertion in three patients with spastic quadriplegic cerebral palsy who had previously undergone thoracolumbar fusions for scoliosis. Insertion was successful in all three patients; no complications of catheter disconnection, catheter dislodgment, or cerebrospinal fluid leakage occurred. Follow-up review ranged from 10 to 28 months postoperatively (mean 17 months). The posterior cervical approach for intrathecal baclofen pump insertion is a safe and effective alternative for patients who have previously undergone thoracolumbar spine fusions and in whom the traditional lumbar approach is not feasible.

Adolescent↗
PubMed1994

Perspectives on opioid tolerance from basic research: behavioural studies after spinal administration in rodents.

For tolerance development studies, computer modelling and statistical tests suggested that the equation which best described the decrement of analgesic effect was best served by an exponential decay function. Further analysis of the time course data led to the tentative conclusion that all groups of animals became tolerant at the same rate, regardless of drug or dose. A literature search revealed then, as it does now, that although there are many statements regarding the rate of opioid tolerance, there has been little systematic investigation of this. The Holy Grail of obtaining the rates of tolerance for a number of opioid agents in a systematic study is well within grasp. This information will be needed in clinical practice for the rational choice of opioid with regard to rate of the development of tolerance. The working hypothesis that emerges for the magnitude of opioid tolerance is that more potent agonists produce less tolerance. Further confirmation of this hypothesis has been forthcoming. This suggests that clinical use of more potent opioids, such as fentanyl, should be considered as a substitute for morphine in long term treatment regimens. The working hypothesis for cross-tolerance is that agents acting on the same receptors will show cross-tolerance. Cross-tolerance will also be observed among agents acting on different receptors, but only those that exhibit pharmacological synergy after short term administration. Asymmetry of cross-tolerance can occur, as the magnitude of this cross-tolerance is determined by the relative potency of the toleragen with regard to that of the probe agent. Given the additional factor of receptor selectivity with agents of different receptor classes, types and subtypes, new studies need to be designed combining the toleragen with a selective antagonist to determine the precise receptor mediation of the magnitude of tolerance, and thus cross-tolerance. For example, the delta opioid DADLE infused with a mu selective opioid antagonist would produce an animal strictly tolerant at delta receptors, as DADLE has been implicated to have some effects at mu receptors. In any event, consideration of the quantitative measures of cross-tolerance are extremely important to help shape a rationale treatment plan for patients who may become tolerant to a particular class of analgesics. In general, direct toleragen administration by constant dose, constant rate infusion into local central nervous system (CNS) regions will provide the most rigorous tolerance studies for examination of the pharmacodynamic theories of tolerance, as adaptations in processes affecting central bioavailability, such as dispositional changes in the blood-brain barrier or fibrous encapsulation of an implanted subcutaneous pellet, are circumvented. The above considerations also are relevant for studies of tolerance and cross-tolerance after intracerebroventricular administration or, in general, for tolerance studies after systemic administration. The possibility of probe administration to the same region of CNS that was rendered tolerant, as in the Y-catheter method, further enhances the focus on the pharmacodynamic mechanisms of tolerance without the ancillary and literally peripheral concerns of a dispositional nature. A posological approach to these studies cannot be overemphasized, as it is only through such time consuming and costly experiments that rigorous, quantitative data can be obtained. Such data may help to guide the hand of the physician towards rational therapeutic intervention in the treatment of patients with chronic pain and opioid tolerance.

Analgesics, Opioid↗
PubMed2005

Pain management, including intrathecal pumps.

Even when managed according to guidelines, approximately 14% of cancer patients have unrelieved pain or unacceptable side effects, and there is good evidence that patients still are not receiving optimal therapy. Implantable drug delivery systems (IDDS) administer small amounts of drugs directly to the spinal cord and reduce systemic narcotic exposure by a factor of 300 to one. In a large randomized trial of 202 patients with pain scores of 7.5 or higher, despite 200 mg or more of morphine or equivalent narcotics, IDDS gave better clinical success than comprehensive medical management (84.5% vs 70.8%, P=0.05). Pain scores were reduced by 52% versus 39%, drug toxicity scores were reduced by 50% versus 17%, and IDDS patients lived longer. Even the most refractory pain patients--those failed by a month of comprehensive medical management by experts--when subsequently provided with IDDS, had a 27% reduction in pain scores and a 50% reduction in drug side effects. Given multiple positive small cohort studies and a positive high-power randomized trial, IDDS should be considered as the best treatment for this population.

Drug Delivery Systems↗
PubMed1999

Gabapentin attenuates nociceptive behaviors in an acute arthritis model in rats.

In this study, we investigated the effectiveness of gabapentin (Neurontin), administered spinally with a microdialysis fiber, in reducing nociceptive behavioral responses induced by a knee joint inflammation model. This model is produced by injection of the knee joint with kaolin and carrageenan in rats. The resultant knee joint inflammation produces a secondary hyperalgesia to radiant heat applied to the hindpaw. Both pretreatment and post-treatment protocols were examined. Spinal administration of gabapentin (10 mg/ml) infused 1.5 h before induction of knee joint inflammation, although having no effect on the baseline, prevented the development of heat hyperalgesia. Gabapentin also prevented the development of other pain-related behaviors scored subjectively. Gabapentin had no effect, however, on the joint circumference increase typical in this model. In animals with fully developed knee joint inflammation, gabapentin produced a reversal of heat hyperalgesia. The paw withdrawal latency responses and subjective pain scores were no longer significantly different from baseline, but joint circumference increases remained. These data suggest that gabapentin is an effective antinociceptive agent when administered either before or after induction of knee joint inflammation acting through a central neurogenic mechanism.

Acetates↗
PubMed1983

Narcotics for acute postoperative pain. Is intramuscular administration passé?

Intramuscular (IM) injection of narcotic has been the mainstay of postoperative analgesia. However, problems inherent in IM administration--pulmonary dysfunction and inadequate pain control due to variable peak levels of drug concentration and variable absorption rate--have resulted in continuing efforts to find a more desirable method of administration. Intravenous (IV) infusion on a continuous or self-administered intermittent basis controls pain more effectively than IM injection. The total amount of drug required is significantly less and pulmonary dysfunction seems to occur less frequently. Some investigators are studying injection of narcotic into the epidural or subarachnoid space of the spine as a means of providing postoperative analgesia. This method provides an unusually intense, prolonged, and segmental analgesic action, as well as greater improvement in respiratory dynamics than with IV infusion. Although the advantages of the IV and spinal methods seem to outweigh the disadvantages, further research is needed before they can be recommended as alternatives to the standard IM method used to control postoperative pain.

Humans↗
PubMed1998

[New methods for transurethral electroresection of the prostate from the anesthesiologic viewpoint].

Intravascular absorption of large volumes of solution without electrolytes is a common problem in transurethral resection of the prostate. In the present study we compared two different methods of resection (TURP vs. Vaporization TURP; 20 patients in each group) regarding fluid absorption and loss of blood. In addition, we report on 60 patients who had Vapo-TURP. The operations were performed by different very experienced surgeons. In both groups, spinal anaesthesia and standard regimes of infusion were used. The amount of fluid absorbed was measured by the ethanol method (2 vol.% ethanol; Widmark-formula). Haemoglobin, haematocrit and electrolytes were determined at set times. Ten of the 20 patients in the TURP group showed blood-alcohol levels > 0.1%/1000. In the Vapo-TURP group, only five of 57 patients (three patients with perforation of the prostate capsula were excluded) showed positive levels of blood-alcohol (< 0.05%/1000; fluid absorption < 150 ml). The difference was statistically significant (p = 0.002). Sixty minutes after the beginning of the procedures, the values of haemoglobin and haematocrit were significantly lower in the TURP group (7.68 +/- 0.41 vs. 7.38 +/- 0.64 mmol/l and 0.36 +/- 0.02 vs. 0.34 +/- 0.03). Regarding absorption of fluid and bleeding, Vapo-TURP was superior. From the anaesthesiological point of view, Vapo-TURP should be the method of choice, especially for the elderly.

Aged↗
PubMed2006

Protein phosphatase 2A regulates central sensitization in the spinal cord of rats following intradermal injection of capsaicin.

BACKGROUND: Intradermal injection of capsaicin into the hind paw of rats induces spinal cord central sensititzation, a process in which the responsiveness of central nociceptive neurons is amplified. In central sensitization, many signal transduction pathways composed of several cascades of intracellular enzymes are involved. As the phosphorylation state of neuronal proteins is strictly controlled and balanced by the opposing activities of protein kinases and phosphatases, the involvement of phosphatases in these events needs to be investigated. This study is designed to determine the influence of serine/threonine protein phosphatase type 2A (PP2A) on the central nociceptive amplification process, which is induced by intradermal injection of capsaicin in rats. RESULTS: In experiment 1, the expression of PP2A protein in rat spinal cord at different time points following capsaicin or vehicle injection was examined using the Western blot method. In experiment 2, an inhibitor of PP2A (okadaic acid, 20 nM or fostriecin, 30 nM) was injected into the subarachnoid space of the spinal cord, and the spontaneous exploratory activity of the rats before and after capsaicin injection was recorded with an automated photobeam activity system. The results showed that PP2A protein expression in the spinal cord was significantly upregulated following intradermal injection of capsaicin in rats. Capsaicin injection caused a significant decrease in exploratory activity of the rats. Thirty minutes after the injection, this decrease in activity had partly recovered. Infusion of a phosphatase inhibitor into the spinal cord intrathecal space enhanced the central sensitization induced by capsaicin by making the decrease in movement last longer. CONCLUSION: These findings indicate that PP2A plays an important role in the cellular mechanisms of spinal cord central sensitization induced by intradermal injection of capsaicin in rats, which may have implications in clinical pain therapy.

Animals↗
PubMed1995

[Pressure and flow-profile of different spinal needles].

The flow characteristics of four different types of spinal needles were investigated by measuring the infusion pressure during steady state infusion of either saline or an X-ray contrast agent. Two pencilpoint needles, a Whitacre 22Gauge and a Sprotte 24Gauge, possessed flow characteristics similar to a 22Gauge Quincke point needle. Use of pencilpoint needles for spinal anaesthesia results in a lower incidence of postdural puncture headache compared to the Quincke point needle. We therefore recommended the use of pencilpoint needles for myelography.

Anesthesia, Spinal↗
PubMed1992

Endogenous calcitonin gene-related peptide mediates nonadrenergic noncholinergic depressor response to spinal cord stimulation in the pithed rat.

The role of endogenous calcitonin gene-related peptide (CGRP) in the nonadrenergic noncholinergic depressor response to spinal cord stimulation was studied in the pithed rat in vivo. Pithed rats were given hexamethonium (2 mg/kg per minute i.v.) to block autonomic outflow, and mean blood pressure was artificially maintained at approximately 100 mm Hg with methoxamine (10-15 micrograms/kg per minute i.v.). Electrical stimulation of the spinal cord at the level of the lower thoracic vertebra (T9-12) caused a fall in blood pressure in a frequency-dependent (0.5-10 Hz), voltage-dependent (2.5-50 V), and pulse duration-dependent (0.25-8 msec) manner. The heart rate did not change during the depressor response. The depressor response was long lasting, and the maximum response was elicited by stimulation at 4-6 Hz. The neurotoxin tetrodotoxin (100 micrograms/kg i.v.) abolished the depressor response to spinal cord stimulation, whereas treatment with propranolol (0.5 mg/kg per minute i.v.), atropine (0.05 mg/kg per minute i.v.), or a combination of pyrilamine (0.5 mg/kg per minute i.v.) and cimetidine (0.5 mg/kg per minute i.v.) did not affect the response. In pithed rats treated with capsaicin (total dose of 500 mg/kg s.c.), spinal cord stimulation caused a slight depressor response. Exogenous CGRP, but not acetylcholine, isoproterenol, histamine, or substance P, caused a sustained fall in blood pressure that mimicked the spinal cord stimulation-induced depressor response. Continuous infusion of CGRP[8-37] (60 nmol/kg per minute i.v.), a CGRP receptor antagonist, markedly inhibited the depressor responses not only to spinal cord stimulation but also to exogenous CGRP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗