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PubMed1972

Distribution of leucine- 3 H during axoplasmic transport within regenerating neurons as determined by electron-microscope radioautography.

The distribution of leucine-(3)H in neurons was determined by electron-microscope radioautography after infusion of label into the spinal cord or sensory ganglia of regenerating newts. In the nerve cell bodies 3 days after infusion, the highest concentration of label per unit area occurred over the rough-surfaced endoplasmic reticulum. In the large brachial nerves, the silver grains were not distributed uniformly in the axoplasm, indicating that the labeled materials are restricted in their movement to certain regions of the axon. Almost all of the radioautographic grains observed in myelinated nerves could be accounted for by the presence of a uniformly labeled band occupying the area 1500-9000 A inside the axolemma. This region of the axon was rich in microtubules and organelles while the unlabeled central core of the axon contained mainly neurofilaments. This observation supports the hypothesis that microtubules are related to axonal transport. In small, vesicle-filled nerve terminals in the blastema, labeled material was restricted to a thin zone a short distance beneath the plasma membrane while the central region of the terminal was largely unlabeled. The peripheral pattern of labeling in the nerve endings is consistent with successive addition of newly synthesized proteins at the periphery of the growth cone and release of substances such as trophic factors at the nerve terminal.

Animals↗
PubMedDate not supplied

Comparative flow rates of saline in commonly used spinal needles including pencil-tip needles.

BACKGROUND AND OBJECTIVES: Certain characteristics of spinal needles that can influence their clinical usefulness were examined, namely, flow rates, internal diameters, and size of orifices of pencil-type needles. METHODS: Flow rates of 0.9% sodium chloride solution were measured in spinal needles with an infusion pressure of 10 mmHg at isothermic and steady-state conditions. In 15 different types, a new needle was used for each experiment, and 6 experiments were performed with each needle type for a total of 90 experiments. The Hagen-Poisseuille Law for laminar flow was used to calculate the internal diameters. RESULTS: The flow rates of needles of the same gauge varied considerably depending on the manufacturer. Compared with 26-gauge ultrathin-wall spinal needle produced by the same manufacturer (Braun, Bethlehem, Pennsylvania), the flow rate through 29-gauge spinal needle was 18% that of the former needle. The flow rate through 27-gauge Quincke Whitacre needle (Becton Dickinson, Rutherford, New Jersey) was not statistically different from that through 26-gauge needle by the same manufacturer. By arbitrarily choosing < or = 2 seconds to be the in vitro desirable period for saline to traverse the needle from one end to the other, all needles with the exception of 29-gauge and standard 26-gauge Quincke Braun needles met this criterion. The length and size of the orifices of Whitacre needles were found to be significantly smaller than those of Sprotte needles (Havel, Cincinnati, Ohio). The orifice of Sprotte needle was longer than the known thickness of the dura while that of the Whitacre needle was smaller. CONCLUSIONS: Needles of the same gauge do not necessarily have the same flow rate. Flow rate correlates well with internal, not external, diameter. By considering < or = 2 seconds to be the desirable time for saline to traverse a spinal needle, all, except two, meet this criterion. The orifice of Whitacre needle has more desirable features than that of Sprottle needle. Anesthesiologists are encouraged to use 27-gauge needles since their flow rate is not slower than that of 26-gauge needles.

Needles↗
PubMed1993

Effect of RP 67580, a non-peptide neurokinin1 receptor antagonist, on facilitation of a nociceptive spinal flexion reflex in the rat.

1. In order to examine the contribution of neurokinin1 (NK1) receptors to facilitation of a spinal nociceptive reflex in the rat, we have investigated the effects of RP 67580 (3aR, 7aR)-7,7-diphenyl-2(1-imino-2-(2-methoxyphenyl/ethyl)perhydrois oindole)), a non-peptide neurokinin1 (NK1) receptor antagonist, selective for the rodent receptor sub-type, on the activity of individual motorunits. These results were compared with the effects of RP 68651, the inactive 3aS, 7aS enantiomer of RP 67580, as a control for non-specific activity. 2. Experiments were performed on 15 rats anaesthetized with a continuous i.v. infusion of alphaxalone/alphadalone and spinalized at T9-10. Single unit recordings of motorunit activity from biceps femoris/semitendinosus were made with a concentric needle electrode. In each experiment, a vehicle dose followed by 4 sequential rising doses of either RP 67580 or RP 68651 were given at 15 min intervals. High intensity electrical stimuli were applied to the hindlimb receptive field of the motorunit at a rate of 1 per 60 s throughout the experiment to establish a baseline. A conditioning stimulus (20 of these stimuli at 1 Hz) was delivered 5 min after each dose and the effect of the size of the baseline response examined. 3. The conditioning stimulus evoked a facilitation of the baseline at the start of all experiments (mean increase +/- s.e. mean = 151 +/- 20%). RP 67580 attenuated this facilitation, with an ID50 (+/- s.e. mean) of 2.5 +/- 4.2 micrograms kg-1, i.v., whereas RP 68651 at doses of up to 3 mg kg-1, i.v. did not. There was no statistically significant effect of drug on the baseline reflex, nor on the response to the conditioning stimulus. Doses of 300 and 3000 microg kg-1 of both RP 67580 and RP 68651 evoked small depressor effects on systemic arterial blood pressure.4. We conclude that the facilitation of a spinal flexor reflex by noxious conditioning stimuli in the rat is mediated by NK1 receptors whereas the baseline reflex is not. The results suggest that brain penetrantNK1 receptor antagonists may have central anti-nociceptive effects.

Animals↗
PubMed2001

[Treatment of pain in cancer with systemically administered opioids].

The World Health Organization guidelines for cancer pain relief have been proven efficacious in 90% of the patients with cancer pain. The patient's self-report of pain is the focus of treatment. When initiating treatment, controlled-release preparations of opioids are generally favoured, and are combined with immediate release morphine to prevent or treat 'breakthrough' pain and to enable the optimum opioid dosage to be calculated. (Breakthrough pain is a transient increase in pain in a patient who has stable, persistent pain treated with opioids.) In patients with an unfavourable balance between analgesia and side effects, the following strategies may be useful, together with appropriate treatment of the side effects: Sequential opioid trials (so-called opioid rotation) is an approach which is effective in 50-70% of the patients. Changing the route of opioid administration is successful in 70-95% of the patients. When selecting an invasive technique, continuous subcutaneous infusion is medically preferred. Spinal analgesia is an alternative. Knowledge of the relative potency of opioid drugs and of their biologic availability is needed to guide changes in drugs or routes of administration.

Analgesics, Opioid↗
PubMed1971

Ammonium and chloride extrusion: hyperpolarizing synaptic inhibition in spinal motoneurons.

The reversal potential of postsynaptic inhibition shifts toward resting membrane potentials in cat spinal motoneurons after intravenous infusion of ammonium salts(1 to 3 millimoles per kilogram of body weight). Simultaneously, the depolarizing action of intracellularly injected chloride ions on the inhibitory membrane is enhanced and recovery therefrom is prolonged. Passive membrane properties remain unaltered. The results indicate a blocking of active extrusion of chloride which normally maintains a high ionic gradient for hyperpolarizing inhibition.

Action Potentials↗
PubMed1977

Norepinephrine-induced reflex bradycardia after central administration of angiotensin II.

Central angiotensin effects may include baroreceptor alterations and/or ventilated, were given angiotensin intravertebrally (10 ng/kg/min), into a lateral cerebroventricle (0.4 microgram/min) or intravenously (10 ng/kg/min). Surgery was completed under methoxyflurane anesthesia; wounds were periodically infiltrated with viscous tetracaine and the methoxyflurane discontinued. The experiments were performed with the brain unanesthetized to optimize detection of an angiotensin effect on the cardioinhibitory component of the baroreceptor reflex. Bradycardia was evoked by norepinephrine injections (2 microgram/kg i.v.). Intraventricular and intravertebral angiotensin increased basal mean blood pressure 16 mm Hg (p less than 0.05); norepinephrine-induced pressor responses and bradycardia were unaffected by the peptide. Intravenous angiotensin did not affect basal blood pressure; a 16 mm Hg increase (p less than 0.05) in the norepinephrine pressor response with no change in bradycardia was observed. Atropine reversed the norepinephrine bradycardia and increased the pressor response in all cats, thus demonstrating the integrity of the reflex. We conclude that centrally administered angiotensin produces no change in the cardioinhibitory reflex to an acute pressor stimulus. The possibility of a peripheral effect of the peptide exists. The hypertensive response observed in the conscious spinal cats after central angiotensin infusions could be due to vasopressin release and/or action of the peptide at cardiovascular sites at high spinal levels.

Angiotensin II↗
PubMed2006

[Relation between glucose concentrations in cerebrospinal fluid and sensory and motor block during spinal anesthesia with hyperbaric bupivacaine].

OBJECTIVE: To study the relation between cerebrospinal fluid (CSF) glucose levels, the highest level of sensory block, and the duration of motor block after intrathecal injection of 2 mL of hyperbaric bupivacaine. To determine CSF glucose levels upon recovery from motor block. PATIENTS AND METHODS: A prospective study of 34 patients administered a spinal anesthetic in continuous infusion through a 22-gauge catheter. CSF samples were extracted through the catheter 5, 10, 15, 20, 30, 45, and 60 minutes after start of infusion and upon motor recovery. After each extraction the intensity of the motor block was assessed; the intensity of the sensory block was assessed after each extraction up to 20 minutes. RESULTS: Glucose concentrations in CSF tended to decrease from 5 minutes (1027.07 [SD 349.04] mg dL(-1)) until full motor recovery (247.50 [20.39] mg dL(-1)). The probability of finding a motor block at a CSF glucose concentration of 287.5 mg dL(-1) or higher was less than 5%. We identified a positive correlation between the highest level of sensory block and the duration of full motor block (r=0.62, P<0.01) and between CSF glucose levels at the moment of greatest sensory block and upon full motor recovery (r=0.50, P<0.01). CONCLUSIONS: After continuous spinal anesthesia with hyperbaric bupivacaine, glucose concentrations in CSF are directly related to the highest level of sensory block, the course of the blockade, and its reversal.

Aged↗
PubMed2000

Downregulation of TrkA expression in primary sensory neurons after unilateral lumbar spinal nerve transection and some rescuing effects of nerve growth factor infusion.

Peripheral nerve injury results in sprouting of sympathetic and sensory nerve terminals around large diameter neurons in the dorsal root ganglia (DRG), but the underlying mechanism is not clear. Current study sought to examine changes of the nerve growth factor (NGF) receptor TrkA in DRG and spinal cord after a spinal nerve transection by an immunohistochemical technique and to investigate effects of NGF on the expression of TrkA protein in the same animal model. In the control rat, TrkA immunoreactivity was localized to about 55 +/ -1% of total neurons in DRG and to laminae I and II of the spinal cord. The percentage of TrkA immunoreactive neurons in DRG and TrkA staining intensity of spinal cord were reduced 1 week after the nerve lesion. The changes became maximal 2 weeks, but recovered partially 4 weeks after the lesion. The size of TrkA immunoreactive neurons dramatically shifted to smaller sizes, becoming more remarkable 4 weeks after the lesion. In the contralateral DRG, the percentage of TrkA immunoreactive neurons also decreased significantly. Exogenous NGF delivered to DRG for 2 weeks partially reversed the reduction of TrkA expression as well as atrophy of TrkA immunoreactive neurons. No TrkA immunoreactive basket was found around neuronal somata. Our data show that unilateral peripheral nerve injury results in dynamic downregulation of TrkA in sensory neurons in bilateral DRG and spinal cord, and that TrkA expression in sensory neurons is partially regulated by target-derived NGF.

Animals↗
PubMed2003

Continuous intrathecal infusion of SB203580, a selective inhibitor of p38 mitogen-activated protein kinase, reduces the damage of hind-limb function after thoracic spinal cord injury in rat.

P38 mitogen-activated protein kinase (MAPK) is one of the key enzymes in apoptosis induction pathways. We tested continuous intrathecal infusion of SB203580, a selective inhibitor of p38-MAPK, after spinal cord compression injury by a 20 g weight for 40 min at the 11th vertebra level-thoracic spinal cord. SB203580 (1 microg/day) was infused for 1 week after the compression. Hind-limb function was evaluated by measuring the frequency of 'standing' posture; raising fore limbs and sustaining body weight with hind-limbs. One-week after the compression, frequency of standing spinal cord injured rat was decreased to about half of that in sham operated animals which underwent laminectomy without compression. The frequency of standing in rats infused SB203580 recovered 2-3 weeks after the spinal cord injury, on the other hand, vehicle animals infused with saline did not recover. Myelin staining by Luxol fast blue showed severe myelin degradation in vehicle animals in lateral and dorsal funiculi. Apoptotic cells, detected by TUNEL staining, appeared in lateral funiculi of spinal cord injured rats. The application of SB203580 decreased the number of apoptotic cells. The SB203580-treated animals showed no significant degeneration of myelin structure. These results suggest that inhibition of p38-MAPK is one candidate for therapeutic agents against neurological deficits after spinal cord injury.

Animals↗
PubMed2001

An intraaortic solution trial to prevent spinal cord injury in a rabbit model.

OBJECTIVES: to evaluate the effectiveness of an intraaortic delivered solution on preventing spinal cord injury. DESIGN: forty rabbits were allocated into five equal groups. MATERIALS AND METHODS: one clamp was placed just distal to the left renal artery, and another was placed just above the iliac bifurcation for 40 min. Group 1 was not infused (control group). Through a 24G vascular catheter inserted into the isolated aortic segment, 20 ml of LR solution at room temperature (Group 2) 20 ml of LR solution at 3 degrees C (Group 3), and 20 ml of LR solution at 3 degrees C containing 30 mg/kg of methylprednisolone (Group 4) were infused over 3 min. In Group 5, 10 mg/kg of vitamins E and C were delivered two days before the experiment, and 20 ml of LR solution at 3 degrees C containing 30 mg/kg of methylprednisolone, and 10 mg/kg of vitamins E and C was infused at the operation. Postoperative spinal cord function was assessed using Tarlov's criteria. RESULTS: the neurologic status of Groups 3, 4, and 5 was significantly superior to that of Groups 1 and 2. No paraplegia was observed in Groups 4 and 5. Spastic paraplegia occurred in all rabbits of Groups 1 and 2, and in 20% of Group 3. In the electron microscopic evaluation of spinal cord specimens, normal histologic structure was observed in Groups 4 and 5, whereas, some derangements were observed in all others. CONCLUSIONS: intraaortic infusion of a hypothermic blended solution containing methylprednisolone, vitamins C and E provided best protection against postischaemic spinal cord dysfunction.

Animals↗
PubMedDate not supplied

Labour analgesia guided by echocardiography in a parturient with primary dilated cardiomyopathy.

PURPOSE: To evaluate the effects of intrathecal analgesics on cardiac function during labour analgesia using echocardiography in a parturient with idiopathic dilated cardiomyopathy (DCM). CLINICAL FEATURES: Induction of labour was planned in a 35-yr-old primiparous woman suffering from DCM. In order to stabilize hemodynamics in this patient, we induced continuous spinal analgesia with an infusion of fentanyl and epinephrine. Although her analgesia was well maintained for three hours during the first stage of labour, the patient complained of pain towards the second stage of labour. At this point, we administered bupivacaine intrathecally to alleviate her pain. Transthoracic echocardiography showed that the left ventricular end-diastolic and systolic dimensions, as well as the ejection fraction were not impaired by use of these analgesic medications. CONCLUSION: Measurement of left ventricular dimensions by echocardiography allowed us to monitor the patient's response to intrathecal analgesic medications. In this patient with DCM, analgesia with intrathecal fentanyl and bupivacaine was well tolerated.

Adult↗
PubMed2004

Resveratrol, a red wine polyphenol, protects spinal cord from ischemia-reperfusion injury.

OBJECTIVE: The cardioprotective effect of red wine has been attributed to resveratrol. The resveratrol-induced protection against ischemia-reperfusion (I/R) injury has been documented in heart, kidney, and brain. Resveratrol scavenges free O(2) radicals and upregulates nitric oxide (NO). However, the presence of resveratrol-induced spinal cord protection against I/R injury has not been reported in the literature. The objective of this study was to evaluate the effects of resveratrol on neurologic functions, histopathologic changes, and NO metabolism following temporary spinal cord ischemia (SCI) in rabbits. Material and methods SCI was induced with occlusion of the infrarenal aorta in rabbits. In addition to the sham group (group S, n = 7), group C (n = 7) received vehicle 30 minutes before ischemia. Group R1 (n = 7) and R10 (n = 7) received 1 mg/kg and 10 mg/kg resveratrol instead of vehicle, respectively. Blood samples were taken to obtain nitrite/nitrate levels during the surgical procedure. After neurologic evaluation at the 48th hour of reperfusion, lumbar spinal cords were removed for histopathologic examination and malondialdehyde measurement as a marker of oxidative stress. RESULTS: Five animals in group C had paraplegia while 5 in group R10 had normal neurologic functions. The average Tarlov score of group R10 was significantly higher than that the score of group C (4.1 +/- 1.2, vs 1.2 +/- 2.2; P =.014). Histopathologic examination revealed higher neuronal viability index in group R10 compared with that of group C (0.82 +/- 0.24 vs. 0.46 +/- 0.34; P =.018). Nitrite/nitrate levels decreased in group C (from 357 +/- 20.15 micromol/L to 281 +/- 47.9 micromol/L; P <.01) whereas they increased both in group R1 and group R10 (from 287+/-28 micromol/L to 310 +/- 33.9 micromol/L and from 296 +/- 106 micromol/L to 339 +/- 87 micromol/L, respectively) during SCI. Malondialdehyde levels of group R10 was lower than those of group C (55 +/- 12.9 nmol/mg protein vs 83.9 +/- 15.1 nmol/mg protein; P =.001, respectively). CONCLUSIONS: In this model of SCI, resveratrol decreased oxidative stress, increased NO release, and protected spinal cord from I/R injury. Resveratrol-induced neuroprotection is probably mediated by its antioxidant and NO promoting properties. Before considering the clinical use of this natural antioxidant, further research is warranted about its mechanism of effects, timing, and optimum dose. CLINICAL RELEVANCE: Paraplegia that results from spinal cord ischemia is a catastrophic complication of thoracic and thoracoabdominal aorta surgical procedures. Despite several surgical modifications and pharmacologic approaches, paraplegia has not been totally eliminated. On clinical grounds, the efficiency of currently used pharmacologic agents to prevent spinal cord injury during thoracic and thoracoabdominal aorta surgery is very limited and their benefit is controversial. Preischemic infusion of resveratrol protects the spinal cord from ischemia reperfusion injury in rabbits. Following clarification of the underlying protective mechanism, optimal dose, and timing, resveratrol may used in humans as an adjunct to eliminate this catastrophic complication.

Animals↗
PubMed2005

Intravenous immunoglobulin ameliorates experimental autoimmune encephalomyelitis and reduces neuropathological abnormalities when administered prophylactically.

BACKGROUND AND METHODS: Immunomodulation with intravenous immunoglobulin (IVIG) represents a way of interfering with the disease process in multiple sclerosis (MS). In this study, the effects of IVIG on neurological symptoms and central nervous system (CNS) pathology were evaluated in experimental autoimmune encephalomyelitis (EAE), an MS animal model. EAE was induced in susceptible Dark Agouti rats by active immunization with a spinal cord homogenate, and infusions of 1 g/kg IVIG were given prophylactically or therapeutically. RESULTS: The administration of IVIG at the time of immunization significantly suppressed the development of neurological symptoms compared with infusions of placebo (mean EAE score 0.6+/-0.3 versus 2.3+/-0.4). Moreover, the prophylactic IVIG administration resulted in a significant inhibition of the inflammatory response in CNS tissue (inflammation score 1.1+/-0.2 versus 1.8+/-0.2 after placebo). No beneficial effects were obtained by therapeutic IVIG infusions as the EAE disease course and the degree of inflammation and demyelination in the CNS were not different from animals receiving treatment with placebo. CONCLUSIONS: The present study indicates that IVIG reduces the symptoms of EAE by suppression of the CNS inflammation that characterizes CNS pathology in these animals. Taking into account data from clinical trials of IVIG in MS, the results further suggest that IVIG acts primarily during the induction phase of the immune response thus preventing the development of relapses in MS.

Animals↗
PubMed2000

Development of hypertension induced by subpressor infusion of angiotensin II: role of sensory nerves.

Long-term administration of a subpressor dose of angiotensin II (Ang II) leads to pressor hyperresponsiveness and slow development of hypertension. Our preliminary data show that mRNA expression for calcitonin-gene related peptide in dorsal root ganglia was significantly increased by subpressor infusion of Ang II. To determine the role of sensory nerves in the development of hypertension induced by subpressor infusion of Ang II, newborn Wistar rats were given 50 mg/kg SC capsaicin on the 1st and 2nd days of life. After the weaning period, male rats were divided into 4 groups and subjected to the following treatments for 2 weeks: capsaicin+Ang II (150 ng. kg(-1). min(-1) SC by osmotic pumps, CAP-AII), capsaicin+vehicle (CAP), control+Ang II (CON-AII), and control+vehicle (CON). The results show that mean arterial pressure was significantly elevated in both Ang II-infused rats compared with non-Ang II-treated rats (P<0.05), and it was higher in CAP-AII than in CON-AII rats (P<0.05). The 24-hour urinary and sodium excretions were lower in CAP-AII than in CON-AII, CAP, and CON rats (P<0.05). These data demonstrated that sensory denervation exacerbates the development of hypertension and impairs renal excretory function when a subpressor dose of Ang II is given. These results indicate that activation of sensory nerves, either by Ang II or by other hormonal or hemodynamic factors, plays a compensatory role in promoting urine and sodium excretion and attenuating elevated blood pressure initiated by Ang II.

Angiotensin II↗
PubMed2002

In vivo infusions of exogenous growth factors into the fourth ventricle of the adult mouse brain increase the proliferation of neural progenitors around the fourth ventricle and the central canal of the spinal cord.

Stem cells isolated from the fourth ventricle and spinal cord form neurospheres in vitro in response to basic fibroblast growth factor (FGF2)+heparin (H) or epidermal growth factor (EGF)+FGF2 together. To determine whether these growth factor conditions are sufficient to induce stem cells within the fourth ventricle and spinal cord to proliferate and expand their progeny in vivo, we infused EGF and FGF2, alone or together, with or without H, into the fourth ventricle for 6 days via osmotic minipumps. Animals were injected with bromodeoxyuridine (BrdU) on days 4, 5 and 6 of infusion in order to label cells proliferating in response to the growth factors. Infusions of EGF+FGF2+H into the fourth ventricle resulted in the largest proliferative effect, a 10.8-fold increase in the number of BrdU+ cells around the fourth ventricle, and a 33.5-fold increase in the number of BrdU+ cells around the central canal of the spinal cord, as compared to vehicle infused controls. The majority of the cells were nestin+ after 6 days of infusion. Seven weeks post-infusion, 22 and 30% of the number of BrdU+ cells induced to proliferate after 6 days of EGF+FGF2+H infusions were still detected around the fourth ventricle and central canal of the spinal cord, respectively. Analysis of the fates of the remaining cells showed that a small percentage of BrdU+ cells around the fourth ventricle and in the white matter of the spinal cord differentiated into astrocytes and oligodendrocytes. BrdU+ neurons were not found in the brainstem or in the grey matter of the cervical spinal cord 7 weeks post-infusion. These results show that endogenous stem cells and progenitors around the fourth ventricle and central canal of the spinal cord proliferate in response to exogenously applied growth factors, but unlike in the lateral ventricle where they generate some new neurons, they only produce new astrocytes and oligodendrocytes at 7 weeks post-infusion.

Animals↗
PubMed2007

Plasma and cerebrospinal fluid concentrations of indomethacin in children after intravenous administration.

The objective of this study was to evaluate the cerebrospinal fluid (CSF) permeation of indomethacin in healthy children. The participants (n = 31, aged 4-144 months) received indomethacin (0.35 mg/kg) as a 10-minute intravenous infusion prior to surgery under spinal anaesthesia. A single CSF and plasma sample from each individual was collected 14 to 225 minutes after the infusion. Indomethacin concentrations were determined from the CSF, plasma, and protein-free plasma. Total plasma, protein-free plasma, and CSF concentrations of indomethacin ranged between 90 and 2200 ng/mL (median, 780 ng/mL), 0.3 and 0.8 ng/mL (median, 0.5 ng/mL), and 0.2 and 5.0 ng/mL (median, 1.4 ng/mL), respectively. The CSF to plasma concentration ratio remained less than 0.01. There was no correlation between the administration time and CSF concentrations. Eleven children developed 12 nonserious adverse effects, from which 5 were central nervous system (CNS) effects (agitation). In conclusion, indomethacin permeated into the CSF of children, which enables both desired and adverse CNS effects of indomethacin.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

A prospective, randomized, double-blind comparison of epidural and intravenous sufentanil infusions.

BACKGROUND: The site of action (spinal vs. central) of epidurally administered lipid-soluble opioids has been the subject of controversy. We compared the efficacy, plasma concentration and side effects of epidural and intravenously administered sufentanil for postoperative pain relief. METHODS: Using a double-blind, prospective design, 50 patients scheduled for intraabdominal operations during combined epidural-general anesthesia were randomized into one of two groups. Patients in group 1 (n = 24) received a 1-microgram/ml sufentanil infusion epidurally at 0.2 microgram.kg-1.h-1 and a saline infusion intravenously at the same rate. Patients in group 2 (n = 26) received a 1-microgram/ml sufentanil infusion intravenously at 0.2 microgram.kg-1.h-1 and a saline infusion epidurally at the same rate. Intravenous morphine sulfate was available in 2-mg increments to all patients in the postanesthesia care unit until visual analogue scale (0-100 mm) pain score was < or = 30. Then, a patient-controlled intravenous pump providing morphine on demand (1 mg with a 10-min lockout) was begun. Blood samples were drawn for sufentanil plasma levels and patients were assessed for pain, sedation and nausea for the 48 h after commencement of the infusions. RESULTS: Similar visual analogue pain, sedation, and nausea scores were found between the patients in the two groups. No differences were found in supplemental morphine requirements and plasma sufentanil concentrations between the patients in the two groups. A higher incidence of excessive sedation requiring infusion decrease was infusion decrease was found in the intravenous group (six vs. one, P < 0.05). CONCLUSIONS: Many clinical similarities were found when epidural and intravenous sufentanil infusions were compared. The higher incidence of excessive sedation in the patients receiving intravenous sufentanil could not be explained on the basis of plasma sufentanil concentrations alone. This study indicates that little clinical difference exists between epidural and intravenous administration of sufentanil.

Aged↗