Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Infusions, Spinal”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1984

Failure of IV atropine to abolish nasal irritation caused by chlormethiazole infusion in elderly patients undergoing spinal anaesthesia.

The efficacy of intravenous atropine in abolishing the nasal irritation of chlormethiazole was assessed. Forty elderly patients undergoing transurethral resection of prostate under spinal anaesthesia were studied. One ml of either atropine sulphate (0.6 mg) or normal saline was administered intravenously in a double-blind fashion 10 minutes prior to infusion of 0.8% chlormethiazole edisylate. A loading infusion of 5 ml X min-1 of the chlormethiazole solution was followed by a variable rate of infusion in order to maintain a predetermined state of sedation--i.e. where the patient lapsed into sleep but was easily awakened to obey commands. Sneezing was the commonest side-effect occurring in 45% and 70% of patients in atropine and saline groups respectively. This was not effectively abolished by IV atropine in incremental doses of 0.6 mg up to 1.8 mg. Because of the sneezing and restlessness, four patients in the atropine group required general anaesthesia to improve operating conditions. These side-effects of chlormethiazole may limit its use as a sedative for surgery in this elderly age group.

Aged↗
PubMed1997

Prevention of hypotension during spinal anaesthesia for caesarean section: ephedrine infusion versus fluid preload.

We compared the efficacy of prophylactic ephedrine infusion over fluid preloading in prevention of maternal hypotension during spinal anaesthesia for Caesarean section. Forty-six women undergoing elective Caesarean section at term were allocated randomly to receive either intravenous fluid preloading with Hartmann's solution 20 ml.kg-1 (fluid group) or prophylactic intravenous ephedrine 0.25 mg.kg-1 (ephedrine group). Moderate hypotension was defined as > or = 20% reduction in systolic blood pressure and severe hypotension as > or = 30% reduction in systolic blood pressure. Maternal uterine circulation was measured using Doppler ultrasound in 11 parturients before and after spinal anaesthesia. There was a lower incidence of severe hypotension in the ephedrine group compared with the fluid group (35% vs. 65%, p = 0.04), although the incidence of moderate hypotension was similar. Mean umbilical venous pH was higher in the ephedrine group than in the fluid group (7.33 vs. 7.29, p = 0.02) and the number of patients shivering was lower in the ephedrine group (2 vs. 9, p = 0.02). No difference was found between pre- and postspinal uterine artery pulsatility indices in either group. We conclude that prophylactic ephedrine infusion alone is at least as good as fluid preload alone in combating the hypotension associated with spinal anaesthesia for Caesarean section.

Anesthesia, Obstetrical↗
PubMed1997

BDNF prevents and reverses adult rat motor neuron degeneration and induces axonal outgrowth.

To assess the therapeutic potential of brain-derived neurotrophic factor (BDNF) in clinics, we extensively investigated the effects of BDNF on adult motor neurons in a rat spinal root avulsion model. Intrathecal administration of BDNF immediately after the spinal root avulsion greatly protected against the motor neuron cell death. BDNF also showed a protective effect on the atrophy of soma and on the reduction of transmitter-related enzymes such as choline acetyl transferase and acetylcholine esterase. Very interestingly, BDNF induced axonal outgrowth of severely damaged motor neurons at the avulsion site. The BDNF administration following 2-week treatment with phosphate-buffered saline after avulsion prevented further augmentation of cell death and reversed cholinergic transmitter-related enzyme deficiency. BDNF was demonstrated to possess a wide variety of biological effects on survival, soma size, cholinergic enzymes, and axonal outgrowth of adult motor neurons. These results provide a rationale for BDNF treatment in motor neuron diseases such as spinal cord injury and amyotrophic lateral sclerosis.

Acetylcholinesterase↗
PubMed2002

Topical application of dynorphin A (1-17) antiserum attenuates trauma induced alterations in spinal cord evoked potentials, microvascular permeability disturbances, edema formation and cell injury: an experimental study in the rat using electrophysiological and morphological approaches.

Dynorphin is a neuropeptide that is present in high quantities in the dorsal horn of the spinal cord. The peptide is actively involved in pain processing pathways. However, its involvement in spinal cord injury is not well known. Alteration in dynorphin immunoreactivity occurs following a focal trauma to the rat spinal cord. Infusion of dynorphin into the intrathecal space of the cord results in ischemia, cell damage and abnormal motor function. Antibodies to dynorphin when injected into the intrathecal space of the spinal cord following trauma improve motor recovery, reduce edema and cell changes. However, influence of dynorphin on trauma induced alteration in spinal cord bioelectrical activity is still not known. Spinal cord evoked potentials (SCEP) are good indicator of spinal cord pathology following trauma. Therefore, in present investigation, influence of dynorphin antibodies on trauma induced changes in SCEP were examined in our rat model. In addition, spinal cord edema formation, microvascular permeability disturbances and cell injury were also investigated. Our results show that topical application of dynorphin antiserum (1 : 200) two min before injury markedly attenuated the SCEP changes immediately after injury. In the antiserum treated animals, a significant reduction in the microvascular permeability, edema formation and cell injury was observed in the traumatised spinal cord. These observations suggest that (i). dynorphin is involved in the altered bioelectrical activity of the spinal cord following trauma, (ii). the peptide actively participates in the pathophysiological processes of cell injury in the spinal cord trauma, and (iii). the dynorphin antiserum has potential therapeutic value for the treatment of spinal cord injuries.

Animals↗
PubMed2004

Concentrations of propofol in cerebral spinal fluid: target-controlled infusion.

BACKGROUND: Although the performance of target-controlled infusion (TCI) have been studied extensively, the accuracy and safety of a TCI system that targets the effect site remains to be demonstrated. This study was to investigate the relations of TCI of propofol to its concentrations in cerebral spinal fluid (CSF), the effect-site concentrations and bispectral index (BIS). METHODS: Twelve mongrel dogs were used for investigations. The target effect-site concentration was set at 3 microg/ml and the infusion was lasted for 15 minutes. CSF and blood samples were then collected and propofol concentrations were determined by using high performance liquid chromatography with fluorescence detection. BIS and hemodynamic data were monitored continuously. RESULTS: The predicted plasma concentrations were generally overestimated. Median performance error (MDPE) and absolute median performance error (MDAPE) were -10.0% and 29.9% respectively. Propofol CSF concentrations were much lower than its effect-site concentrations. Changes in BIS were consistent with propofol concentrations in CSF, both of which changed direction at 5 minutes while the effect-site concentrations relatively lagged behind. Better correlation (r(2) = 0.9195) was found between BIS and CSF concentrations, when compared with that between BIS and effect-site concentrations (r(2) = 0.554). CONCLUSION: With 1% enflurane inhaled, the inconsistency of drug effect to the effect-site concentrations may result from inaccuracy of pharmacokinetic parameters. CSF may show effect-site concentrations more accurately than plasma when using target effect-site concentration infusion.

Anesthetics, Intravenous↗
PubMed1975

Effects of several beta-blockers on blood pressure in the rat.

Effects of practolol, alprenolol and pindolol on blood pressure in the rat were studied. Also effects of these three beta-blocking agents on blood pressure and heart rate in spinal rats during adrenaline infusion were studied and compared with those of propranolol. The beta-blocking agents produced a sustained pressor action in the rat, and in the spinal rat infused with adrenaline. The magnitude of the pressor action induced by the beta-blockers was in the following order: pindolol larger than or equal to propranolol larger than or equal to alprenolol greater than practolol. Minimum doses of these beta-blockers required to cause a pressor action in the spinal rat infused with adrenaline were in the following order; practolol greater than alprenolol larger than or equal to propranolol larger than or equal to pindolol. The magnitude of the pressor action produced by the same dose of these beta-blockers and minimum doses of these beta-blockers required to cause a pressor action in the spinal rat infused with adrenaline seemed to be roughly proportional to their beta-receptor blocking activities. It was concluded that the minimum doses of these beta-blockers required to cause a pressor action and the magnitude of the pressor action induced by the beta-blockers in the spinal rat infused with adrenaline could be used to compare their beta-blocking activities and that practolol, a cardioselective beta-blocker, seems to block not only cardiac beta-receptor but to some extent also peripheral vascular beta-receptors.

Adrenergic beta-Antagonists↗
PubMed1991

Plasma fibronectin and complement following infusion of colloidal solutions after spinal anaesthesia.

A randomized study of 30 patients undergoing uncomplicated surgery under spinal anesthesia was conducted to assess the influence of colloids on the kinetics of plasma fibronectin and complement. Both are opsonins of the reticuloendothelial system; moreover fibronectin is concerned with host resistance against septic complications following trauma and surgery. The patients were assigned to receive either Ringer's lactate (Group 1), gelatin (Group 2) or dextran 40 (Group 3). Blood samples were withdrawn before colloids or Ringer's infusion and during the 4 postoperative days. There was a reduction in plasma fibronectin throughout the study in groups 1 and 3, but an increase in group 2 by 24 h. The adhesion of plasma fibronectin to gelatin was maximal 1 h after infusion (44%) and remained significant up to day 2 in group 2. There was no relationship in groups 1 and 3. C3 and C4 components of complement exhibited a low value in the early post-operative period, due to hemodilution. This study shows an in vivo fibronectin-gelatin interaction, and suggests that gelatin infusion inhibits the increased shift of plasma fibronectin at the site of tissue injury after surgery.

Adult↗
PubMed2000

Continuous intrathecal fluid infusions elevate nerve growth factor levels and prevent functional deficits after spinal cord ischemia.

Continuous intracerebroventricular or intrathecal infusions of neurotrophic factors have been reported to prevent neuronal degeneration, stimulate axonal sprouting and ameliorate behavioral deficits in various models of CNS injury and aging. In the present study, the ability of intrathecal infusions of recombinant human nerve growth factor (NGF) to reduce functional deficits following spinal cord ischemia was investigated. Adult rabbits underwent intrathecal cannulation and continuous infusions of either 300 microg/ml recombinant human NGF or artificial CSF (vehicle) at a rate of 143 microl/day for 7 days prior to induction of spinal cord ischemia. Continuous infusions were maintained after induction of ischemia. Four days later, both NGF-treated and vehicle-infused subjects showed a significant amelioration of functional motor deficits compared to lesioned, non-infused subjects (P<0.05). The average duration of tolerated ischemia increased from 23.4+/-1.8 min in lesioned, non-infused subjects to 35.5+/-3.1 min in lesioned, artificial CSF-infused subjects and 35.6+/-4.7 min in NGF-infused subjects (mean+/-S.E.M.). Significantly elevated NGF protein levels were attained within the spinal cords of both NGF-treated subjects and artificial CSF-infused subjects, although levels were substantially higher in NGF-treated subjects (9.8+/-3.8 ng/g in NGF-infused vs. 2.0+/-0.4 ng/g in vehicle-infused and only 0.4+/-0.2 ng/g in lesioned, non-infused animals). These findings indicate that the process of intrathecal cannulation and fluid infusion elicits alterations in the spinal cord environment that are neuroprotective, including spontaneous elevations in NGF levels.

Animals↗
PubMed1982

Tolerance and cross tolerance to morphine after chronic spinal D-Ala2-D-Leu5-enkephalin infusion.

The development of tolerance and cross tolerance to morphine at spinal cord levels on the tall flick inhibition was studied in rats tolerant to D-Ala2-D-Leu5-enkephalin (DADL). The long term intrathecal infusion of DADL was accomplished by means of osmotic minipumps. Chronic intrathecal infusion of DADL for 5 days caused a shift of dose response curves of both DADL and morphine sulfate injected intrathecally to the right indicating that tolerance and cross tolerance to morphine had developed after long term intrathecal infusion of DADL. The shift of the dose response curve of DADL was parallel, whereas that of morphine was non-parallel and flattening. Concomitant intrathecal infusion of naloxone which was more sensitive in blocking mu-opioid receptor than delta-opioid receptor blocked the development of cross tolerance to morphine while the development of tolerance to DADL was left unaffected. The studies present the evidence that two types of opioid receptors, delta- and mu-opioid in the spinal cord of rats are involved in the development of tolerance by chronic DADL exposure.

Animals↗
PubMed2004

Simultaneous development of bilateral retrobulbar and intradural spinal masses following donor lymphocyte infusions for acute lymphoblastic leukemia relapsing after bone marrow transplantation.

The authors describe a 6-year-old boy with acute lymphoblastic leukemia in relapse after bone marrow transplantation. Complete remission was obtained after reinduction chemotherapy followed by donor lymphocyte infusions. Ten months later, right-sided proptosis and exotropia developed, with back pain and leg paralysis. Computed tomography revealed bilateral orbital masses. Magnetic resonance imaging demonstrated abnormal signal intensity in the T4-6 vertebral bodies and an intradural mass on the left posterior side of the spinal canal. Although bone marrow aspiration was negative, orbital mass biopsies revealed CD10-positive lymphoblasts. Chimerism analysis of bone marrow and peripheral blood showed full donor alleles. Local radiotherapy and chemotherapy resulted in neurologic improvement.

Bone Marrow↗
PubMed1998

Schwann cells genetically modified to secrete human BDNF promote enhanced axonal regrowth across transected adult rat spinal cord.

The infusion of BDNF and NT-3 into Schwann cell (SC) grafts promotes regeneration of brainstem neurones into the grafts placed in adult rat spinal cord transected at T8 (Xu et al., 1995b). Here, we compared normal SCs with SCs genetically modified to secrete human BDNF, grafted as trails 5 mm long in the cord distal to a transection site and also deposited in the transection site, for their ability to stimulate supraspinal axonal regeneration beyond the injury. SCs were infected with the replication-deficient retroviral vector pL(hBDNF)RNL encoding the human preproBDNF cDNA. The amounts of BDNF secreted (as detected by ELISA) were 23 and 5 ng/24 h per 106 cells for infected and normal SCs, respectively. Biological activity of the secreted BDNF was confirmed by retinal ganglion cell bioassay. The adult rat spinal cord was transected at T8. The use of Hoechst prelabelled SCs demonstrated that trails were maintained for a month. In controls, no SCs were grafted. One month after grafting, axons were present in SC trails. More 5-HT-positive and some DbetaH-positive fibres were observed in the infected vs. normal SC trails. When Fast Blue was injected 5 mm below the transection site (at the end of the trail), as many as 135 retrogradely labelled neurones could be found in the brainstem, mostly in the reticular and raphe nuclei (normal SCs, up to 22, mostly in vestibular nuclei). Numerous neurones were labelled in the ventral hypothalamus (normal SCs, 0). Also, following Fast Blue injection, a mean of 138 labelled cells was present in dorsal root ganglia (normal SCs, 46) and spinal cord (39 vs. 32) rostral to the transection. No labelled spinal neurones rostral to the transection were seen when SCs were not transplanted. Thus, the transplantation of SCs secreting increased amounts of BDNF improved the regenerative response across a transection site in the thoracic cord. Moreover, the enhanced regeneration observed with infected SCs may be specific as the largest response was from neurones known to express trkB.

Adult↗
PubMed2026

Comparison of a Modified Regimen of Prophylactic Phenylephrine Boluses Versus Variable Rate Infusion During Elective Cesarean Delivery Under Spinal Anesthesia: A Noninferiority Randomized Double-Blind Study.

BACKGROUND: Prophylactic phenylephrine boluses have been found to be as effective as variable rate infusions during elective cesarean delivery but require a higher number of physician interventions to maintain blood pressure near baseline values. Therefore, there is a need to find a feasible regimen of bolus administration that is equally efficacious to the infusion regimen while at the same time requires a comparable number of physician interventions and is thus non-inferior to the infusion regimen. METHODS: Healthy pregnant women with term, uncomplicated, singleton pregnancies undergoing elective cesarean delivery under spinal anesthesia were randomly divided into two groups. The Bolus group received a phenylephrine bolus 100 &#x3bc;g immediately after spinal anesthesia and then at every systolic blood pressure value <90% of the baseline. The infusion group received a prophylactic variable-rate infusion of phenylephrine beginning at 50 &#x3bc;g/min and titrated to maintain systolic blood pressure at 90-99% of baseline. The primary outcome was the number of physician interventions needed to maintain the target systolic blood pressure; the secondary outcomes included phenylephrine requirements, incidence of hypotension/hypertension/bradycardia, umbilical arterial and venous blood gas analysis, Apgar scores, and maternal complications. The primary outcome was analyzed in terms of non-inferiority using a non-inferiority margin of two interventions. RESULTS: Eighty patients were included in the study. The median (interquartile range [IQR]) number of physician interventions was 6 (5-8) in the infusion group and 3 (2-4) in the bolus group (P < .001). The difference of medians (95% confidence interval [CI]) between the two groups was -3 (-4 to -2). Phenylephrine requirements were higher in the infusion group (630 [426-765] &#x3bc;g) compared to the bolus group (300 [200-400] &#x3bc;g; P < .001). Blood pressure was higher at certain time points in the infusion group, but overall accuracy of blood pressure control was not different between the groups. Incidence of hypotension, hypertension, and bradycardia, neonatal outcomes, and maternal complications did not differ between the groups. CONCLUSIONS: The modified regimen of prophylactic boluses is non-inferior to variable rate prophylactic phenylephrine infusion in terms of physician interventions needed to maintain systolic blood pressure within the target range and maternal and neonatal outcomes.

Humans↗
PubMed1988

Neurologic deficits and neuronal injury in rats resulting from nonopioid actions of the delta opioid receptor antagonist ICI 174864.

The delta opioid receptor antagonist ICI 174864 produces postural abnormalities and barrel rolling after i.c.v. injection and hindlimb and tail flaccidity after spinal subarachnoid injection in rats. These effects appear to result from nonopioid characteristics of ICI 174864 because they are neither shared nor blocked by other opioid antagonists (naloxone, ICI 154129 and WIN 44,441-3) and are produced by two compounds (ICI 174644 and ICI 178173) that are structurally related to ICI 174864 but lack its delta antagonist properties. Barrel rolling and hindlimb paralysis are also produced by dynorphin A-related peptides; however, rats failed to demonstrate tolerance or cross-tolerance to the hindlimb paralytic actions of ICI 174864 or dynorphin A (1-13) after 7 days of continuous spinal intrathecal infusion of either of these compounds. Whereas hindlimb responses to low doses of ICI 174864 (1.6-6.2 nmol intrathecally) were usually transient, higher doses (6.2-25 nmol intrathecally) produced persistent hindlimb motor dysfunction, altered nociception, priapism, hindlimb edema, bladder infarction and atony and urinary incontinence. Neuronal and axonal changes in the lumbosacral spinal cords of rats with persistent and transient neurologic deficits provided direct evidence of the neuropathologic actions of ICI 174864 (3.1 and 6.2 nmol) and ICI 174644 (25 nmol). These results indicate that 1) use of ICI 174864 as a selective delta opioid receptor antagonist is potentially compromised by its nonopioid neuropathologic actions and 2) ICI 174864 and dynorphin A-related peptides are unique among opioid agonists and antagonists in sharing barrel rolling and hindlimb paralytic effects. A similar mechanism of action may underlie the shared nonopioid actions of these peptides.

Animals↗
PubMedDate not supplied

Regression pattern of amplitude of electrocardiographic waves during intravenous infusion in intact, buffer nerve denervated and spinal dogs.

Electrocardiographic (ECG) amplitude changes during clinically feasible rate of infusion of normal saline (NS), Ringer-Locke (RL) solution and tender coconut water (TCW) upto a dose of 100 ml/kg in paraldehyde (PLD) and chloralose and urethane (C&U) anaesthetised dogs were studied. The infusion caused a net decrease in P and QRS amplitudes but had varied effect on T wave amplitude in intact PLD and C&U anaesthetised dogs. Infusion of RL in vagotomised and/or carotid sinus (CS) denervated dogs and in spinal dogs indicated that these neural pathways had a significant effect on basal amplitude of ECG waves but their influence on infusion induced ECG changes was only marginal; in this the vagi seem to have a greater influence than the other pathways. The T wave changes during infusion were independent of simultaneous P and QRS changes and appeared to depend on the ionic composition of the infusion fluid. TCW infusion was very well tolerated, particularly by the C&U anaesthetised dogs. It would seem that the evaluation of ECG from patients on parenteral fluid be done in the context of the present observation that infusion per se decreases the amplitude of ECG.

Animals↗
PubMed1988

A comparison of propofol and midazolam by infusion to provide sedation in patients who receive spinal anaesthesia.

Twenty patients scheduled for orthopaedic surgery under spinal anaesthesia received by intravenous infusion either 1% propofol or 0.1% midazolam at a rate adjusted to maintain adequate sedation as judged on a five-point scale. No other anaesthetic or analgesic drugs were given. The mean time to reach the required level of sedation was similar in both groups and the quality and ease of control of sedation were good in all patients. Mean infusion rates were 3.73 mg/kg/hour for propofol and 0.27 mg/hg/hour for midazolam. Airway maintenance was excellent and there were no side effects other than restlessness of the arms in one patient in each group. Recovery, judged by ability to open the eyes and recall date of birth, was significantly more rapid after propofol than after midazolam (2 and 10 minutes respectively after the end of infusion) and two patients in the latter group were unduly drowsy in the initial postoperative period. Pre- and postoperative amnesia were greater in the midazolam group but no patient had recall of peri-operative events. Psychometric tests showed significantly better recovery of higher mental function after propofol for up to 2 hours after surgery.

Anesthesia Recovery Period↗
PubMed2002

The neuropeptide FF analogue, 1DMe, reduces in vivo dynorphin release from the rat spinal cord.

Intrathecal infusion of the neuropeptide FF analogue, [D-Tyr1, (NMe)Phe3]neuropeptide FF (1DMe; 0.1 microm-0.1 mm) in anaesthetized rats produced a concentration-dependent decrease in the spinal outflow of dynorphin A (1-8)-like material, which persisted for at least 90 min after treatment with 10 microm-0.1 mm of the compound. Co-administration of d-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP; 1 microm) to block spinal micro-opioid receptors did not modify this effect, whereas naltrindole (10 microm) totally prevented it and nor-binaltorphimine (10 microm) reduced the post-effect. These data suggest that 1DMe triggers the release of endogenous opioids that stimulate mainly delta-opioid receptors, and secondarily kappa-opioid receptors, thereby exerting a negative influence on dynorphin A (1-8)-like material outflow. Because dynorphin has pronociceptive properties, such a decrease in spinal dynorphin A (1-8)-like material release might underlie the long-lasting antinociceptive effects of intrathecally administered neuropeptide FF and analogues.

Animals↗
PubMed2001

Recovery after high-dose methylprednisolone and delayed evacuation: a case of spinal epidural hematoma.

Spinal epidural hematoma (SEH) is rare and not without serious sequelae. We report a patient who developed Brown-Séquard syndrome from SEH after fluoroscopic-guided cervical steroid injection and favorable response to methylprednisolone (MP). A 56-year-old man reported immediate sharp shooting pain to the upper extremities on introduction of epidural toughy needle. A total of 5 mL of 0.2% ropivacaine and 120 mg methylprednisolone acetate suspension was administered at the C6-7 interspace. Within half an hour, a neurologic deficit occurred at C7-8 and right Brown-Séquard syndrome developed. Once SEH was suspected (3 hours after onset of neurologic deficit), a protocol of high-dose MP intravenous infusion was initiated. Immediate incomplete recovery of motor, sensory, and sphincteric functions was noted within 30 minutes of infusion. Emergency spinal C6-T2 bilateral decompressive laminectomies and evacuation SEH were performed within an expected delay (10 hours from the onset of neurologic deficit). Fluoroscopic guidance does not take the place of adherence to meticulous technique. An unexplained neurologic deficit after invasive spinal procedures should raise the concern for SEH. Early recognition and emergent evacuation remain the mainstay management for SEH. This case suggests some neuroprotection from MP in cases of cervicothoracic cord compression secondary to traumatic SEH. When potential risks for SEH exist, it is advisable not to administer local anesthetic so as not to interfere with neurologic assessment and delaying the diagnosis.

Anti-Inflammatory Agents↗