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PubMed1996

Initial stabilization and medical management of acute spinal cord injury.

Despite intensive preventive efforts, acute spinal cord injury remains a significant public health problem. The pathophysiology of this type of injury involves both the primary, or initial, mechanical injury and secondary injury mechanisms such as ischemia, lipid peroxidation and intracellular calcium influx. Initial management includes immobilization of the injured spine, maintenance of the airway, systemic oxygen delivery and treatment of neurogenic shock. All patients with acute spinal cord injury should receive an intravenous bolus of methylprednisolone, 30 mg per kg, within eight hours of injury, followed by an infusion of 5.4 mg per kg per hour for 23 hours. Transfer to a regional acute spinal cord injury unit for definitive management should be accomplished as soon as the patient's condition is stabilized.

Acute Disease↗
PubMed1989

Spinal vs. supraspinal sites of action of the alpha 2-adrenergic agonists clonidine and ST-91 on the acoustic startle reflex.

Previous work has shown that stimulation of alpha 2-adrenergic receptors depresses the startle responses in rats. The present study suggests that this depressant effect involves supraspinal rather than spinal alpha 2-adrenergic receptors because intraventricular but not intrathecal infusion of the hydrophilic alpha 2-adrenergic agonist ST-91 depressed the acoustic startle reflex. To determine the point in the acoustic startle pathway where alpha 2-adrenergic receptor activation might ultimately alter neural transmission, startle responses were elicited electrically from different points along the acoustic startle pathway after systemic administration of clonidine. Clonidine depressed acoustically-elicited startle and startle elicited by electrical stimulation of the ventral cochlear nucleus to a comparable magnitude and over a similar time course. It also partially depressed startle elicited by electrical stimulation of the nucleus reticularis pontis caudalis (RPC). Taken together, these data suggest that alpha 2-adrenergic stimulation depresses startle by acting on supraspinal receptors, but that this effect is ultimately expressed, at least in part, by actions at both spinal and brainstem levels of the acoustic startle response pathway. The results are compared to other drugs known to affect the startle reflex.

Acoustic Stimulation↗
PubMed1987

Intraosseous infusion flow rates in hypovolemic "pediatric" dogs.

We tested a 20-gauge, 2 1/2-inch spinal needle and a 13-gauge, 3 1/2-inch bone marrow needle with Ringer's lactate delivered by gravity and 300 mm Hg pressure in vitro and in hypovolemic puppies to ascertain in vivo intraosseous flow rates and to determine the effects of catheter size and anatomic factors on flow rate. In vitro flow was significantly faster than in vivo flow (P = .001). In vivo, mean flow rates were 11 mL/min for the 20-gauge needle and 13 mL/min for the 13-gauge needle by gravity. The mean flows by 300 mm Hg pressure for the same needles were 24 mL/min and 29 mL/min. While the in vivo flow rates were significantly greater for the 13-gauge versus the 20-gauge needle, the differences were not clinically significant (2 mL/min difference by gravity and 5 mL/min difference by pressure). The clinically comparable in vivo rates for the two needles tested indicated that the rates are dependent on flow through the bone marrow rather than the size of the needle. The data suggest that while intraosseous infusion is a rapid technique for gaining vascular access, the flow rates achieved may not be sufficient for the definitive treatment of severe hypovolemic or hemorrhagic shock alone.

Animals↗
PubMed2000

Survival effects of BDNF and NT-3 on axotomized rubrospinal neurons depend on the temporal pattern of neurotrophin administration.

This study shows that both BDNF and NT-3 can prevent cell death in axotomized adult rat rubrospinal neurons (RSNs), but that the efficacy of neuroprotection depends on the temporal pattern of treatment. At 8 weeks after cervical spinal cord injury, 51% of the RSNs had died. Subarachnoidal BDNF infusion into the cisterna magna for 4 weeks resulted in neuronal hypertrophy and 71% survival. Continuous infusion for 8 weeks into the lumbar subarachnoidal space with either BDNF or NT-3 gave similar survival rates, while a combination of BDNF and NT-3 resulted in 96% survival, although the cells were atrophic. When administration of either BDNF or NT-3 was delayed and performed during postoperative weeks 5-8, the number of surviving neurons was increased compared to early treatment. Delayed treatment with a combination of BDNF and NT-3 resulted in complete survival and a reduction in neuronal atrophy. A decreased expression of TrkB receptors and microtubule-associated protein-2 in the RSNs after axotomy was counteracted by BDNF and NT-3. Microglial activity remained increased even when complete cell survival was achieved. Thus, the combination of neurotrophins as well as the temporal pattern of treatment need to be adequately defined to optimize survival of injured spinal tract neurons.

Afferent Pathways↗
PubMed1999

The neuroprotective effects of intrathecal administration of the selective N-type calcium channel blocker ziconotide in a rat model of spinal ischemia.

PURPOSE: Spinal cord ischemia and resulting paraplegia represent a major complication associated with surgical repair of the thoracoabdominal aorta. Although the mechanism of spinal neuronal degeneration during ischemia is unclear, it may involve excessive calcium influx via N-type voltage-sensitive calcium channels (VSCCs). The neuroprotective capacity of intrathecal (IT) administration of the selective N-type VSCC blocker ziconotide, previously shown to be potently analgesic, was studied. METHODS: In a rat aortic occlusion model, spinal cord ischemia was induced for 8, 9, or 10 minutes by occluding the descending thoracic aorta. Ziconotide was administered IT as (1) a continuous infusion of 300 or 600 ng/kg/h initiated 24 hours before ischemia and continuing an additional 24 hours or (2) a 0.3 microgram bolus injected 45 minutes before the induction of ischemia. Animals were allowed to live for 24 hours, and recovery of motor function was evaluated during this period. Spinal cords were processed using a silver impregnation technique and microtubule-associated protein type II (MAP2) immunohistochemistry. RESULTS: Continuous IT infusion of ziconotide provided significant protection against 8- and 9-minute occlusions, but not 10-minute occlusions, as indicated by recovery of motor function, degree of spinal neuronal degeneration, and loss of MAP2 immunoreactivity. Acute IT pretreatment with ziconotide provided transient protection during the initial 4 hours of reperfusion; however, this protective effect was no longer present at 24 hours. CONCLUSION: These data implicate N-type VSCC activation in spinal neuronal degeneration caused by transient spinal ischemia, because selective blockade of this channel by continuous IT infusion of ziconotide was protective against injurious intervals of spinal ischemia. Based on these findings, ziconotide may provide both neuroprotection and preemptive analgesia for aortic aneurysm surgery.

Analysis of Variance↗
PubMed2003

Intravenous administration of human umbilical cord blood cells in a mouse model of amyotrophic lateral sclerosis: distribution, migration, and differentiation.

Amyotrophic lateral sclerosis (ALS), a multifactorial disease characterized by diffuse motor neuron degeneration, has proven to be a difficult target for stem cell therapy. The primary aim of this study was to determine the long-term effects of intravenous mononuclear human umbilical cord blood cells on disease progression in a well-defined mouse model of ALS. In addition, we rigorously examined the distribution of transplanted cells inside and outside the central nervous system (CNS), migration of transplanted cells to degenerating areas in the brain and spinal cord, and their immunophenotype. Human umbilical cord blood (hUCB) cells (10(6)) were delivered intravenously into presymptomatic G93A mice. The major findings in our study were that cord blood transfusion into the systemic circulation of G93A mice delayed disease progression at least 2-3 weeks and increased lifespan of diseased mice. In addition, transplanted cells survived 10-12 weeks after infusion while they entered regions of motor neuron degeneration in the brain and spinal cord. There, the cells migrated into the parenchyma of the brain and spinal cord and expressed neural markers [Nestin, III Beta-Tubulin (TuJ1), and glial fibrillary acidic protein (GFAP)]. Infused cord blood cells were also widely distributed in peripheral organs, mainly the spleen. Transplanted cells also were recovered in the peripheral circulation, possibly providing an additional cell supply. Our results indicate that cord blood may have therapeutic potential in this noninvasive cell-based treatment of ALS by providing cell replacement and protection of motor neurons. Replacement of damaged neurons by progeny of cord blood stem cells is probably not the only mechanism by which hUCB exert their effect, since low numbers of cells expressed neural antigens. Most likely, cord blood efficacy is partially due to neuroprotection by modulation of the autoimmune process.

Alanine↗
PubMed2002

Opioid agonists differentially regulate mu-opioid receptors and trafficking proteins in vivo.

Chronic opioid agonist treatment produces tolerance and in some cases opioid receptor internalization and down-regulation. Both morphine and etorphine induce tolerance; however, only etorphine produces mu-opioid receptor (muOR) down-regulation. In vitro studies implicate dynamin-2 (DYN-2) and G-protein receptor kinase-2 (GRK-2) in these processes. Therefore, we examined etorphine and morphine effects on regulation of GRK-2 and DYN-2 in mouse spinal cord. Mice were treated for 7 days with etorphine (200 microg/kg/day infusion) or morphine (40 mg/kg/day infusion + one 25-mg implant pellet). Controls were implanted with a placebo pellet. On the 7th day after implantation mice were tested for i.t. [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) analgesia. In other mice, spinal cord was removed for [(3)H]DAMGO binding studies or GRK-2 and DYN-2 protein and mRNA abundance were determined. Both etorphine and morphine produced significant tolerance (ED(50) shift = 7.6- and 7.3-fold for morphine and etorphine, respectively). Etorphine decreased spinal muOR density by approximately 30%, whereas morphine did not change muOR density. Etorphine increased ( approximately 70%) DYN-2 protein abundance and decreased its mRNA (31%), whereas it had no effect on GRK-2 protein and mRNA abundance. Morphine had no effect on either DYN-2 or GRK-2 protein or mRNA abundance. These data raise the possibility that unequal receptor regulation by etorphine and morphine might be due to differential regulation of trafficking proteins. Overall, receptor down-regulation associated with chronic etorphine treatment may accelerate dynamin-related activity. Finally, the decrease in DYN-2 mRNA may be related to stabilization of DYN-2 protein abundance, which might inhibit transcription.

Analgesics, Opioid↗
PubMed1979

Bronchial angiography and intraarterial chemotherapy with mitomycin-C in bronchogenic carcinoma. Anatomy, technique, complications.

Bronchial angiography and intraarterial infusion of mitomycin-C were successfully performed in 39 of 47 patients with bronchogenic carcinoma. More than one course was given to several patients. No neurologic complications occurred and the side effects were insignificant. The pertinent anatomy of the bronchial and spinal arteries is summarized and a comprehensive description of the angiography and infusion technique is given. It is important that the infused artery is not occluded by the catheter and that the drug is properly diluted to avoid complications. The method appears to be of therapeutic value in the treatment of pulmonary carcinoma.

Aged↗
PubMed1989

Cholinergic systems in the rat brain: IV. Descending projections of the pontomesencephalic tegmentum.

Descending projections from cholinergic neurons in the pedunculopontine and laterodorsal tegmental nuclei, collectively referred to as the pontomesencephalotegmental (PMT) cholinergic complex, were studied by use of the fluorescent retrograde tracers fluorogold, true blue, or Evans Blue in combination with choline acetyltransferase (ChAT) immunohistochemistry of acetylcholinesterase (AChE) pharmacohistochemistry. Pedunculopontine somata positive for ChAT or staining intensely for AChE were retrogradely labeled with fluorescent tracers following infusions into the motor nuclei of cranial nerves 5, 7, and 12. ChAT-positive cells in both the pedunculopontine and laterodorsal tegmental nuclei demonstrated projections to the vestibular nuclei, the spinal nucleus of the 5th cranial nerve, deep cerebellar nuclei, pontine nuclei, locus ceruleus, raphe magnus nucleus, dorsal raphe nucleus, median raphe nucleus, the medullary reticular nuclei, and the oral and caudal pontine reticular nuclei. Fluorescent tracers used in combination with AChE pharmacohistochemistry corroborated these projections and, in addition, provided evidence for cholinergic pontomesencephalic projections to the lateral reticular nucleus and inferior olive. The majority of retrogradely labeled neurons demonstrating ChAT-like immunoreactivity were found ipsilateral to the injection site, but, in all cases, tracer-containing cholinergic cells contralateral to the infused side of the brain were detected also. More retrogradely labeled cells containing ChAT were observed in the pedunculopontine tegmental than in the laterodorsal tegmental nucleus following tracer injections at all sites with the exceptions of the locus ceruleus and dorsal raphe nucleus where the converse profile was observed. None of the pedunculopontine or laterodorsal tegmental cells immunopositive for ChAT or stained intensely for AChE contained retrogradely transported tracers following dye infusions into the cerebellar cortex or cervical spinal cord. Triple-label experiments using two tracers infused into different sites in the same animal revealed that individual ChAT-immunoreactive cells in the PMT cholinergic complex projected to more than one hindbrain site in some cases and had ascending projections as well. Certain ChAT-positive somata in the pedunculopontine and laterodorsal tegmental nuclei were found in close association with several fiber tracts, including the superior cerebellar peduncle, lateral lemniscus, dorsal tegmental tract, and medial longitudinal fasciculus.

Acetylcholinesterase↗
PubMed2005

[Advantage of ropivacaine for postoperative epidural analgesia following leg orthopedic surgery].

BACKGROUND: Epidural administration of local anesthetics may lead to effective pain relief. However, tachyphylaxis or other problems following prolonged epidural anesthesia may develop and in many cases difficulties exist in the maintenance of the similar degree of sensory blockade. The present study was therefore performed to investigate the analgesic effect of continuous postoperative epidural infusion of ropivacaine with fentanyl in comparison with that of bupivacaine or ropivacaine alone. METHODS: After leg orthopedic surgery with lumbar combined spinal-epidural anesthesia, thirty-six patients were randomized to one of the three postoperative epidural infusion groups: bupivacaine 0.125%, ropivacaine 0.2%, or ropivacaine 0.2% with 2.2 microg x ml(-1) (400 microg x 180 ml(-1)) of fentanyl. Continuous epidural infusion was started at a rate of 6 ml x h(-1) with possibility of an additional bolus injection of 3 ml at least every 60 min. Pain was assessed using a 10-cm visual analog scale (VAS) just before and 15 min after epidural bolus injections, and 15-20 h after the start of continuous epidural infusion as the severe at pain through the observation. The spread of analgesia (loss of sharpness in pinprick perception) and motor block (Bromage scale) were evaluated bilaterally. Systolic and diastolic blood pressure and heart rate were also measured. RESULTS: The epidural bolus infusion was associated with a significant decrease of VAS (P < 0.001) and stable blood pressure and heart rate in all groups. The maximal VAS in patients receiving 0.2% ropivacaine+fentanyl was significantly less compared to that in the other two groups. The regression of sensory blockade was significantly prolonged in patients treated with ropivacaine+fentanyl. There was no significant difference in the spread of sensory analgesia between 20 min and 15-20 h after the continuous epidural anesthesia in this group. None of the patients developed adverse effects such as respiratory depression, nausea, and pruritus. CONCLUSIONS: Epidural injection of ropivacaine with fentanyl decreased postoperative pain with stable vital signs in patients undergoing leg orthopedic surgery, as compared to bupivacaine or ropivacaine alone, possibly because of the maintenance of sensory blockade by ropivacaine and enhancement of this sensory blockade by fentanyl.

Adult↗
PubMed1981

Transfer of pethidine to CSF following intravenous administration.

To help delineate the contributions to analgesia evoked by central and spinal opiate receptors, pethidine was administered intravenously to dogs by bolus followed by infusion. Plasma and cerebrospinal fluid were sampled and assayed for pethidine. Cerebrospinal fluid concentrations followed a similar time course to plasma but with lower concentrations. The average cerebrospinal fluid:plasma ratio was 0.4 and resembled the fraction of unbound pethidine in plasma. It was concluded that cerebrospinal fluid concentrations after intravenous administration were so low that spinal action would be unlikely.

Animals↗
PubMed1984

Tachycardia, hypertension and decreased reflex bradycardia produced by striatal lesions induced by kainic acid.

The effects of intra-striatal injection of kainic acid on cardiovascular function were assessed in urethane-anesthetized rats. Intra-striatal administration of 2 micrograms of kainic acid (in a volume of 0.5 microliter) produced both tachycardia and hypertension. The tachycardia induced by intra-striatal injection of kainic acid was antagonized by either prior bilateral vagotomy or spinal transection of the animals (at C7). On the other hand, the hypertension induced by intra-striatal administration of kainic acid was antagonized by prior bilateral vagotomy, but not spinal transection. In addition, reflex bradycardia was produced by intravenous infusion of adrenaline in rats. Over the dose range (1.25-5.0 micrograms/kg, i.v.) of adrenaline used, a dose-dependent bradycardia was obtained. It was found that pretreatment of animals with intra-striatal injection of kainic acid, although causing no change in the adrenaline-induced pressor effect, did reduce the adrenaline-induced bradycardia. Intravenous administration of same dose of kainic acid had no effect on these cardiovascular responses. Thus, the data indicate that striatal neurones are involved in the central control of cardiovascular function.

Animals↗
PubMed1999

A case of spinal cord compression syndrome by a fibrotic mass presenting in a patient with an intrathecal pain management pump system.

A 45-year-old woman presented with increasing low back pain, progressive anesthesia in her lower extremities and difficulty ambulating. She had a history of chronic low back pain problems for which, 26 months earlier, she had an intrathecal infusion pump permanently placed for pain and spasm control. Urgent magnetic resonance imaging (MRI) of the lumbar spine revealed a mass at the site of the tip of the intrathecal catheter with high grade spinal cord compression at the level of L-1. At surgical laminectomy the compressing lesion was found to be a reactive tissue fibroma. As more patients receive these devices the physician should consider cord compression syndrome in patients presenting with symptoms of increasing low back pain, anesthesia and progressive proprioceptive loss.

Anesthesia, Spinal↗
PubMed2006

Bladder overactivity and hyperexcitability of bladder afferent neurons after intrathecal delivery of nerve growth factor in rats.

Nerve growth factor (NGF) has been proposed as an important mediator inducing bladder overactivity under pathological conditions such as spinal cord injury, bladder outlet obstruction, or cystitis. We therefore examined the effects of chronic NGF treatment on bladder activity and the properties of bladder afferent neurons. In adult female rats, NGF (2.5 microg/microl) was infused continuously into the intrathecal space at the L6-S1 level of spinal cord for 1 or 2 weeks using osmotic pumps (0.5 microl/h). Bladder afferent neurons were labeled with axonal transport of Fast Blue injected into the bladder wall. After intrathecal injection of NGF, cystometrograms under an awake condition showed bladder overactivity revealed by time-dependent reductions in intercontraction intervals and voided volume. ELISA analyses showed significant increases in NGF levels in L6-S1 dorsal root ganglia of NGF-treated rats. In patch-clamp recordings, dissociated bladder afferent neurons exhibiting tetrodotoxin (TTX)-resistant action potentials from NGF-treated animals were larger in diameter and had significantly lower thresholds for spike activation compared with sham rats. In addition, the number of TTX-resistant action potentials during 600 ms depolarizing pulses was significantly increased time dependently after 1 or 2 weeks of NGF application. The density of slowly inactivating A-type K+ currents was decreased by 52% in bladder afferent neurons with TTX-resistant spikes after 2 week NGF treatment. These results indicate that increased NGF levels in bladder afferent pathways and NGF-induced reduction in A-type K+ current density could contribute to the emergence of bladder overactivity as well as somal hypertrophy and hyperexcitability of bladder afferent neurons.

Animals↗
PubMed1989

[Superselective bronchial arterial catheterization via a sheath catheter (SS-BAC)].

Bronchial artery infusion therapy including embolization of the artery has been widely used in the treatment of lung cancer and also for the treatment of hemoptysis due to various lung diseases. However, some serious complications such as spinal cord lesion, tracheobronchial fistula formation and so on have been documented in the literature and these complications are attributed to anatomical characteristics of the bronchial artery having a common trunk with feeding arteries to the spinal cord, esophagus and trachea. To prevent these hazardous events we attempted to infuse and embolize the proper bronchial artery with high selectivity by using catheter-in-catheter technique. A Cook green catheter, 7.2 Fr. size, was wedged in the intercostobronchial trunk artery by a Seldinger technique and then a small catheter, 3.0 Fr. size, was passes through the former catheter to the proper bronchial artery beyond the orifices of other feeding arteries. In 26 out of 30 patients who underwent this procedure we successfully performed this superselective bronchial artery catheterization and the 26 patients consisted of 15 patients with lung cancer and one with metastatic lung tumor who were treated with bronchial artery infusion therapy and ten with various lung diseases who were treated with bronchial artery embolization because of hemoptysis. Bronchial artery infusion therapy including embolization has gained higher safety and effectiveness by means of this superselective catheterization.

Adult↗
PubMed1989

The syndrome of inappropriate antidiuretic hormone secretion and its effect on blood indices following spinal fusion.

Red blood cell indices in four adolescent and preadolescent patients with documented inappropriate antidiuretic hormone secretion (SIADH) following spinal fusion were examined for evidence of dilution. The blood indices in these preoperative patients demonstrated evidence of dilution on both the intracellular and extracellular levels. The major factors causing these dilutional effects were elevated ADH, intravenous fluid overloading, and mobilization of "third space" fluids. It appears that extracellular dilution secondary to these factors results in spuriously low blood indices (namely, hemoglobin, hematocrit, and red blood cells) during the postoperative period. These findings suggest that an awareness of SIADH and avoiding intravenous fluid overloads by accurately managing intraoperative and postoperative fluids will decrease the dilutional effects observed on blood indices and perhaps save patients from unwarranted transfusions.

Adolescent↗
PubMed2003

Intraputamenal infusion of GDNF in aged rhesus monkeys: distribution and dopaminergic effects.

Site-specific delivery of trophic factors in the brain may be important for achieving therapeutic efficacy without unwanted side effects. This study evaluated the site-specific infusion of glial cell line-derived neurotrophic factor (GDNF) into the right putamen of aged rhesus monkeys. After 4 weeks of continuous infusion at a rate of 22.5 microg/day, GDNF had diffused up to 11 mm from the catheter openings in the putamen into the rostral putamen, internal capsule, external capsule, caudate nucleus, and globus pallidus. Anisotropic flow along the external capsule tracts carried GDNF into the anterior amygdaloid area. Backflow of GDNF along the catheter track from the frontal cortex infiltrated juxtaposed corpus callosal and cortical tissue. GDNF was carried by retrograde transport to dopamine neurons in the ipsilateral substantia nigra, stimulating an 18% increase in the number of tyrosine hydroxylase (TH)-positive dopamine neurons and a 28% increase in dopamine neuron perikaryal size. Also, TH-positive fiber density was increased in the ipsilateral globus pallidus, caudate nucleus, and putamen. Anatomic effects from GDNF stimulation of the dopaminergic system were restricted to the ipsilateral hemisphere. Retrograde GDNF labeling was also present in a few TH-positive neurons in the locus coeruleus and a large cluster of TH-negative neurons in the ventral anterior thalamus. Anterograde transport of GDNF was evident in axons in the pyramidal tract from the cerebral peduncle to the caudal spinal cord. Tissue injury from the intraparenchymal catheter and continuous infusion was confined primarily to a narrow zone surrounding the track and was mild to moderate in severity.

Aging↗
PubMed2003

The effects of volatile anesthetics on nonadrenergic, noncholinergic depressor responses in rats.

UNLABELLED: The effects of volatile anesthetics on nonadrenergic, noncholinergic (NANC) transmission mediated by calcitonin gene-related peptide (CGRP) are unclear. We studied the effects of isoflurane, halothane, and sevoflurane on NANC depressor responses to electrical spinal cord stimulation in pithed rats whose mean arterial blood pressure was maintained near 120 mm Hg by continuous infusion of methoxamine. Autonomic outflow was blocked by hexamethonium. After 30 min of inhalation of different concentrations of anesthetics, spinal cord stimulation at the lower thoracic level (10 V at 4 Hz; duration, 1 ms) was applied for 30 s to induce a NANC depressor response. Isoflurane at 2% and halothane at 1.5% attenuated NANC depressor responses significantly, whereas isoflurane at 1%, halothane at 0.75%, and sevoflurane at 2% or 4% did not. Volatile anesthetics did not attenuate the release of CGRP after spinal cord stimulation, whereas isoflurane at 2% and halothane at 1.5% significantly inhibited depressor responses to exogenously administered CGRP. Sevoflurane at 4% did not significantly affect CGRP-induced depressor responses. Thus, isoflurane and halothane at large concentrations attenuate NANC depressor responses by attenuating the depressor action of CGRP, not CGRP release. IMPLICATIONS: The anesthetics isoflurane and halothane attenuate nonadrenergic, noncholinergic depressor responses mediated by calcitonin gene-related peptide in the rat without affecting the release of the peptide.

Anesthetics, Inhalation↗