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 775 records · Page 43Linked to original sources
PubMed1978

Effect of autonomic neural blockade on verapamil-induced suppression of the accelerated ventricular escape beat in ouabain-treated dogs.

The effect of autonomic neural blockade on verapamil-induced suppression of the accelerated ventricular escape beat (AVE) was evaluated in anesthetized dogs pretreated with ouabain. Ouabain (53 +/- 2 microgram/kg, n = 45) was administered in divided doses until simultaneous electrical stimulation of the right atrium and ventricle triggered an AVE. The escape interval of the AVE was stable over a 150-min time period in a group of control animals. Verapamil was infused (20 microgram/kg/min) until the escape interval increased at least 50% or until the AVE was abolished. The total amount of verapamil in milligrams per kilogram that produced this effect was defined as the verapamil endpoint. The verapamil endpoint in vagotomized animals was not significantly different from a group of intact controls. In contrast, the verapamil endpoint in animals pretreated with propranolol, hexamethonium, guanethidine, bretylium or spinal section was significantly less than the control group. Propranolol, hexamethonium, guanethidine or spinal section alone increased the escape interval by a maximum of 12%. Infusion of norepinephrine in spinal animals treated with verapamil restored the AVE. These data indicate that sympathetic nerve activity contributes to the genesis of the AVE and antagonizes the antiarrhythmic effect of verapamil on the escape beat.

Animals↗
PubMed1997

Cardiac performance during unilateral lumbar spinal block after crystalloid preload.

PURPOSE: The haemodynamic effects of crystalloid preload were evaluated in a randomised blind study in 20 ASA status I-II, 50-80 yr-old patients, undergoing unilateral spinal anaesthesia for leg surgery produced with low doses of hyperbaric bupivacaine. METHODS: Baseline non-invasive blood pressure (oscillometry), heart rate, stroke volume and cardiac index (transthoracic electrical bioimpedance) were recorded. Then, patients were randomly allocated to receive 10 ml.kg-1 Ringer's Lactate solution over 20 min (preload group, n = 10) or no crystalloid infusion (no-preload group, n = 10). Spinal block was performed using 8 mg hyperbaric bupivacaine 0.5% injected slowly at the L2-L3 interspace (0.02 ml.sec-1 through a 25-gauge Whitacre needle) with patients lying on their operated side and with the needle opening directed towards the dependent side. Lateral decubitus position was maintained for up to 15 min after anaesthetic injection to facilitate hyperbaric bupivacaine distribution towards dependent regions of the subarachnoid space. Haemodynamic variables were recorded 5, 10, 15 and 30 min after spinal injection, while sensory level and motor block were evaluated 10, 15 and 30 min after anaesthetic injection on both operated and unoperated side. RESULTS: No differences of upper sensory level and motor block were observed between the two groups on the operated and non-operated sides. Diastolic blood pressure was decreased compared with baseline in the no-preload group only (P = .0001). Systolic arterial pressure and heart rate did not change in either group. Stroke volume and cardiac index were decreased in the no-preload group compared with both baseline (P = .02; P = .001) and the preload group (P = .04; P = .02). CONCLUSION: Crystalloid preload influences cardiovascular function during spinal block, and may be useful when very low bupivacaine doses and lateral decubitus are used to achieve unilateral spinal block.

Aged↗
PubMed2005

Ziconotide, an intrathecally administered N-type calcium channel antagonist for the treatment of chronic pain.

Ziconotide is a novel peptide that blocks the entry of calcium into neuronal N-type voltage-sensitive calcium channels, preventing the conduction of nerve signals. N-type calcium channels are present in the superficial laminae of the dorsal horn of the spinal cord. In various animal models of pain, intrathecal administration of ziconotide blocked nerve transmission and nociception. The United States Food and Drug Administration recently approved ziconotide intrathecal infusion for the management of severe chronic pain in patients who require intrathecal therapy and who are intolerant of or refractory to other treatment, such as systemic analgesics, adjunctive therapies, or intrathecal morphine. The drug has a narrow therapeutic window and a lag time for the onset and offset of analgesia and adverse events. In early clinical trials, frequent and severe psychiatric and central nervous system adverse effects were associated with rapid intrathecal infusion (0.4 microg/hr) and frequent up-titration (every 12 hrs). Therefore, patients with psychiatric symptoms are not candidates for this drug. Drug trials of external intrathecal catheters and microinfusion devices demonstrated a 3% risk of meningitis. A low initial infusion rate of 0.1 microg/hour and limiting infusion rate increases to 2-3 times/week are now recommended. Patients responsive to intrathecal ziconotide require an implanted infusion system to receive long-term therapy.

Calcium Channel Blockers↗
PubMed1992

N-methyl-D-aspartate (NMDA) and opioid receptors mediate dynorphin-induced spinal cord injury: behavioral and histological studies.

Both N-methyl-D-aspartate (NMDA) and opioid receptors have been implicated in the pathophysiology of traumatic spinal cord injury and dynorphin-induced paralysis. The present studies compared the effects of the non-competitive NMDA antagonist dextrorphan (Dex) and the kappa-selective opioid antagonist nor-binaltorphimine (nor-BNI) on the acute motor deficits and chronic neuropathological alterations caused by intrathecally administered dynorphin A-(1-17) (Dyn A). Infusion of Dyn A into the rat lower thoracic spinal subarachnoid space produced acute, reversible hindlimb paresis. Histological evaluations of spinal cord sections from these animals at 2 weeks post-infusion revealed ventral grey matter necrosis, neuronal loss and gliosis as well as axonal loss in adjacent white matter; however, there was minimal alteration in serotonin immunocytochemistry caudal to the injury zone. Dex or non-BNI pretreatment each significantly (P less than 0.05) reduced, and to a similar degree, the acute motor deficits and certain histological changes associated with Dyn A administration. These findings further support the hypothesis that dynorphin-induced spinal cord injury involves both NMDA receptors and opioid receptors.

Animals↗
PubMed1992

Methylprednisolone for acute spinal cord injury.

Treatment with high-dose intravenous methylprednisolone is safe and may be associated with significant neurologic improvement in acute spinal cord injury patients. Accurate calculation and administration of the prescribed therapy and identification and assessment of complications should be incorporated into the overall standard of care for the acute spinal cord injury patient.

Acute Disease↗
PubMed2004

[Short-acting beta 1-adrenergic blocker is useful for anesthetic management of cesarean section in a patient with Marfan syndrome].

The aortic root dilatation and its dissection are the most catastrophic events in pregnancy with Marfan syndrome as has been reported. It has been shown that prophylactic beta-adrenergic blocker is effective in reducing the aortic distensibility. However, its fetal toxicity should be considered. It includes hypoglycemia, neonatal apnea and bradycardia. Landiolol hydrochloride is a new beta-adrenergic blocker of which greatest advantages are its short duration of action, rapid clearance and high beta 1-selectivity. This drug has not been evaluated in its maternal and fetal effects on human pregnancy. We report a case of Marfan syndrome complicated with 49 mm annuloaortic ectasia. She received landiolol for the prevention of aggravated aortic root dilatation during cesarean section. After the administration of spinal anesthesia, she was treated with landiolol by continuous infusion at a rate of 0.003 to 0.005 mg.kg-1.min-1 until delivery of 1764 g infant with Apgar scores of 5 (1 min) and 8 (5 min). We could maintain maternal hemodynamics stable and good post cesarean uterus contraction. No severe adverse effects were observed in the infant. In conclusion, it is useful for maintaining the hemodynamics stable in a pregnant woman with Marfan syndrome and keep the infant safe from any adverse effects by infusing of landiolol.

Adrenergic beta-Antagonists↗
PubMed1986

Atrial natriuretic peptide decreases circulatory capacitance in areflexic rats.

The short-term hemodynamic response to atrial natriuretic peptide appears to be partly mediated by decreased venous return, which could result from increased circulatory capacitance or decreased blood volume. To determine if rat atrial natriuretic peptide 99-126 (0.5 microgram/kg/min IV for 30-70 minutes) dilated capacitance vessels or decreased blood volume, mean circulatory filling pressure (measured during brief circulatory arrest by inflating an intraatrial balloon) and blood volume (51Cr-erythrocytes) were measured in anesthetized rats. Mean circulatory filling pressure, central venous pressure, and blood volume decreased by 0.4 mm Hg, 0.5 mm Hg, and 3.4 ml/kg, respectively. To determine the total circulatory pressure-volume relationship without influence from autonomic reflexes, mean circulatory filling pressure and blood volume were measured in spinal-cord-transected rats before and immediately after infusing or withdrawing 5 ml blood. Atrial natriuretic peptide decreased mean circulatory filling pressure, central venous pressure, and blood volume by 0.9 mm Hg, 1.7 mm Hg, and 8.0 ml/kg, respectively, and displaced the pressure-volume relationship toward the pressure axis by decreasing extrapolated unstressed volume. Similar results were obtained in spinal-cord-transected rats that had initial vascular tone restored to a greater level by norepinephrine infusion. In anephric rats, atrial natriuretic peptide decreased central venous pressure by 0.3 mm Hg and blood volume by 1.6 ml/kg. The results indicate that short-term infusion of atrial natriuretic peptide reduced circulatory capacitance in rats and suggest that this reduction resulted from diminished blood volume due to urinary fluid loss followed by passive vascular recoil and active venoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed2000

The effect of spinal ibuprofen on opioid withdrawal in the rat.

UNLABELLED: This study examines the effect of spinal ibuprofen on the behavioral manifestations associated with the opioid abstinence syndrome. Rats (n = 8 per group) were infused for 5 days with morphine and then pretreated with a spinal bolus dose of ibuprofen before systemic naloxone antagonism (300 microg). Groups included ibuprofen S(+) 1. 36, 13.6, and 136 nmol, and ibuprofen R(-) 136 nmol. A separate group of saline-infused rats was given ibuprofen S(+) 136 nmol before naloxone antagonism. Ibuprofen S(+), but not R(-), dose-dependently and stereospecifically blocked opioid withdrawal hyperalgesia but did not significantly alter other signs of the opioid abstinence syndrome. We conclude that hyperalgesia associated with opioid withdrawal can be blocked by spinally administered ibuprofen, and suggest that there may be a role for spinal prostaglandins in the enhancement of nociception observed in association with the opioid abstinence syndrome. IMPLICATIONS: This study shows that spinal ibuprofen blocks opioid withdrawal hyperalgesia in the rat in a stereospecific fashion, implicating the likely release of spinal prostaglandins during withdrawal and their possible role as neuromodulators in the enhancement of nociception that accompanies this phenomenon.

Animals↗
PubMed2001

Epinephrine increases the neurotoxic potential of intrathecally administered lidocaine in the rat.

BACKGROUND: Epinephrine is commonly added to lidocaine solutions to increase the duration of spinal anesthesia. Despite this common usage, the effect of epinephrine on the neurotoxic potential of this anesthetic is not known. The current experiments investigated whether adding epinephrine increases functional impairment or histologic damage induced by spinal administration of lidocaine in the rat. METHODS: Eighty rats were divided into four groups to receive an intrathecal injection of normal saline containing either 5% lidocaine, 5% lidocaine with 0.2 mg/ml of epinephrine, 0.2 mg/ml of epinephrine, or normal saline alone. Animals were assessed for persistent sensory impairment using the tail-flick test administered 4 and 7 days after infusion. Animals were then killed, and the spinal cord and nerve roots were prepared for neuropathologic evaluation. RESULTS: Rats given 5% lidocaine developed persistent sensory impairment and histologic damage, and the addition of epinephrine resulted in a further significant increase in injury. Sensory function in animals given epinephrine without anesthetic was similar to baseline and did not differ from saline. Histologic changes in animals treated with epinephrine alone did not differ significantly from saline controls. CONCLUSIONS: The neurotoxicity of intrathecally administered lidocaine is increased by the addition of epinephrine. When making clinical recommendations for maximum safe intrathecal dose of this anesthetic, one may need to consider whether the solution contains epinephrine.

Anesthesia, Spinal↗
PubMed1981

A simple safe method for continuous infusion epidural analgesia in obstetrics.

Continuous infusion epidural anaesthesia may reduce the risks of hypotension, high spinal block and intravenous injection associated with repeated bolus injections. However, controlling the rate of a simple infusion is difficult and infusion pumps are expensive and bulky. We describe a method for continuous infusion epidural anesthesia using a 6 ml/hr capillary infusion device (Intraflo CFS-06F Sorenson Research Co., Salt Lake City, Utah) and bupivicaine 0.25 per cent. In a study of 50 patients, 35 (70 per cent) had adequate pain relief with the infusion alone for a mean time until delivery of 5 hours (range 2 to 13 hours). A further 11 patients (22 per cent) required only one top-up for the second stage of labour after a mean pain-free time of 5.4 hours (range 1.5 to 9.7 hours). There were no maternal or foetal complications related to the technique of continuous infusion used. No block went higher than the ninth thoracic dermatome at any time.

Anesthesia, Epidural↗
PubMed1997

Tachyphylaxis and sensitization to nicotine-induced tachycardiac and pressor effects after nicotine infusions.

This work examined the effects of nicotine on mean arterial pressure and heart rate in non-anesthetized spinal rats. Nicotine (200 mg/kg) was administered as a single bolus, as infusions lasting 7.5, 15 or 30 min, and as a post-infusion bolus. A nicotine bolus increased pressure and rate. These effects were less marked as the rate of infusion decreased. The infusions affected differentially the effects of a subsequent bolus. Thus, while tachycardia was decreased, the blood pressure rise was increased. An initial transient bradycardia was observed after bolus administration, but not during infusions; this effect was unchanged after post-infusion boluses. Pharmacological analysis indicated that tachycardia and bradycardia were predominantly due to ganglionic stimulation, while adrenal and sympathetic nerve catecholamine release played a major role in the pressor response. These results indicate that slow nicotine infusions do not induce tachyphylaxis for all of the cardiovascular effects of a subsequent bolus, and that development of acute tolerance appears to depend on the mechanism of action of the response.

Animals↗
PubMed1998

Supersensitivity of spinal opioid receptors to antagonists in intrathecal butorphanol and morphine dependence.

The purpose of this investigation was to evaluate changes in the sensitivity of spinal opioid receptors to selective antagonists in rats rendered dependent on intrathecal (i.t.) butorphanol and morphine. Using quantitative autoradiography, competitive binding assays with selective opioid antagonists were performed in the spinal cord sections of i.t. butorphanol- and morphine-dependent rats in which withdrawal was precipitated by i.t. naloxone. In butorphanol-dependent rats, the spinal kappa-opioid receptor developed a greater degree of antagonist supersensitivity than the spinal delta- and mu-opioid receptors did. In contrast, the spinal mu-opioid receptor became more sensitive than the delta-opioid receptor in morphine-dependent rats. These results indicate that differential supersensitivity of spinal opioid receptors was induced after chronic i.t. infusions of butorphanol and morphine.

Animals↗
PubMed2004

Modulation of rodent spinal cord radiation tolerance by administration of platelet-derived growth factor.

PURPOSE: To examine the role of platelet-derived growth factor (PDGF) for ameliorating radiation myelopathy of the cervical spinal cord in a rodent model. METHODS AND MATERIALS: After developing the technique for cannulation of the basal cistern, initial animal experiments were conducted to test the feasibility of intrathecal continuous infusion of PDGF in a model of cervical spinal cord irradiation in adult Fisher F-344 rats and to determine the most effective dose level of PDGF. Subsequently, the dose-modification factor was determined in a larger group of rats. Irradiation was given in 2 fractions (16 Gy followed by 14-24 Gy) and animals were examined for the development of paresis. RESULTS: The initial dose-finding experiment revealed significant differences in the incidence of radiation myelopathy (100% in saline-treated control rats, 25% with the most effective dose of PDGF, up to 100% with less effective doses). The most effective dose of PDGF was 0.014 mug per day. Subsequent experiments revealed a median effective dose (ED(50)) of 35.6 Gy (95% confidence interval, 34.7-36.5 Gy) for animals receiving this dose of PDGF in contrast to 33.8 Gy (33.4-34.3 Gy) for the control group (p = 0.003). The dose-modification factor obtained with this dose of PDGF was 1.05. CONCLUSIONS: Intrathecal administration of PDGF concomitant to irradiation of the cervical spinal cord in rats was feasible. Treatment with PDGF significantly increased the tolerance of the spinal cord. The PDGF experiments should be viewed as a proof of principle that brief therapeutic intervention in the earliest phase of damage induction can reduce late effects in the spinal cord. They form the basis for further studies of growth factor administration in this particular model.

Animals↗
PubMedDate not supplied

c-fos expression as a marker of central cardiovascular neurons.

Immunohistochemical detection of Fos, the protein product of the immediate-early gene c-fos, was evaluated as a functional marker of central neurons sensitive to a change of blood pressure/blood volume. Controlled hemorrhage and infusion of the hypotensive agent nitroprusside or hydralazine induced the appearance of Fos-immunoreactivity (Fos-IR) in several prominent groups of central neurons: the piriform cortex, bed nucleus of the stria terminalis, islands of Calleja, subfornical organ, central nucleus of the amygdala, parabrachial nucleus, supraoptic and paraventricular nuclei, pontine A5, locus ceruleus, ventrolateral medulla, the nucleus of the solitary tract, area postrema, and intermediolateral cell column in the spinal cord. Elevation of blood pressure by infusion of phenylephrine caused the appearance of Fos-IR in fewer groups of neurons: the bed nucleus of the stria terminalis, central nucleus of the amygdala, parabrachial nucleus, the nucleus of the solitary tract and area postrema. The differential distribution of Fos neurons in hypotensive versus hypertensive animals underscores the potential application of Fos as a metabolic marker in identifying a network of neurons responding to a specific cardiovascular challenge. Further, simultaneous characterization of the transmitter phenotype of Fos-containing neurons offers an additional advantage of this method over other conventional tract-tracing techniques.

Animals↗
PubMed1977

Autonomic afferents at T1 in elicitation of volume-induced tachycardia in the dog.

Intravenous infusion of blood elicited tachycardia in anesthetized dogs with beta-receptor blockade (dogs with vagal efferents intact but cardiac sympathetic efferents blocked) and bradycardia in dogs with combined beta-receptor blockade and rhizotomy at T1 (dogs with vagal efferents intact but cardiac sympathetic efferents plus autonomic afferents at T1 blocked). This suggests that tachycardia elicited by volume in infusion may be partly due to a reflex with its afferent pathway at the T1 segment of the spinal cord and its efferent pathway in the vagi. Moreover, infusion evoked bradycardia in dogs with right-sided rhizotomy at T1, which was not significantly different from the response elicited in dogs with bilateral rhizotomy at T1. Additionally, the tachycardia response induced in dogs with ventral or dorsal rhizotomy at T1 was significantly different from the bradycardia response elicited in dogs with both dorsal and ventral rhizotomy at T1. These results suggest that the afferent pathway predominates on the right side, and its entry at T1 may be via both dorsal and ventral roots.

Afferent Pathways↗
PubMed2006

Combined spinal epidural analgesia for labor with and without 3 ml of 1.5% epidural lidocaine.

BACKGROUND: Lidocaine is used as a 'test dose' to detect misplacement of epidural catheters. When administered immediately after the initiation of a combined spinal epidural for labor analgesia, it was found to interfere with motor function. The authors hypothesized that an epidural test dose of 3 ml of 1.5% lidocaine injected immediately after the initiation of combined spinal epidural analgesia and followed by a continuous epidural infusion would prolong the duration of analgesia and decrease the incidence of breakthrough pain. MATERIAL/METHODS: Sixty nulliparous parturients were recruited for this randomized controlled trial. Combined spinal epidural analgesia was performed with intrathecal levobupivacaine 2.5 mg and fentanyl 25 microg. The patients were randomized into three groups: group L receiving 3 ml of 1.5% epidural lidocaine, group S 3 ml of normal saline, and group C the control group receiving no test solution. An epidural infusion of 0.1% levobupivacaine and 2 microg of fentanyl/ml at 10 ml/hr was initiated immediately. Their need for supplementary analgesia, duration of analgesia, sensory block, motor block, side-effects, and overall satisfaction were recorded. RESULTS: The breakthrough pain rate in all groups were similar. Their mean duration of analgesia (mean survival times) were not significantly different. Group C had the lowest incidence of lower limb motor block. The satisfaction scores were significantly highest in group L. CONCLUSIONS: The administration of epidural lidocaine and saline immediately after intrathecal levobupivacaine 2.5 mg and fentanyl 25 microg did not reduce the incidence of breakthrough pain in combined spinal epidural labor.

Analgesia, Epidural↗
PubMed2006

Spinal cord compression in a patient with a pain pump for failed back syndrome: a chalk-like precipitate mimicking a spinal cord neoplasm: case report.

OBJECTIVE AND IMPORTANCE: The use of intrathecal morphine has been effective with few complications for chronic intractable pain of both benign and malignant origins. A rare but serious problem that exists is the formation of an inflammatory mass at the catheter tip of the pain pump. CLINICAL PRESENTATION: We report the case of a 67-year-old female patient with failed back syndrome who presented with sensory complaints and back pain. INTERVENTION: Magnetic resonance imaging revealed impingement on the thoracic cord by a mass. The mass was originally thought to be a spinal cord tumor; however, operation and chemical analysis of the mass showed that it was a bupivacaine precipitate at the tip of the catheter of the pain pump. CONCLUSION: This is the first such case, to our knowledge, of a bupivacaine precipitate mimicking a spinal cord tumor.

Aged↗
PubMed1998

Does postsynaptic alpha 1-adrenergic receptor supersensitivity contribute to autonomic dysreflexia?

Quadriplegics often experience periods of severe hypertension known as autonomic dysreflexia. Clinically, these events have been well documented, but the mechanisms for mediating autonomic dysreflexia remain unclear. We used a chronic rat model to investigate the potential development of supersensitivity at postsynaptic alpha 1-adrenergic receptors as a contributing factor to the exaggerated sympathetic response characteristic of autonomic dysreflexia. Adult male Wistar and Sprague-Dawley rats were anesthetized and given spinal transection at T5. After 30 days, rats were reanesthetized and arterial and venous catheters implanted. Twenty-four hours later, colorectal distension (CRD) was used to evoke autonomic dysreflexia in conscious, spinalized rats. To gauge changes in alpha 1-receptor sensitivity, we assessed mean arterial pressure (MAP) in response to intravenous phenylephrine (PE) infusions. No consistent differences were observed between intact and spinalized rats. Therefore, supersensitivity of alpha 1-receptors cannot completely account for the hypertensive bouts associated with autonomic dysreflexia. In addition, while attempting to develop an appropriate model for autonomic dysreflexia, we discovered that spinalized Wistar rats exhibited MAP responses characteristic of autonomic dysreflexia, whereas lesioned Sprague-Dawley rats did not, when subjected to CRD. Thus Wistar rats provide a better animal model for autonomic dysreflexia.

Adrenergic alpha-Agonists↗