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PubMed2006

Lesions in sheep following administration of a vaccine of a Freund's complete adjuvant nature used in the control of ovine paratuberculosis.

CASE HISTORIES: Occurrences of adverse reactions in seven sheep flocks in Australia following vaccination against paratuberculosis where veterinary attention was requested are reviewed. All cases occurred within the 3-year period following commencement of use of a vaccine of a Freund's complete adjuvant nature, at a time when approximately six million doses of vaccine had been administered. CLINICAL FINDINGS: In the first case, 26/58 (45%) Merino sheep vaccinated as adults had palpable tissue reactions at or near the site of vaccination; enlarged prescapular lymph nodes were palpated in 17 (29%), and nine (16%) sheep had both palpable lesions at the site of vaccination and enlarged prescapular lymph nodes. The reactions included caseous nodules up to 5.5 cm in diameter. In the other cases, fistulating or granulomatous wounds were occasionally found at the recommended site of injection behind the ear, and myiasis was rare. Occurrences of inappropriate choice of injection site were recorded, including injection into the axilla of two Merino rams, and lesions in the tissues of the maxilla and nose of almost 50% of 350 Border Leicester lambs. Four outbreaks of progressive paralysis due to injection into cervical musculature were reported, described as "OJD staggers" by producers. DIAGNOSIS: Granulomatous cellulitis and lymphadenitis associated with oil droplets typical of "oil granulomata". Injection of vaccine into the dorsal cervical area resulted in progressive paralysis due to myonecrosis and suspected granulomatous leptomeningitis. CLINICAL RELEVANCE AND CONCLUSIONS: Although lesions at and near the site of injection are common, adverse reactions to vaccination were rare and included mortality from cervical spinal injection, production losses from injection in the maxilla or axilla or if myiasis resulted, and potential marketing losses if animals or carcasses are discounted as a result of the lesions. Risk factors for adverse reactions included inadequate restraint of sheep, breed of sheep, experience of the operator, poor injection technique, and inappropriate placement of vaccine. Increasing attention to the proper restraint of animals, restricting vaccination to the recommended site behind the ear, careful placement of the vaccine into subcutaneous tissue to avoid drainage of vaccine material into tissues such as the spinal cord, and post-vaccination supervision to address welfare concerns should adverse reactions occur are recommended.

Animals↗

PubMed1990

Effects of inositol, 1,4,5-trisphosphate injections into cat spinal motoneurons.

Inositol 1,4,5-trisphosphate (IP3) was injected iontophoretically into cat spinal motoneurons in pentobarbital-anaesthetized cats and nonanaesthetized, decerebrate cats. Injections of IP3 induced a long-lasting, reproducible hyperpolarization without consistent change in input resistance. The peak amplitude of post-spike afterhyperpolarization (AHP) was significantly increased by IP3 when the membrane potential was adjusted to the control level. Intracellular injections of Ca2+ chelators, which depressed the Ca2(+)-activated AHP, prevented the IP3-induced long-lasting hyperpolarization, suggesting that IP3 acts by a Ca2(+)-dependent mechanism. Intracellular injections of myo-inositol did not consistently induce hyperpolarizations. Also intracellular injections of Li+, which blocks IP3 catabolism, did not prevent the IP3-evoked hyperpolarization. These data suggest that IP3 itself, rather than its breakdown product myo-inositol, is mainly responsible for the hyperpolarizing effect. Possible mechanisms for the IP3-induced hyperpolarization are discussed.

Anesthesia↗

PubMed1997

The addition of phenylephrine contributes to the development of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine.

BACKGROUND: Recent reports indicate that transient neurologic symptoms commonly occur after single-injection spinal anesthesia with lidocaine. Information regarding tetracaine has been limited to a single case report. In addition, little is known about the cause of these symptoms or the cofactors that affect their occurrence. The present study sought to determine whether the presence of phenylephrine or the concentration of glucose in the anesthetic solution affects the incidence of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine. METHODS: One-hundred sixty patients classified as American Society of Anesthesiologists physical status I or II who were scheduled for elective surgery on a lower limb or perineum were sequentially assigned to one of four equal groups to receive intrathecal 0.5% tetracaine in 7.5% or 0.75% glucose, with or without 0.125% phenylephrine. Patients were evaluated on postoperative day one for the presence of pain, dysesthesia, or both in the legs or buttocks by an investigator unaware of the drug given. RESULTS: Symptoms were present in 10 patients (12.5%) receiving a spinal anesthetic containing phenylephrine, but in only one patient (1.3%) receiving spinal anesthesia without phenylephrine. There was no significant difference in the incidence of symptoms between groups receiving 7.5% glucose and those receiving 0.75% glucose (8.8% and 5% of patients, respectively). CONCLUSIONS: These results suggest that adding phenylephrine to tetracaine for spinal anesthesia increases the potential for transient neurologic symptoms, but that the concentration of glucose does not affect their occurrence.

Adult↗

PubMedDate not supplied

Analgesic efficacy and side effects of subarachnoid sufentanil-bupivacaine administered to women in advanced labor.

BACKGROUND AND OBJECTIVES: Previous studies of labor analgesia using subarachnoid sufentanil (alone or with adjuvants) have focused on women in the early first stage of labor. This study prospectively evaluated analgesia and side effects of subarachnoid sufentanil (10 micrograms) plus bupivacaine (2.5 mg) in parturients with cervical dilation of 7 cm or more. METHODS: In an open-label, nonrandomized trial, 32 parturients in the late first stage of labor, who had requested regional anesthesia, consented to subarachnoid injection of sufentanil (10 micrograms) and bupivacaine (2.5 mg). Patients rated their pain by a verbal pain score (0-10 scale) prior to regional anesthesia, 5 minutes after subarachnoid injection, and every 20 minutes thereafter until delivery or request for additional analgesia. Blood pressure, pruritus, Bromage motor block score (0-3), mode of delivery, and need for supplemental analgesics were recorded. RESULTS: Lumbar puncture was successful in 30 women. Pain scores (mean +/- SD) were 8.7 +/- 1.0 prespinal and 0.7 +/- 1.5 5 minutes postinjection, and remained less than 5 for 130 minutes after the spinal injection. Of these 30 patients, 24 had unassisted vaginal delivery, 4 had instrumental vaginal delivery (3 vacuum, 1 low forceps), and 2 had cesarean delivery. Of the 28 patients who delivered vaginally, 19 did not require supplemental analgesics and had a delivery pain score of 5 or lower. Blood pressure decreased after spinal analgesia (P < .05), and necessitated treatment in three patients. The Bromage motor block score was 0 in 26 patients and 1 in 4 patients. Pruritus was noted by 22 patients. CONCLUSION: In parturients with cervical dilation of 7 cm or more, subarachnoid sufentanil-bupivacaine produces rapid analgesia with an effective duration of approximately 130 minutes.

Adult↗

PubMed1995

Multiplicative interaction between intrathecally and intracerebroventricularly administered morphine for antinociception in the mouse: effects of spinally and supraspinally injected 3-isobutyl-1-methylxanthine, cholera toxin, and pertussis toxin.

1. Either intrathecal (i.t.) or intracerebroventricular (i.c.v.) administration of morphine alone at the dose of 0.2 microgram slightly increased inhibition of the tail-flick response. However, combined i.t. and i.c.v. injections of morphine at the same dose increased the inhibition of the tail-flick response in a synergistic manner. 2. Cholera toxin (CTX, 0.05 to 0.5 microgram) pretreated i.t. or i.c.v. for 24 hr or pertussis toxin (PTX, 0.05 to 0.5 microgram) for 6 days dose-dependently attenuated inhibition of the tail-flick response induced by combined i.t. and i.c.v. injection of morphine. 3. 3-Isobutyl-1-methylxanthine (IBMX, 0.001 to 0.1 ng) pretreated i.t. for 10 min dose-dependently attenuated the inhibition of the tail-flick response induced by combined i.t. and i.c.v. injections of morphine. However, IBMX pretreated i.c.v. for 10 min was not effective in attenuating the inhibition of the tail-flick response induced by combined i.t. and i.c.v. injections of morphine. 4. It is concluded that both spinal and supraspinal CTX- and PTX-sensitive G-proteins are involved in the antinociception produced by morphine-induced multiplicative interaction between spinal and supraspinal sites. However, only spinal but not supraspinal cAMP phosphodiesterase is involved in mediating antinociception induced by morphine-induced multiplicative interaction.

1-Methyl-3-isobutylxanthine↗

PubMed2004

Spinal manipulation postepidural injection for lumbar and cervical radiculopathy: a retrospective case series.

OBJECTIVE: To describe the safety and potential therapeutic benefit of spinal manipulation postepidural injection in the nonsurgical treatment of patients with cervical and lumbar radiculopathy. METHODS: The study design was a retrospective review of outcomes of 20 cervical and 60 lumbar radiculopathy patients who underwent spinal manipulation postepidural injection in a hospital setting. Patients received either fluoroscopically guided or computed tomography (CT)-guided epidural injection of a combination of lidocaine and Depo-Medrol. The manual therapy consisted of an immediate postepidural application of flexion distraction mobilization and then high-velocity, low-amplitude spinal manipulation to the affected spinal regions. Outcome criteria were empirically defined as significant improvement, temporary improvement, or no change. The minimum follow-up time for all patients was 1 year. RESULTS: There were no complications associated with spinal manipulation, whereas 3 complications associated with the epidural injection procedure were noted. Of lumbar spine patients, 36.67% (n = 22) noted significant improvement, 41.67% (n = 25) experienced temporary improvement, and 21.67% (n = 13) reported no change. Of the patients undergoing spinal manipulation after cervical epidural injection, 50% (n = 10) noted significant improvement, 30% (n = 6) experienced temporary improvement, whereas 20% (n = 4) exhibited no change. CONCLUSIONS: These data suggest that spinal manipulation postepidural injection is a safe nonsurgical procedure to use in the treatment of the patient with radiculopathy of spinal origin. This is also the first report of the use of spinal manipulation postepidural injection in the cervical spine.

Adult↗

PubMedDate not supplied

Discitis after lumbar epidural corticosteroid injection: a case report and analysis of the case report literature.

OBJECTIVE: The primary objective is to document the first case report of discitis after a lumbar epidural corticosteroid injection. The second objective is to analyze the case report literature to identify clinical features and trends of patients with infectious complications after spinal injections. DESIGN: Single case report. A MEDLINE and EMBASE literature search was conducted using key words from the names of commonly performed spinal procedures, including epidural corticosteroid, selective nerve root, transforaminal epidural, facet joint, and sacroiliac joint injections. SETTING: Pain medicine clinic at a tertiary medical center. PATIENT: A 64-year-old man with an 8-year history of left lower extremity radicular pain and recurrent pulmonary infections was referred for a lumbar epidural corticosteroid injection. Six weeks following the injection, the patient returned with a 4-week history of worsening right-sided paraspinous pain without associated recurrent pneumonia. Magnetic resonance imaging revealed a right-sided L5-S1 disc extrusion with discitis and a right L5-S1 discectomy was performed. Cultures of disc material and blood showed growth of coagulase-negative Staphylococcus, and a transesophageal echocardiogram showed no evidence of endocarditis. The patient received 6 weeks of intravenous antibiotics and he had symptomatic recovery at 3-month follow-up. RESULTS: Including our patient, the literature search identified 27 case reports of infectious complications. Similar clinical features and significant trends were evident in five categories including predisposing factors, symptom presentation, diagnostic evaluation, etiological organisms, and treatment outcomes. CONCLUSIONS: The identified clinical features and trends could prove useful to the practitioner when an infectious complication is suspected or has occurred.

Adrenal Cortex Hormones↗

PubMed2004

Nicotine attenuates oxidative stress, activation of redox-regulated transcription factors and induction of proinflammatory genes in compressive spinal cord trauma.

Pathophysiology of neurodegeneration following spinal cord injury (SCI) involves alterations of cellular redox status, activation of transcription factors and induction of proinflammatory genes. In addition, recent evidence indicates that nicotine can induce potent neuroprotective effects. To study the influence of nicotine on the redox signaling pathways in relationship to SCI, moderate contusions of spinal cords at the level of T-10 were induced in rats treated or untreated with nicotine. Cellular oxidative stress, DNA binding activity of redox-responsive transcription factors (AP-1, NF-kappaB and CREB) as well as mRNA levels of inflammatory genes (MCP-1 and TNF-alpha) were determined in the thoracic and lumbar regions of the spinal cords. Nicotine was administrated 2 h after the SCI in a single i.p. injection at the dose of 0.35, 3.5 or 7 mg/kg, and rats were sacrificed 3 h following such an injection. Spinal cord trauma was associated with a significant increase in oxidative stress, and activation of NF-kappaB, AP-1 and CREB, as well as overexpression of MCP-1 and TNF-alpha in both the thoracic and lumbar regions. Nicotine administration following the SCI markedly attenuated, especially in the lumbar region, these oxidative and proinflammatory responses. These protective effects of nicotine were fully reversed by inhibition of neuronal nicotinic receptors by mecamylamine. The present results indicate that nicotine administration can attenuate the oxidative injury to spinal cords and suggest that neuronal nicotinic receptors can be attractive targets for neuroprotective therapy.

Animals↗

PubMed2000

Norepinephrine release from spinal synaptosomes: auto-alpha2 -adrenergic receptor modulation.

BACKGROUND: Clonidine produces analgesia after spinal injection by activating alpha2-adrenergic receptors. Recently, clonidine has been demonstrated to increase spinal release of norepinephrine (NE) in vivo, in contrast to that anticipated by classic presynaptic autoinhibition. The purpose of the current study was to determine if clonidine could inhibit release of NE in a preparation of spinal cord tissue lacking synaptic circuits. METHODS: Crude synaptosomes were prepared from male Sprague-Dawley rat spinal cord, loaded with [3H]NE, and stimulated by potassium chloride to release [3H]NE. Samples were incubated with clonidine in the absence or presence of various inhibitors. To study the effect of alpha2a-adrenergic receptor subtypes, some animals were pretreated with an oligodeoxynucleotide (ODN) composed of a sense or antisense sequence to a portion of this receptor. RESULTS: Potassium chloride produced a concentration-dependent increase in [3H]NE release, and this release was inhibited by clonidine with a concentration producing 50% maximal inhibition (IC50) of 1.3 microm. The effect of clonidine was inhibited by the alpha2-adrenergic antagonists, yohimbine and idazoxan, but not by alpha1-adrenergic, muscarinic, or opioid antagonists. Intrathecal pretreatment with antisense ODN to alpha2A-adrenergic receptors reduced alpha2A-adrenergic receptor protein expression compared with sense ODN control and also reduced clonidine-induced inhibition of [3H]NE release. CONCLUSIONS: These data demonstrate the existence of classic autoinhibitory alpha2-adrenergic receptors in the spinal cord, probably of the alpha2Asubtype. They further suggest that clonidine-induced stimulation of spinal NE release must occur from indirect actions, presumably due to activation of a spinal circuit.

Adrenergic alpha-Agonists↗

PubMed1987

Efferent projections of the paratrigeminal nucleus in the rat.

The efferent projections of the paratrigeminal nucleus in the rat were investigated by means of retrograde transport techniques. Injections were made in most of the supraspinal structures known to receive afferents from the spinal cord or the trigeminal nucleus caudalis. Spinal injections were also performed. Dense paratrigeminal efferents were seen to be directed to the nucleus of the solitary tract and to the peribrachial area, the latter including the cuneiformis and parabrachial nuclei. Projections were mostly ipsilateral. These results are discussed in relation to a possible role of the paratrigeminal nucleus in thermoreception and/or vegetative regulation processing.

Animals↗

PubMed1988

Studies on dopamine-, tyrosine hydroxylase- and aromatic L-amino acid decarboxylase-containing cells in the rat diencephalon: comparison between formaldehyde-induced histofluorescence and immunofluorescence.

The morphology, number and distribution of catecholaminergic neurons, as visualized either with the aluminum-catalysed formaldehyde method for catecholamines or with the immunohistochemical method for the catecholamine-synthesizing enzymes tyrosine hydroxylase and aromatic L-amino acid decarboxylase, respectively, were analysed within the rat dorsal hypothalamus, ventral thalamus and adjoining regions (A11 and A13 cell groups). Both polyclonal rabbit and monoclonal mouse tyrosine hydroxylase antibodies were used in elution-restaining and double-staining experiments, respectively. Some of the animals also received spinal injections of the fluorescent tracer True Blue in order to retrogradely label cells projecting to the spinal cord. With respect to the number and distribution of catecholaminergic neurons in the A11 and medial A13 cell groups, including the spinal-projecting subpopulation, the results obtained with the two methods were very similar, indicating that within these regions of the CNS the two methods in principle visualize identical cell populations. However, the catecholaminergic cells were distinctly larger and their processes appeared more extensive with the immunohistochemical method. Animals processed for immunohistochemistry exhibited a lower total number of retrogradely labelled cells in the A11 area than those analysed with aldehyde-induced fluorescence despite the fact that both methods revealed similar numbers of retrogradely labelled tyrosine hydroxylase-positive and catecholamine-containing cells, respectively. The reason for these discrepancies, which are probably of methodological nature, are discussed. While this study shows that the results obtained with the two methods within the A11 and medial A13 cell group are very similar and thus strengthens the earlier proposed concept of the organization of the diencephalospinal dopaminergic system, it also documents that in intermingling and nearby CNS regions there are cell bodies which cannot be demonstrated with the aldehyde fluorescence method, but which still contain tyrosine hydroxylase and/or aromatic L-amino acid decarboxylase-like immunoreactivity. One explanation is low levels of enzyme and/or dopamine combined with a comparatively low sensitivity of the histochemical method. Thus, neurons containing both enzymes are probably dopaminergic, even if catecholamine fluorescence cannot be demonstrated. Neurons containing tyrosine hydroxylase, but lacking both aldehyde induced fluorescence and aromatic L-amino acid decarboxylase, may also still be dopaminergic.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Descending projections from the caudal medulla oblongata to the superficial or deep dorsal horn of the rat spinal cord.

The location of neurons in the caudal medulla oblongata that project to the superficial or deep dorsal horn was studied in the rat, by means of retrograde labelling from confined spinal injection sites. The tracer cholera toxin subunit B was injected into laminae I-III (fuve rats) or I-V (three rats) at C4-7 spinal segments. Neurons projecting to the superficial dorsal horn were located in the dorsomedial part of the dorsal reticular nucleus ipsilaterally, the subnucleus commissuralis of the nucleus tractus solitarius bilaterally, and a region occupying the lateralmost part of the ventrolateral reticular formation between the lateral reticular nucleus and the caudal pole of the spinal trigeminal nucleus, pars caudalis, bilaterally. Neurons projecting to the deep dorsal horn, which were only labelled when laminae I-V were filled by the tracer, occurred in the dorsomedial and ventrolateral parts of the dorsal reticular nucleus and in the ventral reticular nucleus bilaterally. A few cells were located in the above described lateralmost portion of the ventrolateral reticular formation bilaterally and in the ventral portion of the ipsilateral cuneate nucleus. In the light of previous data demonstrating that dorsal horn neurons project to the dorsal reticular nucleus, the ventrolateral reticular formation, and the nucleus tractus solitarius, and that neurons in these three medullary regions are involved in pain inhibition at the spinal level, the descending projections demonstrated here suggest the occurrence of spino-medullary-spinal loops mediating the analgesic actions elicited in each nucleus upon the arrival of nociceptive input from the dorsal horn.

Animals↗

PubMed2005

Managing chronic pain with encapsulated cell implants releasing catecholamines and endogenous opiods.

Spinal injections (intrathecal) of norepinephrine and/or opiod agonists are antinociceptive and when administered together may act in synergy. Spinal implants of adrenal chromaffin cells are an effective method for sustained delivery of the analgesic substances norepinephrine and enkephalin to the central nervous system (CNS). One method of packaging and implanting cell-loaded devices into the intrathecal space of recipients is by encapsulating the cell suspensions in a polymer membrane prior to implantation. Cells/tissue packaged within an encapsulating membrane obviate the need for immunosuppressive therapies in transplant recipients. In addition, device output can be quantified prior to implantation, and following the removal of the spinal implant. The ability to retrieve the devices with the present tubular configuration also confers an additional margin of safety over unencapsulated chromaffin cell implants. This paper reviews the research and clinical observations of cellular transplants containing adrenal chromaffin cells for relieving chronic pain. Encapsulated cell technology is discussed with an emphasis on our experiences developing pain-modulating clinical devices. The human-sized prototype devices were loaded with enzymatically isolated bovine chromaffin cells and maintained in vitro for 7 - 8 days in serum-free media. Two days prior to implantation, each device was assayed by static incubation to measure catecholamine and met-enkephalin output, and qualified devices (n = 6) were implanted into the sheep subarachnoid space for 6 weeks. Following a 6 week in life period, the retrieval forces of prototype devices were measured during removal from the subarachnoid space. Static incubation of the devices immediately following retrieval and after a 24 hour re-incubation period were used to quantify norepinephrine and met-enkephalin secretion profiles. This study demonstrated the safety, retrievability and maintenance of pharmacologically active encapsulated chromaffin cell-loaded devices with human implant dimensions.

Animals↗

PubMedDate not supplied

Histopathologic changes in primate spinal cord after single and repeated epidural phenol administration.

BACKGROUND AND OBJECTIVES: Epidural phenol for control of pain and spasticity has been advocated for clinical use. This study determined the histopathologic changes that follow single and repeated epidural administration of phenol in saline in nonhuman primates. METHODS: Nine primates received 0.5 mL of either 3% phenol in saline (n = 4) or 6% phenol in saline (n = 5) via lumbar epidural injection. Two additional primates received three consecutive daily epidural doses of 0.5 mL of 3% phenol in saline. Finally, 5 unoperated primates and 5 primates that received only 2 mL of radiographic contrast material served as control subjects. Two weeks after the epidural injection, spinal cords were removed and processed for histopathologic study by a neuropathologist blinded to the solution administered. RESULTS: None of the control animals demonstrated histopathologic changes. One animal that received 6% phenol died 3 days after injection. All phenol-treated animals demonstrated predominantly posterior root damage. Spinal cord damage was seen in all animals receiving 6% phenol, in 2 animals receiving 3% phenol single doses, and in neither animal receiving 3% phenol multiple doses. Anterior root damage occurred in all phenol-treated animals except the 4 that received single 3% phenol injections. Animals that received 6% phenol demonstrated greater lower extremity motor weakness than those in the other groups, but no clear correlation existed between extent of histopathologic changes and motor weakness. CONCLUSIONS: Motor weakness, anterior root damage, and direct cord injury were noted in primates following epidural administration of phenol in concentrations below what has been reported for clinical use in humans. Since it is more difficult to control the spread of epidural versus subarachnoid phenol, the risks of epidural phenol may outweigh the benefits relative to subarachnoid administration.

Animals↗

PubMed2000

Caesarean section for placenta praevia: a retrospective study of anaesthetic management.

A retrospective survey of anaesthesia for Caesarean section (CS) for placenta praevia was performed, covering the period between January 1, 1984 and December 31, 1998. Three hundred and fifty consecutive cases of placenta praevia were identified. Overall a regional technique was used 60% of the time. Five women had a placenta accreta which required Caesarean hysterectomy: one had general anaesthesia (GA) throughout and four initially received a single-shot spinal injection. Of these latter four cases, two were converted to GA during the hysterectomy and two continued with spinal anaesthesia throughout. Two other women (both GA), suffered postoperative thrombotic episodes (one pulmonary embolus and one cerebral thrombosis) but made full recoveries. Control of blood pressure when using regional anaesthesia (RA), even in the presence of considerable haemorrhage, was not a problem. Statistical regression models indicated that RA was associated with a significantly reduced estimated blood loss and reduced need for blood transfusion. This retrospective survey finds no data to support the much quoted aphorism that RA is contraindicated for CS in the presence of placenta praevia.

Anesthesia, Epidural↗

PubMed1951

An evaluation of cesarean section.

The risks of cesarean section have been reduced in step with the increase in safety of all major surgical procedures. In a series of 13,153 deliveries, 1,265 (9.6 per cent) were by cesarean section. There were three obstetrical maternal deaths in 11,888 cases in which delivery was by the vaginal route-0.025 per cent. In the series of 1,265 deliveries by cesarean section there was one death attributable to the operation-0.08 per cent. The total uncorrected fetal loss following cesarean section was 3.8 per cent. This compares favorably with fetal loss of 3.2 per cent in the vaginal delivery group in this series, and with fetal loss rates reported from large obstetrical centers. Anesthesia by spinal injection is the method of choice in cesarean section. There were no maternal deaths or accidents attributable to spinal anesthetic, and in no case was it felt that fetal death was attributable to it. The incidence of maternal morbidity in the cesarean section group following spinal anesthesia was 15.8 per cent-less than half the incidence of morbidity following inhalation anesthesia.

Anesthesia, Spinal↗

PubMed1983

[Spinal concentrations of amoxicillin in purulent meningitis in children].

Hundred and fifteen children suffering of purulent meningitis (S.pneumoniae: 19; H.influenzae: 44; N.meningitidis; 23; others: 29) were treated by amoxicillin 200 mg/kg/day in four intramuscular injections. Spinal taps for assay of antibiotic levels in the CSF were taken 1 or 3 or 6 hours after the injection. The levels were respectively for this samples of 6.9 -1.7-1.4 micrograms/ml during the first 48 hours of treatment and 4.4-1.7-1.9 after one week. The concentrations CSF/serum were from 5 to 9.8 per cent at the beginning of treatment.

Amoxicillin↗

PubMed1984

Centrally induced vasopressor and sympathetic nerve responses to carbachol in rats.

Blood pressure rose when carbachol was injected into the cerebral ventricles in conscious rats, but the heart rate fell. When rats were later anesthetized with urethane to allow recording of abdominal sympathetic nerve activity, carbachol injected similarly produced the following biphasic responses: initial vasodepression followed by a sustained pressor phase accompanied by corresponding changes in peripheral sympathetic nerve activity. The heart rate was transiently suppressed following the injection. Spinal section abolished the initial hypotensive phase and accompanying bradycardia and made the response purely pressor. By contrast, intravenous injections elicited purely vasodepressor responses. Thus, carbachol administered centrally caused vasopressor responses possibly via both activation of sympathetic vasomotor centers and a release of pituitary hormones. Since anesthesia attenuated the pressor responses and made them biphasic, these results indicate that central cholinergic mechanisms are inhibited during anesthesia and that a sympatho-inhibitory mechanism of cholinergic receptors exists behind the pressor responses, as disclosed during anesthesia.

Anesthesia↗