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Dental trouble & apnea (lidocaine abstracts)

K. Bennett klmwb at cybergal.com
Mon Feb 8 01:13:39 EST 1999


I have also had SEVERE seizures from Lidocaine injections in Dental Offices. I
found that I don't have that reaction from it if it is the type WITHOUT
EPINEPHRINE!!! NO EPI...The injections usually are given with this included to
help keep the med localized for longer...without it, it takes about 30 minutes
before you have to have another shot! Tell the folks you deal with "NO EPI" and
your shakes can be "normal" terror from sounds of drilling and smells of YOUR
teeth being drilled!

Also, I recently had a root canal redone, and they told me that they weren't
gonna use Lidocaine at all because they preferred (?not sure heard exactly
rightly?) DARVOCAINE? for that?

Ask...

K. Bennett

"The more I know, the more I know I need to know more."
(By:  A Smart Person...?)

Rauni wrote:

> I have has seizures after shots of lidocaine. I don't know if that is
> common or not. Makes going to the dentist difficult. I need a melogram
> and can't get one because of my reaction to lidocaine.  BTW I also
> have a seizure disorder
>
> On Tue, 02 Feb 1999 00:38:12 GMT, Brian Sandle
> <bsandle at southern.co.nz> wrote:
>
> >Apologies for a lengthy article. Perhaps more attention should be given
> >to disturbance of the breathing stimulus mechanism in the sinus area.
> >
> >I have ben asking about licdocaine neurological effects on
> >sci.med.dentistry and bionet.neuroscience.
> >
> >Now I wonder whether lidocaine may affect a person with a tendency to
> >multiple sclerosis in the breathing centre, perhaps, then sleep apnea
> >could set in and produce more nerological symptoms.
> >
> >Or the dental work might produce disturbance in the sinus which could
> >reduce breathing stimulus.
> >
> >My left nostril gets a bit more blocked with pressure since an upper big
> >molar root canal. Now it is 6 days since and I woke with a more blocked
> >nostril than before. It has cleared a bit.
> >
> >I have been having some of the neurological troubles mentioned by
> >stigmata1, but they have been clearing a bit since the root canal. The
> >dentist found a fair bit of pus under the root dressing which had been in
> >for a month.
> >
> >Brian Sandle
> >
> > ***********************
> >   Sleep Apnea
> >   Author:   prepster <prepster at mindspring.com>
> >   Date:   1999/01/14
> >   Forum:   alt.support.sleep-disorder
> >
> >I have had Sleep Apnea for a while and only recently took action on it. My
> >doctor says he wants to correct a deviated nasal septum, remove my tonsils
> >and do an UPPP.
> >
> >I refuse to do the UPPP; it is painful with side effects and has a low
> >success rate...comments? Would it also help to have my adenoids removed?
> >**********************
> >
> >   Re: Chronic Pain Down Right since April
> >   Author:   Barry Kaplan <kaplanfamily at worldnet.att.net>
> >   Date:   1998/12/22
> >   Forums:   alt.support.chronic-pain, alt.med.fibromyalgia
> >   more headers author posting history prev next
> >   _________________________________________________________________
> >
> >Dave,
> >What did they fill the root canal with?
> >The most common root canal filling material is called "gutta percha" and it
> >is fairly innocuous.
> >In years past, two other materials were used.  One is called "silver
> >points".  They are not good, but they shouldn't cause the pain you are
> >reporting.  They just corrode over time.
> >The other material that is out of favor is called "sargenti paste" This
> >stuff can be real bad news.  I have heard of syptoms similar to yours, but
> >not NEARLY as bad nor widespread in distribution.
> >However, it is also possible that the thing causing the pain may not have
> >been of dental origin.  The distribution of the nerves in the mouth has
> >nothing to do with the nerves in your arm and leg. If you reported the pain
> >and tic only in your face, I might suspect things like trigeminal neuralgia
> >(tic Douluoroeux).
> >I know you said you saw 23 doctors, but there are two things you need to be
> >certain to do (if you haven't already). First of all, I would make sure I
> >had a second opinion onthe root canal by a board certified endodontist (root
> >canal specialist)
> >Secondly, you might consider seeing a neurologist about your other
> >complaints.
> >It is possible that the tooth you had the root canal done on may not have
> >been the problem. I have never seen mouth pain refer farther than the
> >sinuses or neck.  You may have had a different problem to begin with.
> >
> >There are at least two physicians that often respond to posts an this
> >newsgroup.  Hopefully Mike, Todd ,and anyone else with anything to add will
> >pipe up
> >
> >Barry (DDS)
> >
> >
> >
> >stigmata1 at hotmail.com wrote in message <75p0a9$tug$1 at nnrp1.dejanews.com>...
> >>I hope there's an answer! In April of 1998 I went to get some routine
> >dental
> >>work done, and found that I required a root canal, which I assented to.
> >>Almost immediately after the procedure, I started experiencing excrutiating
> >>pain in that tooth, which seemed to inflame the entire right side of my
> >face.
> >>It was so bad I wanted to be knocked out and have it removed on site.
> >>However, since I'm 23 all doctors advised me against removal and assured me
> >>that within a month the pain would subside. Well, the pain became so bad
> >>twice that I went to the emergency room because I couldn't take it, and
> >they
> >>gave me Percocet, Which I ended up being on for about two months. During
> >this
> >>time period, I started feeling a burning pain sensation "creeping" down my
> >>arm and my leg, as well as the already established pain in my face, eye,
> >>saggital plan, which led to a facial tic that I have to this day. But as
> >this
> >>pain started creeping down my extremities, I found it more and more
> >difficult
> >>to move my hand and my foot, writing was very difficult, I had trouble
> >>holding the pen. Gradually, the excruciating pain gave way to a lesser
> >pain,
> >>and I was moved off of Percocet down to Hydrocodone, Then just OTC pain
> >>relievers. I'm not lying prostrate in pain anymore, but I still have a
> >>constant, low level pain that's down the right side of my body. When I sigh
> >>or yawn or exhale deeply, I feel "bolts" of pain race down my right arm
> >until
> >>it 'hits' at the tips of the fingers. I also experience a phenomenon
> >when I
> >>hold my computer mouse, where my right hand will get 'cold shots' all over
> >>the top of my hand when surrounding the mouse. There seem to be pain focal
> >>points at the top of my spine and the bottom, and I feel the pain connected
> >>and start to run down what feels like the center of my leg and arm where
> >the
> >>limb is subumerged in a burning sensation. Anyone know what this is, how it
> >>came about, and the cure?
> >>
> >>Any answers appreciated,
> >>
> >>Dave Canova,
> >>stigmata1 at hotmail.com
> >>
> >*********************
> >
> >   Neurology 1992 Nov;42(11):2088-93
> >
> >Lidocaine unmasks silent demyelinative lesions in multiple sclerosis.
> >
> >    Sakurai M, Mannen T, Kanazawa I, Tanabe H
> >
> >   Department of Neurology, School of Medicine, University of Tokyo,
> >   Japan.
> >
> >   Blockage of a small number of sodium channels may prevent impulse
> >   conduction in some demyelinated segments of nerve fibers with low
> >   safety factors, thereby unmasking subclinical demyelinative lesions.
> >   On the basis of this hypothesis, lidocaine, a sodium channel blocker,
> >   was administered intravenously to 28 MS patients and to 19 normal
> >   subjects and seven patients with nondemyelinating diseases. As
> >   predicted, lidocaine (mean plasma level, 2.7 micrograms/ml) elicited
> >   reversible subclinical symptoms in 23 of the MS patients, but it had
> >   not effect on the control subjects. We made a quantitative study of
> >   the visual functions (visual acuity, color vision, visual evoked
> >   potential [VEP]) that were impaired in 15 MS patients. Of the 23
> >   affected eyes, nine showed normal VEPs, indicative of the test's
> >   sensitivity to focal lesions. This test should be useful in the
> >   diagnosis of MS and in the evaluation of the subclinical activity of
> >   MS as well.
> >
> >   PMID: 1331868, UI: 93063903
> >   Masui 1998 May;47(5):570-5
> >
> >[Midazolam for anesthetic induction in neonates].
> >
> >   [Article in Japanese]
> >
> >    Kawakami K, Ohata J, Kadosaki M, Saito I, Iwasawa K, Mitono H
> >
> >   Department of Anesthesiology, Nagano Children's Hospital.
> >
> >   The purpose of this study is to evaluate the effects of midazolam on
> >   circulation, respiration, sedation, and liver function of the
> >   neonates. The study subjects are 27 neonates (body weight 2.1 to 3.8
> >   kg, gestational age at birth 34 to 41 weeks) who underwent surgery in
> >   neonatal period. Of 27, 13 patients received lidocaine (1.5 mg.kg-1)
> >   immediately before tracheal intubation (group L), and 14 had
> >   midazolam (0.1 mg.kg-1) with lidocaine (group ML). We compared the
> >   effects of midazolam in the presence of lidocaine on the following
> >   parameters: (1) the incidence of hypotension (systolic blood pressure
> >   < 50 mmHg) and bradycardia (heart rate < 100 beats.min-1), (2) the
> >   incidence of apnea and desaturation of oxygen (< 80%), (3) the degree
> >   of sedation, and (4) the serum levels of bilirubin and unbound
> >   bilirubin after surgery. In group L, there were hypotension (1/13)
> >   and desaturation (1/13). In group ML, there were desaturation (1/14)
> >   and post-operative apnea (1/14). None in both groups developed
> >   bradycardia or intracranial hemorrhage. A single-dose of lidocaine
> >   induced sedation only in 4 neonates, while combination of midazolam
> >   and lidocaine in 11. None had elevation of either total or unbound
> >   bilirubin after surgery. In conclusion, the titrated dose of
> >   midazolam with lidocaine is useful for anesthetic induction of
> >   neonates, although cares should be taken on its adverse effects such
> >   as hypotension, desaturation, and post-operative apnea.
> >
> >   Publication Types:
> >     * Clinical trial
> >
> >   PMID: 9621667, UI: 98284687
> >     _________________
> >
> >   Anesthesiology 1998 Mar;88(3):761-7
> >
> >Hypoxia causes apnea during epidural anesthesia in rabbits.
> >
> >    Hogan QH, Amuzu J, Clifford PS, Bosnjak ZJ, Kampine JP
> >
> >   Department of Anesthesiology, Medical College of Wisconsin and the
> >   Zablocki Veterans Administration Medical Center, Milwaukee 53226,
> >   USA.
> >
> >   BACKGROUND: Although pulmonary function is minimally changed by
> >   neuraxial blockade in most cases, ventilatory arrest may ensue in
> >   rare cases. The authors examined the mechanism of apnea in a rabbit
> >   model of sudden ventilatory arrest during the combination of epidural
> >   anesthesia and hypoxia. METHODS: Rabbits were studied during
> >   alpha-chloralose sedation and spontaneous ventilation through a
> >   tracheostomy tube. Heart rate and mean arterial pressure were
> >   monitored by intraarterial cannulation. Respiratory rate and tidal
> >   volume were measured by pneumotachograph. Responses were recorded
> >   during administration of oxygen at inspired oxygen concentrations of
> >   11% for 2.5 min and 0% for 40 s, before and after either
> >   thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or
> >   intramuscular lidocaine (15 mg/kg). In a third group of animals,
> >   epinephrine was given intravenously during epidural blockade to
> >   return mean arterial pressure to baseline values before hypoxia. In a
> >   fourth group of animals, which did not get lidocaine, sympathetic
> >   blockade and hypotension were produced with intravenously
> >   administered trimethaphan rather than epidural blockade. RESULTS:
> >   Thoracolumbar epidural anesthesia decreased mean arterial pressure
> >   from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during
> >   hypoxia occurred in 90% of these animals (nine of ten) but in only
> >   11% of animals (one of nine) after intramuscularly administered
> >   lidocaine (P < 0.01). Treatment of epidural hypotension with
> >   epinephrine prevented apnea (zero of nine animals). Apnea during
> >   hypoxia occurred in 50% (three of six) of animals given trimethaphan.
> >   Apnea in all groups was sudden in onset, with no preceding decreases
> >   in respiratory rate or tidal volume. CONCLUSIONS: Epidural anesthesia
> >   results in a narrowed margin of safety for oxygen delivery to the
> >   brain and predisposes subjects to ventilatory arrest during hypoxia.
> >   This results from the combined effects of decreased blood oxygen
> >   content, which is due to decreased inspired oxygen concentration
> >   superimposed on circulatory depression due to neural blockade.
> >
> >   PMID: 9523821, UI: 98181995
> >
> >   Am J Respir Crit Care Med 1995 Jun;151(6):1857-61
> >
> >Effect of upper airway anesthesia on obstructive sleep apnea.
> >
> >    Berry RB, Kouchi KG, Bower JL, Light RW
> >
> >   Department of Medicine, Long Beach VA Medical Center, CA 90822, USA.
> >
> >   We hypothesized that upper airway mechanoreceptors contribute to the
> >   arousal stimulus that occurs with upper airway occlusion in
> >   obstructive sleep apnea (OSA). If so, upper airway anesthesia (UAA)
> >   should reduce the arousal stimulus and impair the arousal response.
> >   To test this hypothesis, we studied the effects of UAA on apnea
> >   duration and the esophageal pressure deflection before arousal in a
> >   group of patients with severe OSA. On two study nights separated by
> >   one week, subjects were monitored for 2 h after lights out. They were
> >   then awakened and either 5 cc of 4% lidocaine or saline (random
> >   order) was dripped into the upper airway via the nose over 10 min.
> >   Another 2 h of monitoring was then performed. Variables on the first
> >   and second parts of the control (C1 and C2) and lidocaine nights (L1
> >   and L2) were compared during non-rapid eye movement sleep using the
> >   analysis of variance. With lidocaine, the mean (+/- SEM) apnea
> >   duration increased from 24.2 +/- 2.6 (L1) to 30.7 +/- 2.3 (L2) s but
> >   with saline the apnea length was unchanged from 23.3 +/- 1.5 (C1) to
> >   23.4 +/- 1.6 (C2) (L2 > [L1, C1, C2], p < 0.01). In addition, the
> >   maximum esophageal pressure deflection (cm H2O) before arousal
> >   increased after lidocaine from 63.6 +/- 14.5 (L1) to 84.1 +/- 14.7
> >   (L2) but after saline was unchanged from 62.1 +/- 15.4 (C1) to 60.0
> >   +/- 15.2 (C2), (L2 > [L1, C1, C2], p < 0.05). We conclude that UAA
> >   impairs the arousal response to airway occlusion. This suggests that
> >   input from upper airway mechanoreceptors during obstructive events
> >   contributes to the total arousal stimulus in patients with OSA.
> >
> >   Publication Types:
> >     * Clinical trial
> >     * Randomized controlled trial
> >
> >   PMID: 7767531, UI: 95285040
> >     _____________________________________________________
> >
> >   Am J Respir Crit Care Med 1995 Apr;151(4):1108-12
> >
> >Topical oropharyngeal anesthesia in patients with obstructive sleep apnea.
> >
> >    Deegan PC, Mulloy E, McNicholas WT
> >
> >   Department of Respiratory Medicine, University College, Dublin,
> >   Ireland.
> >
> >   Topical oropharyngeal anesthesia (TOPA) increases obstructive sleep
> >   apnea (OSA) frequency in both normal subjects and loud snorers. The
> >   effects of TOPA in established OSA were assessed in six male patients
> >   with a mean age (+/- SEM) of 50 +/- 5.3 yr. Following an
> >   acclimatization night, each subject underwent two overnight sleep
> >   studies, randomly assigned to TOPA (10% lidocaine spray and 0.25%
> >   bupivocaine gargle) and control (C) (saline placebo). Patients
> >   demonstrated sleep efficiencies of 93 +/- 2.9% (mean +/- SEM) during
> >   C and 88 +/- 2.9% during TOPA. Overall apnea-hypopnea (AH) frequency,
> >   using inductance plethysmography, showed little change: 21.2 +/- 3.6
> >   on C versus 25.1 +/- 3.5 events/h on TOPA nights (p = 0.12). There
> >   was no significant increase in AH duration with TOPA, and oxygen
> >   desaturation (> or = 4%) frequency was similar: 21.1 +/- 3.9 per hour
> >   during TOPA versus 23.6 +/- 5.9 during C. However, obstructive AHs
> >   showed a change in thoracoabdominal motion from C to TOPA nights,
> >   with an increase in events with abdominal paradox from 3.1 +/- 1.1 to
> >   10.3 +/- 3.1 per hour (p = 0.03), and a reduction in events with
> >   ribcage paradox from 13.1 +/- 1.6 to 8.2 +/- 2.4 per hour (p = 0.08).
> >   Central and mixed AHs demonstrated similar frequencies on both
> >   nights. These data support an impairment of upper airway (UA)
> >   protective reflexes among patients with OSA.
> >
> >   Publication Types:
> >     * Clinical trial
> >     * Randomized controlled trial
> >
> >   PMID: 7697239, UI: 95211324
> >
> >
> >   Brain Res 1991 Sep 27;560(1-2):321-5
> >
> >Trigeminal mediation of the diving response in the muskrat.
> >
> >    Panneton WM
> >
> >   Department of Anatomy and Neurobiology, St. Louis School of Medicine,
> >   MO 63104.
> >
> >   Stimulation of the nasal cavity elicits powerful cardiorespiratory
> >   responses similar to the diving response. In the present study,
> >   bradycardia and apnea were elicited in muskrats by stimulation of the
> >   nasal cavity with ammonia vapors. These responses could be blocked by
> >   injections of 2% lidocaine made bilaterally into the medullary dorsal
> >   horns of the trigeminal sensory complex. However, the bradycardia due
> >   to activation of the baroreceptor reflex with intravenous
> >   phenylephrine was retained. These data implicate trigeminal neurons
> >   in the medullary dorsal horn as modulators of autonomic activity,
> >   especially in the cardiorespiratory adjustments after nasal
> >   stimulation.
> >
> >   PMID: 1760738, UI: 92103521
> >     ________________________________________________________________
> >
> >   Other Formats: [Citation Format] [MEDLINE Format]
> >   Links: [114 medline neighbors]
> >
> >   Am Rev Respir Dis 1991 Apr;143(4 Pt 1):810-3
> >
> >Obstructive sleep apnea following topical oropharyngeal anesthesia in loud
> >snorers.
> >
> >    Chadwick GA, Crowley P, Fitzgerald MX, O'Regan RG, McNicholas WT
> >
> >   Department of Respiratory Medicine, University College, Dublin,
> >   Ireland.
> >
> >   Previous studies support the presence of an upper airway reflex
> >   mechanism that contributes to the maintenance of upper airway patency
> >   during sleep. We investigated the possibility that interference with
> >   this reflex mechanism contributes to the development of obstructive
> >   sleep apnea. Eight otherwise asymptomatic snorers (seven male and one
> >   female), age 39 +/- 5.3 yr (mean +/- SEM), underwent overnight sleep
> >   studies on three successive nights. An acclimatization night was
> >   followed by two study nights randomly assigned to control (C) and
> >   oropharyngeal anesthesia (OPA). On the OPA night topical anesthesia
> >   was induced using 10% lidocaine spray and 0.25% bupivacaine gargle. A
> >   saline placebo was used on night C. All subjects slept well on both
> >   study nights (mean sleep duration was 6.2 h on both study nights),
> >   and sleep stage distribution was similar on both nights. Obstructive
> >   apneas and hypopneas (OAH) rose from 114 +/- 43 during C to 170 +/-
> >   49 during OPA (p less than 0.02). Central apneas and hypopneas (CAH)
> >   were unchanged between the two nights (8 +/- 4.9 versus 7 +/- 3). The
> >   duration of OAH was similar on both study nights (20 +/- 1.9 s during
> >   C versus 20 +/- 1.5 s during OPA). The frequency of movement arousals
> >   terminating OAH tended to be higher during OPA (7 +/- 2.9/h) than
> >   during C (3 +/- 0.7); P = NS. The frequency of oxyhemoglobin
> >   desaturations was also higher during OPA (5 +/- 2.1/h) than during C
> >   (3 +/- 1.4), p less than 0.07.
> >
> >   PMID: 2008992, UI: 91181783
> >     ________________________________________________________________
> >
> >   Other Formats: [Citation Format] [MEDLINE Format]
> >   Links: [109 medline neighbors]
> >
> >   Am Rev Respir Dis 1985 Nov;132(5):972-5
> >
> >The effects of nasal anesthesia on breathing during sleep.
> >
> >    White DP, Cadieux RJ, Lombard RM, Bixler EO, Kales A, Zwillich CW
> >
> >   Inability to breathe through the nose is an increasingly recognized
> >   cause of disordered breathing during sleep. To test the hypothesis
> >   that this respiratory dysrhythmia could result from loss of neuronal
> >   input to respiration from receptors located in the nose, we
> >   anesthetized the nasal passages of 10 normal men during sleep. Each
> >   subject spent 4 consecutive nights in the sleep laboratory while
> >   sleep stages, breathing patterns, respiratory effort, and arterial
> >   oxygen saturation were monitored. Night 1 was for acclimatization
> >   with Nights 3 and 4 being randomized to nasal spraying with either 4%
> >   lidocaine or placebo. On the lidocaine and placebo nights (Nights 3
> >   and 4) the nasal passages were also sprayed with a decongestant to
> >   prevent increased nasal air-flow resistance resulting from mucosal
> >   swelling. To control for the possible effects of this decongestant,
> >   an additional night (Night 2) was included during which the nasal
> >   passages were sprayed with room air. Parallel studies conducted
> >   during wakefulness demonstrated low nasal resistance during the
> >   lidocaine-decongestant regimen. Because of the short duration of
> >   anesthesia with lidocaine, spraying was done at lights out and 2.5
> >   and 5 h later. On the placebo night (decongestant plus saline) there
> >   were 6.4 +/- 1.8 (SEM) disordered breathing events (apneas plus
> >   hypopneas) per subject, whereas with lidocaine (plus decongestant)
> >   this increased fourfold to 25.8 +/- 7.8 events per subject (p less
> >   than 0.05). The majority of the disordered breathing events were
> >   apneas and were fairly evenly distributed between central and
> >   obstructive events. The magnitude of these changes is similar to that
> >   previously reported with complete nasal obstruction. These results
> >   suggest that nasal receptors sensitive to air flow may be important
> >   in maintaining breathing rhythmicity during sleep.
> >
> >   Publication Types:
> >     * Clinical trial
> >     * Randomized controlled trial
> >
> >   PMID: 4062052, UI: 86048887                         this document
> >
> >   Am J Perinatol 1987 Apr;4(2):164-6
> >
> >Lidocaine toxicity after maternal pudendal anesthesia in a term infant with
> >fetal distress.
> >
> >    Bozynski ME, Rubarth LB, Patel JA
> >
> >   There have been many reports of lidocaine toxicity especially after
> >   maternal paracervical block anesthesia. We recently treated a term
> >   infant with evidence of fetal distress who presented with symptoms of
> >   lidocaine toxicity after maternal pudendal anesthesia. The infant
> >   developed apnea and bradycardia soon after birth which responded to
> >   mechanical ventilation and epinephrine. A prolonged Q-T interval was
> >   noted on day 1 which normalized by day 3. Cord blood was assayed and
> >   revealed an elevated lidocaine level. Lidocaine toxicity has been
> >   associated with fetal distress secondary to fetal ion trapping in the
> >   presence of acidosis. Although good response to supportive therapy
> >   occurred in our patient, other methods of therapy such as exchange
> >   transfusion and treatment of seizures may be required in some cases.
> >   Awareness of this now uncommon syndrome will lead to prompt
> >   diagnosis, appropriate work-up, and management.
> >
> >   PMID: 3566884, UI: 87184830
> >     ________________________________________________________________
> >
> >   Other Formats: [Citation Format] [MEDLINE Format]
> >   Links: [169 medline neighbors]
> >
> >   Am J Physiol 1977 Jul;233(1):R30-6
> >
> >Properties of the laryngeal chemoreflex in neonatal piglets.
> >
> >    Lee JC, Stoll BJ, Downing SE
> >
> >   Cardiorespiratory reflex responses to laryngeal chemoreceptor
> >   stimulation were studied in 62 piglets of both sexes varying in age
> >   from 1 to 79 days. The distal trachea was cannulated to provide a
> >   free airway and the proximal end used to introduce fluids into the
> >   laryngeal area. Introduction of either water or milk produced apnea,
> >   bradycardia, and hypertension. Swab application of test fluids to the
> >   laryngeal epithelium produced similar responses. The reflex could be
> >   interrupted by flushing the laryngeal region with saline, by cutting
> >   the superior laryngeal nerves (SLN) or by anesthetizing the laryngeal
> >   epithelium with lidocaine. Electrical stimulation of SLN elicited
> >   identical responses. Respiratory inhibition by the reflex was
> >   enhanced following central depression with chloralose and overridden
> >   by administration of the respiratory stimulant, aminophylline. The
> >   relative potency of the laryngeal reflex was estimated to be
> >   equivalent to about 40% of the dose of chloralose which produced
> >   permanent respiratory arrest. It is concluded that in circumstances
> >   where respiratory drive is reduced the laryngeal inhibitory reflex is
> >   capable of caused persistent apnea and asphyxial death in the young
> >   piglet.
> >
> >   PMID: 18025, UI: 77219523
> >     ________________________________________________________________
> >
> >   Other Formats: [Citation Format] [MEDLINE Format]
> >   Links: [102 medline neighbors]
> >
> >   Rev Bras Pesqui Med Biol 1976 Dec;9(5-6):229-37
> >
> >Lethal effect of the serotonin-xylocaineR association in ganglion-blocked
> >rats.
> >
> >    Valle LB, Oliveira-Filho RM, Armonia PL, Saraceni G Jr, Nassif M, De
> >Lucia R
> >
> >   In rats anestetized with urethane and under ganglionic blockade by
> >   hexamethonium (20 mg/kg, i.v.), the i.v. injection of serotonin (60
> >   mug/kg) determined apnea, ECG alterations and a brief hypotensive
> >   response which is similar to that as elicited when 5-HT is given to
> >   intact rats. During the hypertension which follows that initial
> >   response, apnea is still present along with more severe ECG changes.
> >   After that, blood pressure falls into a prolonged hypotension, which
> >   is invariably accompanied by death. Neither norepinephrine, nor
> >   respiratory analeptics (CoramineR, RemeflinF) were able to prevent
> >   the fatal outcome. Only artificial respiration was found to be useful
> >   in some instances. It was concluded that the association serotonin
> >   plus lidocaine becomes lethal when given to ganglion-blocked rate,
> >   and this toxic effect can be ascribed mainly to the respiratory
> >   depressor activity of the drugs.
> >
> >   PMID: 1013401, UI: 77103742
> >     ___________________________
> >   Z Orthop Ihre Grenzgeb 1974 Oct;112(5):1053-62
> >




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