"K. Bennett" <klmwb at cybergal.com> wrote:
>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?
Carbocaine.
Cheers,
Joel
-----------
>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
>> >
