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Thörn, Sven-Egron
Publications (7 of 7) Show all publications
Ahlstrand, R., Savilampi, J., Thörn, S.-E. & Wattwil, M. (2011). Effects of cricoid pressure and remifentanil on the esophageal sphincters using high-resolution solid-state manometry. Acta Anaesthesiologica Scandinavica, 55(2), 209-215
Open this publication in new window or tab >>Effects of cricoid pressure and remifentanil on the esophageal sphincters using high-resolution solid-state manometry
2011 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 55, no 2, p. 209-215Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Cricoid pressure has been shown to decrease the pressure in the lower esophageal sphincter (LES), increasing the risk of aspiration. Whether this reaction is due to pain associated with the application of cricoid pressure has not been studied. The aim of this study was to compare the effects of cricoid pressure with those of peripheral pain on pressures in the LES, and to study whether remifentanil influences these effects. Data from the upper esophageal sphincter (UES) are also described.

METHODS: Continuous solid-state manometry was performed in 14 healthy volunteers. Initially, the effect of remifentanil (target-controlled infusion with a plasma target concentration of 5.0 ng/ml) was studied, and thereafter, the effects of cricoid pressure and peripheral pain stimulation (cold stimulation). Finally, these two interventions were repeated under ongoing remifentanil infusion.

RESULTS: Remifentanil decreased the LES pressure significantly [ΔP-6.5 mmHg, 95% confidence interval (95% CI) -1.7 to -11.2]. Cricoid pressure application decreased the LES pressure significantly (ΔP-3.7 mmHg, 95% CI -1.4 to 6.1), whereas peripheral pain did not (ΔP 1.2 mmHg, 95% CI -3.5 to 1.1). Under ongoing remifentanil infusion, no cricoid pressure-induced LES relaxation was observed. Cricoid pressure induced high pressures in the area of the UES, 215.7 (±91.2) mmHg without remifentanil vs. 219.4 (±74.2) mmHg with remifentanil.

CONCLUSIONS: Remifentanil as well as cricoid pressure per se induced decreases in LES pressure. However, cricoid pressure-induced changes of the barrier pressure were not significant whether induced with or without an infusion of remifentanil.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2011
National Category
Anesthesiology and Intensive Care
Research subject
Anaesthesiology
Identifiers
urn:nbn:se:oru:diva-15386 (URN)10.1111/j.1399-6576.2010.02367.x (DOI)000286208600010 ()21226863 (PubMedID)2-s2.0-78651516200 (Scopus ID)
Available from: 2011-04-26 Created: 2011-04-26 Last updated: 2018-02-20Bibliographically approved
de Leon, A., Ahlstrand, R., Thörn, S.-E. & Wattwil, M. (2011). Effects of propofol on oesophageal sphincters: a study on young and elderly volunteers using high-resolution solid-state manometry. European Journal of Anaesthesiology, 28(4), 273-278
Open this publication in new window or tab >>Effects of propofol on oesophageal sphincters: a study on young and elderly volunteers using high-resolution solid-state manometry
2011 (English)In: European Journal of Anaesthesiology, ISSN 0265-0215, E-ISSN 1365-2346, Vol. 28, no 4, p. 273-278Article in journal (Refereed) Published
Abstract [en]

BACKGROUND AND OBJECTIVE:

The oesophageal sphincters play an important role in protecting the airway. During manometric studies, administration of an anxiolytic agent is often required to make insertion of the catheter acceptable for the patient. The anxiolytic should not affect the results of the measurements. This study evaluates the effects of two different doses of propofol on the pressures in the oesophageal sphincters. The effect of increased abdominal pressure was also studied.

METHODS:

Twenty healthy volunteers, 10 young (mean age 25 years) and 10 elderly (mean age 71 years), were recruited. The effects of a low dose of propofol [0.3 mg kg(-1) intravenously (i.v.)] and a high dose of propofol (young group 0.9 mg kg(-1) i.v. and elderly group 0.6 mg kg(-1) i.v.) were studied with and without external abdominal pressure.

RESULTS:

There were no statistically significant changes in lower oesophageal sphincter (LOS) pressure after the low dose of propofol. After the high dose, there was an increase in LOS pressure, which was statistically significant in the young group (P < 0.05). The upper oesophageal sphincter (UOS) pressure decreased after both doses of propofol (P < 0.01 for the higher dose and P < 0.05 for the lower dose).

CONCLUSION:

A low dose of propofol (0.3 mg kg(-1) i.v.) leaves the LOS unaffected in young and elderly volunteers and can be used safely as an anxiolytic agent during studies of the LOS without influencing the results. However, the UOS is more sensitive to the effects of propofol and we do not recommend the use of propofol as an anxiolytic agent during manometric studies of the UOS.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2011
National Category
Medical and Health Sciences Anesthesiology and Intensive Care
Research subject
Anaesthesiology
Identifiers
urn:nbn:se:oru:diva-15384 (URN)10.1097/EJA.0b013e3283413211 (DOI)000288196000009 ()21119519 (PubMedID)2-s2.0-79953874254 (Scopus ID)
Available from: 2011-04-26 Created: 2011-04-26 Last updated: 2017-12-11Bibliographically approved
de Leon, A., Thörn, S.-E. & Wattwil, M. (2010). High-resolution solid-state manometry of the upper and lower esophageal sphincters during anesthesia induction: a comparison between obese and non-obese patients. Anesthesia and Analgesia, 111(1), 149-153
Open this publication in new window or tab >>High-resolution solid-state manometry of the upper and lower esophageal sphincters during anesthesia induction: a comparison between obese and non-obese patients
2010 (English)In: Anesthesia and Analgesia, ISSN 0003-2999, E-ISSN 1526-7598, Vol. 111, no 1, p. 149-153Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The prevalence of obesity has increased dramatically in recent decades. The gastrointestinal changes associated with obesity have clinical significance for the anesthesiologist in the perioperative period. The lower esophageal sphincter and the upper esophageal sphincter play a central role in preventing regurgitation and aspiration. The effects of increased intra-abdominal pressure during anesthesia on the lower esophageal sphincter and the upper esophageal sphincter in obese patients are unknown. In the present study we evaluated, with high-resolution solid-state manometry, the upper esophageal sphincter, lower esophageal sphincter, and barrier pressure (BrP) (lower esophageal pressure - gastric pressure) in obese patients during anesthesia induction and compared them with pressures in non-obese patients. METHODS: We studied 28 patients, ages 18 to 72 years, 14 with a body mass index >= 35kg/m(2), who were undergoing laparoscopic gastric bypass, and 14 with a body mass index <= 30kg/m(2), who were undergoing laparoscopic cholecystectomy, using high-resolution solid-state manometry. RESULTS: Upper esophageal sphincter pressure decreased during anesthesia induction in both groups. Lower esophageal sphincter pressure decreased in both groups during anesthesia induction, and it was significantly lower in obese patients than in non-obese patients. The BrP decreased in both groups and was significantly lower in the obese group than in the non-obese group. The BrP remained positive at all times in both groups. CONCLUSION: Lower esophageal sphincter and BrPs decreased in both obese and non-obese patients during anesthesia induction, but were significantly lower in obese patients. Although the BrP was significantly lower, it remained positive in all patients. (Anesth Analg 2010;111:149-53)

National Category
Medical and Health Sciences Surgery
Research subject
Surgery
Identifiers
urn:nbn:se:oru:diva-15389 (URN)10.1213/ANE.0b013e3181e1a71f (DOI)000279281500027 ()
Available from: 2011-04-26 Created: 2011-04-26 Last updated: 2017-12-11Bibliographically approved
Walldén, J., Lindberg, G., Sandin, M., Thörn, S.-E. & Wattwil, M. (2008). Effects of fentanyl on gastric myoelectrical activity: a possible association with polymorphisms of the mu-opioid receptor gene?. Acta Anaesthesiologica Scandinavica, 52(5), 708-715
Open this publication in new window or tab >>Effects of fentanyl on gastric myoelectrical activity: a possible association with polymorphisms of the mu-opioid receptor gene?
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2008 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 52, no 5, p. 708-715Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Opioids have inhibitory effects on gastric motility, but the mechanism is far from clear. Electrical slow waves in the stomach determine the frequency and the peristaltic nature of gastric contractions. The primary aim of this study was to investigate the effects of the opioid fentanyl on gastric myoelectric activity. As there were large variations between the subjects, we investigated whether the variation was correlated to single nucleotide polymorphisms (SNP) of the mu-opioid receptor (MOR) gene. METHODS: We used cutaneous multichannel electrogastrography (EGG) to study myoelectrical activity in 20 patients scheduled for elective surgery. Fasting EGG was recorded for 30 min, followed by intravenous administration of fentanyl 1 microg/kg and subsequent EGG recording for 30 min. Spectral analysis of the two recording periods was performed and the variables assessed were dominant frequency (DF) of the EGG and its power (DP). Genetic analysis of the SNP A118G and G691C of the MOR gene was performed with the polymerase chain reaction technique. RESULTS: There was a significant reduction in DF and DP after intravenous fentanyl. However, there was a large variation between the patients. In eight subjects EGG was unaffected, five subjects had a slower DF (bradygastria) and in six subjects the slow waves disappeared. We found no correlation between the EGG outcome and the presence of A118G or G691C in the MOR gene. CONCLUSIONS: Fentanyl inhibited gastric myoelectrical activity in about half of the subjects. The variation could not be explained by SNP in the MOR gene. Because of small sample size, the results must be regarded as preliminary observations.

Keywords
Adult, Aged, Analgesics, Opioid/metabolism/*pharmacology, Electrophysiology, Female, Fentanyl/metabolism/*pharmacology, Gastrointestinal Motility/*drug effects/*genetics/physiology, Genotype, Humans, Male, Middle Aged, Polymerase Chain Reaction/methods, Polymorphism, Single Nucleotide, Postoperative Nausea and Vomiting/physiopathology/prevention & control, Receptors, Opioid; mu/*genetics, Stomach/physiology
National Category
Medical and Health Sciences Anesthesiology and Intensive Care Surgery
Research subject
Anaesthesiology; Surgery
Identifiers
urn:nbn:se:oru:diva-3395 (URN)10.1111/j.1399-6576.2008.01624.x (DOI)18419726 (PubMedID)
Available from: 2008-12-04 Created: 2008-12-04 Last updated: 2017-12-14Bibliographically approved
Sandin, M., Thörn, S.-E., Dahlqvist, A., Wattwil, L., Axelsson, K. & Wattwil, M. (2008). Effects of pain stimulation on bispectral index, heart rate and blood pressure at different minimal alveolar concentration values of sevoflurane. Acta Anaesthesiologica Scandinavica, 52(3), 420-426
Open this publication in new window or tab >>Effects of pain stimulation on bispectral index, heart rate and blood pressure at different minimal alveolar concentration values of sevoflurane
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2008 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 52, no 3, p. 420-426Article in journal (Other academic) Published
Abstract [en]

Background: The aim of the present study was to examine the level of unconsciousness measured with bispectral index (BIS) at different minimal alveolar concentration (MAC) levels of sevoflurane, and to study the hemodynamic and BIS reactions during noxious stimulation with transcutaneous electrical nerve stimulation (TENS) and an ice water pain test (IWP).

Methods: This study was approved by the Ethics Committee and was performed on 10 healthy, young volunteers (six males and four females), ASA physical status I. Anesthesia was induced and maintained with sevoflurane in an oxygen/air mixture. The volunteers were spontaneously breathing, but if necessary, ventilation was mechanically supported. TENS and IWP were performed at 1.0, 1.5 and 2.0 MAC of sevoflurane.

Results: At 1.0 MAC, there was a significant increase in BIS during pain stimulation both with IWP (P<0.03) and with TENS (P<0.005), but at 1.5 MAC there were no changes. A marked variation in BIS was seen at 2.0 MAC, with periods of burst suppression and periods of high BIS values despite clinical signs of deep anesthesia. These marked variations in BIS were seen before, during and after pain stimulation. One volunteer (# 8) had a short episode of convulsions at 2.0 MAC.

Conclusion: BIS, heart rate and blood pressure increased during pain stimulation at 1.0 MAC but not at 1.5 MAC of sevoflurane. There was a remarkable variation in BIS at 2.0 MAC of sevoflurane, with BIS values indicating wakefulness despite clinical signs of deep anesthesia. This BIS variation is probably caused by epileptogenic activity due to sevoflurane.

Place, publisher, year, edition, pages
Copenhagen: Blackwell Munksgaard, 2008
Keywords
Adult, Anesthesia, Anesthetics; Inhalation/*pharmacology, Blood Pressure/drug effects/physiology, Dose-Response Relationship; Drug, Electrodes; Implanted, Electroencephalography/drug effects, Female, Heart Rate/drug effects/physiology, Humans, Male, Methyl Ethers/*pharmacology, Monitoring; Intraoperative/instrumentation, Pain/physiopathology, Pain Measurement/*drug effects/methods, Pulmonary Alveoli/*metabolism, Transcutaneous Electric Nerve Stimulation/*adverse effects, Unconsciousness/physiopathology
National Category
Medical and Health Sciences Surgery Anesthesiology and Intensive Care
Research subject
Surgery
Identifiers
urn:nbn:se:oru:diva-3396 (URN)10.1111/j.1399-6576.2007.01569.x (DOI)18269392 (PubMedID)
Available from: 2008-12-04 Created: 2008-12-04 Last updated: 2017-12-14Bibliographically approved
Walldén, J., Thörn, S.-E., Lindberg, G. & Wattwil, M. (2008). Effects of remifentanil on gastric tone. Acta Anaesthesiologica Scandinavica, 52(7), 969-976
Open this publication in new window or tab >>Effects of remifentanil on gastric tone
2008 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 52, no 7, p. 969-976Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES: Opioids are well known for impairing gastric motility. The mechanism is far from clear and there is wide interindividual variability. The purpose of this study was to evaluate the effect of remifentanil on proximal gastric tone. MATERIALS AND METHODS: Healthy volunteers were studied on two occasions and proximal gastric tone was measured by a gastric barostat. On the first occasion (n=8), glucagon 1 mg IV was given as a reference for a maximal relaxation of the stomach. On the second occasion (n=9), remifentanil was given in incremental doses (0.1, 0.2 and 0.3 microg/kg/min) for 15 min each, followed by a washout period of 30 min. Thereafter, remifentanil was readministered, and 10 min later glucagon 1 mg was given. Mean intragastric bag volumes were calculated for each 5-min interval. RESULTS: Glucagon decreased gastric tone in all subjects. Remifentanil had a marked effect on gastric tone; we found two distinct patterns of reactions with both increases and decreases in gastric tone and, during the remifentanil infusion, glucagon did not affect gastric tone. CONCLUSIONS: Remifentanil induced changes in gastric tone with both increases and decreases. The effect of remifentanil on gastric tone is probably dependent on the current state of the systems involved.

Place, publisher, year, edition, pages
Copenhagen: Blackwell Munksgaard, 2008
Keywords
Adult, Analgesics, Opioid/*pharmacology, Dose-Response Relationship, Drug, Fasting, Gastrointestinal Agents/administration & dosage, Gastrointestinal Motility/*drug effects/physiology, Glucagon/administration & dosage, Humans, Male, Piperidines/*pharmacology, Reference Values, Stomach/*drug effects/physiology
National Category
Medical and Health Sciences Anesthesiology and Intensive Care Surgery
Research subject
Anaesthesiology; Surgery
Identifiers
urn:nbn:se:oru:diva-3397 (URN)10.1111/j.1399-6576.2008.01685.x (DOI)18494844 (PubMedID)
Available from: 2008-12-04 Created: 2008-12-04 Last updated: 2017-12-14Bibliographically approved
Axelsson, P., Thörn, S.-E., Lövqvist, Å., Wattwil, L. & Wattwil, M. (2006). Betamethasone does not prevent nausea and vomiting induced by the dopamine-agonist apomorphine. Canadian Journal of Anesthesia, 53(4), 370-374
Open this publication in new window or tab >>Betamethasone does not prevent nausea and vomiting induced by the dopamine-agonist apomorphine
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2006 (English)In: Canadian Journal of Anesthesia, ISSN 0832-610X, E-ISSN 1496-8975, Vol. 53, no 4, p. 370-374Article in journal (Refereed) Published
Abstract [en]

PURPOSE: The mechanism of the antiemetic actions of corticosteroids is not known. The purpose of this study was to evaluate if betamethasone can prevent nausea, vomiting or increase of vasopressin induced by apomorphine. Metoclopramide, a dopamine antagonist, was used as a control substance. METHODS: Ten healthy volunteers were studied on three occasions. In a randomized order they were allocated to receive pretreatment with betamethasone 8 mg iv, metoclopramide 10 mg iv, and normal saline 2 mL as placebo on the three different occasions, 15 min before the administration of apomorphine 30 microg x kg(-1) s.c.. After administration of apomorphine, episodes of vomiting were recorded, and the intensity of nausea was estimated by the subject on a visual analogue scale (VAS 0-10 cm). Blood samples for analysis of plasma concentrations of vasopressin were analyzed. RESULTS: One volunteer decided to withdraw, as he experienced akathisia after receiving metoclopramide. During the first two hours after apomorphine, eight of nine volunteers vomited both after betamethasone and placebo. One volunteer did not vomit after betamethasone and placebo but he experienced nausea. None of the volunteers vomited after metoclopramide (P < 0.01 vs betamethasone and placebo). The maximum VAS for nausea was significantly higher after betamethasone and placebo compared to metoclopramide (P < 0.01). The vasopressin levels increased after betamethasone and placebo, but there was no increase in any volunteer after pretreatment with metoclopramide. CONCLUSION: This study demonstrates that betamethasone does not prevent nausea, vomiting and increase of vasopressin induced by apomorphine, whereas metoclopramide prevents apomorphine-induced emesis. Our work suggests that betamethasone does not have dopamine-antagonistic effects.

National Category
Medical and Health Sciences Anesthesiology and Intensive Care
Research subject
Anaesthesiology
Identifiers
urn:nbn:se:oru:diva-11103 (URN)10.1007/BF03022501 (DOI)16575035 (PubMedID)
Available from: 2010-06-16 Created: 2010-06-16 Last updated: 2017-12-12Bibliographically approved

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