Differential effect of propofol on sympathetic neurotransmission in isolated human omental arteries and veins
(1998) In British Journal of Pharmacology 125(1). p.120-126- Abstract
- 1. The present study was undertaken to elucidate the effect of propofol on sympathetic neurotransmission in isolated human omental vessels. 2. Segments of both arteries and veins were exposed to 0, 10(-7), 10(-6), 10(-5) or 10(-4)M propofol, and studied in vitro to determine effects on: (i) isometric tension after electrical field stimulation (EFS) or after exogenous administration of noradrenaline (NA); (ii) EFS-stimulated release of [3H]-NA from vessel segments preincubated with [3H]-NA; (iii) uptake of [3H]-NA. 3. Propofol at 10(-6) M enhanced EFS-induced contraction in artery segments, 10(-7) and 10(-5) M had no effect, and 10(-4) M propofol depressed EFS-induced contraction in both artery and vein segments. 4. Propofol did not affect... (More)
- 1. The present study was undertaken to elucidate the effect of propofol on sympathetic neurotransmission in isolated human omental vessels. 2. Segments of both arteries and veins were exposed to 0, 10(-7), 10(-6), 10(-5) or 10(-4)M propofol, and studied in vitro to determine effects on: (i) isometric tension after electrical field stimulation (EFS) or after exogenous administration of noradrenaline (NA); (ii) EFS-stimulated release of [3H]-NA from vessel segments preincubated with [3H]-NA; (iii) uptake of [3H]-NA. 3. Propofol at 10(-6) M enhanced EFS-induced contraction in artery segments, 10(-7) and 10(-5) M had no effect, and 10(-4) M propofol depressed EFS-induced contraction in both artery and vein segments. 4. Propofol did not affect the response to exogenous NA in artery and vein segments. 5. EFS-stimulated release of [3H]-NA was depressed by 10(-5) and 10(-4) M propofol in artery segments, and by 10(-4) M in vein segments. 6. Uptake of [3H]-NA was depressed by 10(-6)-10(-4) M propofol in artery but not in vein segments. 7. The results suggest that sympathetic neurotransmission is enhanced at clinical concentrations (10(-6) M) of propofol in human omental arteries, but not veins. This may be due to an increased availability of NA in the neuromuscular junction resulting from a reduced presynaptic reuptake. Propofol at probably supraclinical concentrations (10(-5)-10(-4) M) impairs the sympathetic neurotransmission in both human omental arteries and veins, probably due to an inhibitory effect on the NA release from the sympathetic nerves. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1112964
- author
- Wallerstedt, Susanna and Bodelsson, Mikael LU
- organization
- publishing date
- 1998
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Anaesthetic, intravenous, propofol, omental artery, human, sympathetic nervous system: noradrenaline, omental vein
- in
- British Journal of Pharmacology
- volume
- 125
- issue
- 1
- pages
- 120 - 126
- publisher
- Wiley
- external identifiers
-
- pmid:9776351
- scopus:0031705733
- ISSN
- 1476-5381
- DOI
- 10.1038/sj.bjp.0702021
- language
- English
- LU publication?
- yes
- id
- 2a02ab0e-9bad-494d-910e-8411f6691944 (old id 1112964)
- date added to LUP
- 2016-04-01 16:04:21
- date last changed
- 2022-01-28 17:06:17
@article{2a02ab0e-9bad-494d-910e-8411f6691944,
abstract = {{1. The present study was undertaken to elucidate the effect of propofol on sympathetic neurotransmission in isolated human omental vessels. 2. Segments of both arteries and veins were exposed to 0, 10(-7), 10(-6), 10(-5) or 10(-4)M propofol, and studied in vitro to determine effects on: (i) isometric tension after electrical field stimulation (EFS) or after exogenous administration of noradrenaline (NA); (ii) EFS-stimulated release of [3H]-NA from vessel segments preincubated with [3H]-NA; (iii) uptake of [3H]-NA. 3. Propofol at 10(-6) M enhanced EFS-induced contraction in artery segments, 10(-7) and 10(-5) M had no effect, and 10(-4) M propofol depressed EFS-induced contraction in both artery and vein segments. 4. Propofol did not affect the response to exogenous NA in artery and vein segments. 5. EFS-stimulated release of [3H]-NA was depressed by 10(-5) and 10(-4) M propofol in artery segments, and by 10(-4) M in vein segments. 6. Uptake of [3H]-NA was depressed by 10(-6)-10(-4) M propofol in artery but not in vein segments. 7. The results suggest that sympathetic neurotransmission is enhanced at clinical concentrations (10(-6) M) of propofol in human omental arteries, but not veins. This may be due to an increased availability of NA in the neuromuscular junction resulting from a reduced presynaptic reuptake. Propofol at probably supraclinical concentrations (10(-5)-10(-4) M) impairs the sympathetic neurotransmission in both human omental arteries and veins, probably due to an inhibitory effect on the NA release from the sympathetic nerves.}},
author = {{Wallerstedt, Susanna and Bodelsson, Mikael}},
issn = {{1476-5381}},
keywords = {{Anaesthetic; intravenous; propofol; omental artery; human; sympathetic nervous system: noradrenaline; omental vein}},
language = {{eng}},
number = {{1}},
pages = {{120--126}},
publisher = {{Wiley}},
series = {{British Journal of Pharmacology}},
title = {{Differential effect of propofol on sympathetic neurotransmission in isolated human omental arteries and veins}},
url = {{http://dx.doi.org/10.1038/sj.bjp.0702021}},
doi = {{10.1038/sj.bjp.0702021}},
volume = {{125}},
year = {{1998}},
}