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Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells
BACKGROUND: The possibility exists for major complications to occur when individuals are intoxicated with alcohol prior to anesthetization. Halothane is an anesthetic that can be metabolized by the liver into a highly reactive product, trifluoroacetyl chloride, which reacts with endogenous proteins...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2005
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1090549/ https://www.ncbi.nlm.nih.gov/pubmed/15826301 http://dx.doi.org/10.1186/1471-2253-5-3 |
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author | Thiele, Geoffrey M Hill, Gary E Pavlik, Jacqueline A Freeman, Thomas L Tuma, Dean J Duryee, Michael J Klassen, Lynell W |
author_facet | Thiele, Geoffrey M Hill, Gary E Pavlik, Jacqueline A Freeman, Thomas L Tuma, Dean J Duryee, Michael J Klassen, Lynell W |
author_sort | Thiele, Geoffrey M |
collection | PubMed |
description | BACKGROUND: The possibility exists for major complications to occur when individuals are intoxicated with alcohol prior to anesthetization. Halothane is an anesthetic that can be metabolized by the liver into a highly reactive product, trifluoroacetyl chloride, which reacts with endogenous proteins to form a trifluoroacetyl-adduct (TFA-adduct). The MAA-adduct which is formed by acetaldehyde (AA) and malondialdehyde reacting with endogenous proteins, has been found in both patients and animals chronically consuming alcohol. These TFA and MAA-adducts have been shown to cause the release of inflammatory products by various cell types. If both adducts share a similar mechanism of cell activation, receiving halothane anesthesia while intoxicated with alcohol could exacerbate the inflammatory response and lead to cardiovascular injury. METHODS: We have recently demonstrated that the MAA-adduct induces tumor necrosis factor-α (TNF-α) release by heart endothelial cells (HECs). In this study, pair and alcohol-fed rats were randomized to receive halothane pretreatments intra peritoneal. Following the pretreatments, the intact heart was removed, HECs were isolated and stimulated with unmodified bovine serum albumin (Alb), MAA-modified Alb (MAA-Alb), Hexyl-MAA, or lipopolysaccharide (LPS), and supernatant concentrations of TNF-α were measured by ELISA. RESULTS: Halothane pre-treated rat HECs released significantly greater TNF-α concentration following MAA-adduct and LPS stimulation than the non-halothane pre-treated in both pair and alcohol-fed rats, but was significantly greater in the alcohol-fed rats. CONCLUSION: These results demonstrate that halothane and MAA-adduct pre-treatment increases the inflammatory response (TNF-α release). Also, these results suggest that halothane exposure may increase the risk of alcohol-induced heart injury, since halothane pre-treatment potentiates the HEC TNF-α release measured following both MAA-Alb and LPS stimulation. |
format | Text |
id | pubmed-1090549 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-10905492005-05-07 Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells Thiele, Geoffrey M Hill, Gary E Pavlik, Jacqueline A Freeman, Thomas L Tuma, Dean J Duryee, Michael J Klassen, Lynell W BMC Anesthesiol Research Article BACKGROUND: The possibility exists for major complications to occur when individuals are intoxicated with alcohol prior to anesthetization. Halothane is an anesthetic that can be metabolized by the liver into a highly reactive product, trifluoroacetyl chloride, which reacts with endogenous proteins to form a trifluoroacetyl-adduct (TFA-adduct). The MAA-adduct which is formed by acetaldehyde (AA) and malondialdehyde reacting with endogenous proteins, has been found in both patients and animals chronically consuming alcohol. These TFA and MAA-adducts have been shown to cause the release of inflammatory products by various cell types. If both adducts share a similar mechanism of cell activation, receiving halothane anesthesia while intoxicated with alcohol could exacerbate the inflammatory response and lead to cardiovascular injury. METHODS: We have recently demonstrated that the MAA-adduct induces tumor necrosis factor-α (TNF-α) release by heart endothelial cells (HECs). In this study, pair and alcohol-fed rats were randomized to receive halothane pretreatments intra peritoneal. Following the pretreatments, the intact heart was removed, HECs were isolated and stimulated with unmodified bovine serum albumin (Alb), MAA-modified Alb (MAA-Alb), Hexyl-MAA, or lipopolysaccharide (LPS), and supernatant concentrations of TNF-α were measured by ELISA. RESULTS: Halothane pre-treated rat HECs released significantly greater TNF-α concentration following MAA-adduct and LPS stimulation than the non-halothane pre-treated in both pair and alcohol-fed rats, but was significantly greater in the alcohol-fed rats. CONCLUSION: These results demonstrate that halothane and MAA-adduct pre-treatment increases the inflammatory response (TNF-α release). Also, these results suggest that halothane exposure may increase the risk of alcohol-induced heart injury, since halothane pre-treatment potentiates the HEC TNF-α release measured following both MAA-Alb and LPS stimulation. BioMed Central 2005-04-12 /pmc/articles/PMC1090549/ /pubmed/15826301 http://dx.doi.org/10.1186/1471-2253-5-3 Text en Copyright © 2005 Thiele et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Thiele, Geoffrey M Hill, Gary E Pavlik, Jacqueline A Freeman, Thomas L Tuma, Dean J Duryee, Michael J Klassen, Lynell W Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells |
title | Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells |
title_full | Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells |
title_fullStr | Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells |
title_full_unstemmed | Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells |
title_short | Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells |
title_sort | halothane potentiates the alcohol-adduct induced tnf-alpha release in heart endothelial cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1090549/ https://www.ncbi.nlm.nih.gov/pubmed/15826301 http://dx.doi.org/10.1186/1471-2253-5-3 |
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