Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells

Geoffrey Milton Thiele, Gary E. Hill, Jacqueline A. Pavlik, Thomas L. Freeman, Dean J. Tuma, Michael J. Duryee, Lynell Warren Klassen

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

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.

Original languageEnglish (US)
Article number3
JournalBMC Anesthesiology
Volume5
DOIs
StatePublished - Apr 12 2005

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Halothane
Endothelial Cells
Tumor Necrosis Factor-alpha
Alcohols
Lipopolysaccharides
Heart Injuries
Acetaldehyde
Bovine Serum Albumin
Malondialdehyde
Anesthetics
Albumins
Proteins
Anesthesia
Enzyme-Linked Immunosorbent Assay
Liver
Wounds and Injuries
Therapeutics

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells. / Thiele, Geoffrey Milton; Hill, Gary E.; Pavlik, Jacqueline A.; Freeman, Thomas L.; Tuma, Dean J.; Duryee, Michael J.; Klassen, Lynell Warren.

In: BMC Anesthesiology, Vol. 5, 3, 12.04.2005.

Research output: Contribution to journalArticle

Thiele, Geoffrey Milton ; Hill, Gary E. ; Pavlik, Jacqueline A. ; Freeman, Thomas L. ; Tuma, Dean J. ; Duryee, Michael J. ; Klassen, Lynell Warren. / Halothane potentiates the alcohol-adduct induced TNF-alpha release in heart endothelial cells. In: BMC Anesthesiology. 2005 ; Vol. 5.
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AU - Thiele, Geoffrey Milton

AU - Hill, Gary E.

AU - Pavlik, Jacqueline A.

AU - Freeman, Thomas L.

AU - Tuma, Dean J.

AU - Duryee, Michael J.

AU - Klassen, Lynell Warren

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