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Open Access Research article

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

Geoffrey M Thiele123*, Gary E Hill4, Jacqueline A Pavlik12, Thomas L Freeman12, Dean J Tuma12, Michael J Duryee12 and Lynell W Klassen12

Author Affiliations

1 University of Nebraska Medical Center, Department of Internal Medicine, 988090 Nebraska Medical Center, Omaha, NE, 68198-3025, USA

2 Veterans Administration Alcohol Research Center, Omaha Veterans Administration Medical Center, 4101 Woolworth Avenue, Omaha, NE, 68105, USA

3 University of Nebraska Medical Center, Department of Pathology and Microbiology, 986495 Nebraska Medical Center, Omaha, NE, 68198-6495, USA

4 UT South western, Department of Anesthesiology and Pain Management, 5323 Harry Hines Blvd., Dallas, TX, 75390-9072, USA

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BMC Anesthesiology 2005, 5:3  doi:10.1186/1471-2253-5-3

Published: 12 April 2005

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.