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Barnes Steve D. MD; Martin, Lynn D. MD; Wetzel, Randall C. MB, BS, FCCM
Anesthesia & Analgesia: December 1992
ORIGINAL ARTICLE: PDF Only
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To determine whether anesthetics alter endothelial eicosanoid release, cultured bovine pulmonary artery endothelial cells were studied during constant flow and pressure perfusion at two oxygen tensions (hypoxia, 50 ± 2 mm Hg; normoxia, 144 ± 5 mm Hg; mean ± SEM) with and without 1% halothane. Endo-thelialized microcarriers containing ∼5 × 106 cells were loaded into cartridges and perfused (3 mL/min) with Krebs′ solution (pH 7.4, at 37°C) equilibrated with each gas mixture. Eicosanoids (6-keto prostaglandin Flα, thromboxane B2, and total peptidoleu-kotrienes [C4, D4, E4, F4]) were measured by radioimmunoassay and quantified per gram of cellular protein per minute. Eicosanoid release did not vary over time. The 6-keto prostaglandin Flα release increased during hypoxia (normoxia 291 ± 27 vs hypoxia 395 ± 35 ng min−1g protein−1; P < 0.01). Halothane (H) increased release of each eicosanoid during both normoxia and hypoxia: 6-keto prostaglandin Flαnormoxia 291 ± 27 versus normoxia + H 356 ± 32 ng min−1g protein−1, hypoxia 395 ± 35 versus hypoxia + H 464 ± 40 ng-min−1-g protein−1, P < 0.05; thromboxane B2normoxia 19 ± 2 versus normoxia + H 26 ± 2 ng-min−1-g protein−1, hypoxia 20 ± 2 versus hypoxia + H 38 ± 5 ng-min−1g protein−1, P < 0.001; leukotrienenormoxia 363 ± 35 versus normoxia + H 489 ± 52 ng min−1-g protein−1, hypoxia 329 ± 29 versus hypoxia + H 455 ± 39 ng min−1-g protein−1, P = 0.001. We conclude that alteration of endothelial eicosanoid release by halothane and hypoxia could modulate pulmonary vascular tone.

Address correspondence to Dr. Wetzel, Division of Pediatric Anesthesia, The Johns Hopkins Hospital, 600 North Wolfe Street, CMSC 7–110, Baltimore, MD 21287–3711.

© 1992 International Anesthesia Research Society