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Halothane Enhances Pulmonary Artery Endothelial Eicosanoid Release

Departments of Anesthesiology/Critical Care Medicine and Pediatrics, The Johns Hopkins Medical Institutions, Baltimore, Maryland

Abstract

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 x 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 F_l, 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 F_l 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 F_lnormoxia 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.