Inflammation and intimal hyperplasia associated with experimental pulmonary embolism

Abstract

Objective: We tested the hypothesis that a venous thromboembolism to the pulmonary arterial system (pulmonary embolism [PE]) would cause an inflammatory response within the pulmonary arterial (PA) wall marked by elevated cytokines and chemokines and an influx of inflammatory cells. Methods: Experimental PE was induced in 70 rats and confirmed with angiography and O2 saturation depression, and an additional 70 rats underwent sham operations. PA and lung tissue were removed at 3 hours and at 1, 2, 4, 6, 8, and 14 days (n = 10 per time point), were analyzed for proinflammatory cytokines and chemokines, and underwent histologic analysis. Data were analyzed with analysis of variance and the unpaired Student t test. Results: Average gross PE resolution was 40% at 2 days, 90% at 4 days, and 100% at 6 days. Only monocyte chemoattractant protein-1 levels were greater in affected PAs compared with sham PAs at 3 hours, 1 day, and 2 days (137 ± 13 pg/mg protein, 285 ± 40 pg/mg protein, and 249 ± 36 pg/mg protein versus 101 ± 6 pg/mg protein, 150 ± 36 pg/mg protein, and 92 ± 3 pg/mg protein; P