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Increased NO‐synthase activity and beneficial effect of PDE‐5 inhibition by sildenafil in pulmonary hypertension caused by pulmonary embolism (LB646)
Author(s) -
Mizera Roman,
Hodyc Daniel,
Herget Jan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb646
Subject(s) - sildenafil , pulmonary hypertension , hypoxic pulmonary vasoconstriction , medicine , pulmonary embolism , perfusion , vasoconstriction , cardiology , anesthesia , pharmacology
Background Two mechanisms that contribute to pulmonary hypertension after acute pulmonary embolism (PE) are vascular obstruction and vasoconstriction. Vasoconstriction is influenced by NO release. We focused on NO synthase activity, production of NO oxidative products (NOx) and effect of phosphodiesterase‐5 (PDE‐5) blockade by sildenafil on pulmonary hypertension after PE. Methods Using the model of in vivo pulmonary embolism we measured changes of perfusion pressure in isolated rat lungs after blockade of NO‐synthase by L‐NAME and of PDE‐5 by Sildenafil. The NOx concentration was measured before and after PE in venous blood. Results The increase in pulmonary perfusion pressure after L‐NAME administration was higher in rats after PE. NOx plasma concentration was higher after PE than before. Perfusion pressure after PE in rats treated with sildenafil was lower (12.9 ± 0,79 mmHg) than after PE in control group (21.4 ± 3,20 mmHg). Conclusion Experimental PE in rats increases NO‐synthase activity and production of NOx. Administration of sildenafil inhibits pulmonary hypertension after PE. Our study indicates that similarly as in other forms of pulmonary hypertension sildenafil may be beneficial in the treatment of acute pulmonary embolism. Grant Funding Source : Supported by GAUK n. 634112/2012