title: Sildenafil modulates hemodynamics and pulmonary gas exchange.
abstract: The effects of sildenafil (Viagra) on hemodynamics and pulmonary gas exchange remain uncertain. The aim of this study was to investigate what effect sildenafil had on gas exchange. A total of 24 anesthetized pigs were randomly assigned into four groups of six animals each: Group Low received 25 mg of sildenafil, which is equivalent to half the recommended dose for humans; group Normal received 50 mg; group High received 100 mg; and one group served as control. Inert gas and hemodynamic measurements were performed to define dose-dependent effects of sildenafil on cardiac and pulmonary function. Measurements were taken 30, 60, and 90 min after the administration of sildenafil via gastric tube. All doses of sildenafil caused significant increases in intrapulmonary shunt flow (maximum amplitude, 4.4 +/- 0.3 to 11.9 +/- 0.5%; mean +/- SEM), which was reflected by marked decreases in PaO2. Sildenafil elicited some significant increases in cardiac index (CI) (high dose, 142 +/- 10 to 196 +/- 13 ml x kg(-1), mean +/- SEM). Mean arterial pressure was significantly depressed after the high dose of sildenafil. Pulmonary artery pressure was decreased after high-dose sildenafil (maximum amplitude, 16 +/- 1.6 to 14 +/- 1.8, mean +/- SEM). No significant differences between the three treatment groups were found. Sildenafil represents and orally active substance with phosphodiesterase V inhibitory and cardiac output-increasing actions. PaO2 decrease after 50 and 100 mg of sildenafil was observed in the presence of significant rises in pulmonary shunt flow and CI.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria. axel.klleinsasser@uibk.ac.at
authors.forename: A
authors.initials: A
authors.lastname: Kleinsasser
authors.forename: A
authors.initials: A
authors.lastname: Loeckinger
authors.forename: C
authors.initials: C
authors.lastname: Hoermann
authors.forename: F
authors.initials: F
authors.lastname: Puehringer
authors.forename: N
authors.initials: N
authors.lastname: Mutz
authors.forename: G
authors.initials: G
authors.lastname: Bartsch
authors.forename: K H
authors.initials: KH
authors.lastname: Lindner
mesh_terms: D015106:3',5'-Cyclic-GMP Phosphodiesterases; D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; D004305:Dose-Response Relationship, Drug; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D008168:Lung / Q000098:blood supply*; D008297:Male; D010100:Oxygen / Q000097:blood; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D010727:Phosphoric Diester Hydrolases / Q000502:physiology; D010879:Piperazines / Q000494:pharmacology*; D011659:Pulmonary Gas Exchange / Q000187:drug effects*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D011687:Purines; D000068677:Sildenafil Citrate; D013450:Sulfones; D013552:Swine; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D010726:Phosphodiesterase Inhibitors; D010879:Piperazines; D011687:Purines; D013450:Sulfones; D014665:Vasodilator Agents; D000068677:Sildenafil Citrate; D010727:Phosphoric Diester Hydrolases; D015106:3',5'-Cyclic-GMP Phosphodiesterases; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; D010100:Oxygen