Sildenafil modulates hemodynamics and pulmonary gas exchange

Citation
A. Kleinsasser et al., Sildenafil modulates hemodynamics and pulmonary gas exchange, AM J R CRIT, 163(2), 2001, pp. 339-343
Citations number
16
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
ISSN journal
1073449X → ACNP
Volume
163
Issue
2
Year of publication
2001
Pages
339 - 343
Database
ISI
SICI code
1073-449X(200102)163:2<339:SMHAPG>2.0.ZU;2-I
Abstract
The effects of sildenafil (Viagra) on hemodynamics and pulmonary gas exchan ge remain uncertain. The aim of this study was to investigate what effect s ildenafil had on gas exchange. A total of 24 anesthetized pigs were randoml y assigned into four groups of six animals each: Group Low received 25 mg o f sildenafil, which is equivalent to half the recommended dose for humans; group Normal received 50 mg; group High received 100 mg; and one group serv ed as control. Inert gas and hemodynamic measurements were performed to def ine dose-dependent effects of sildenafil on cardiac and pulmonary function. Measurements were taken 30, 60, and 90 min after the administration of sil denafil via gastric tube. All doses of sildenafil caused significant increa ses in intrapulmonary shunt flow (maximum amplitude, 4.4 +/- 0.3 to 11.9 +/ - 0.5%; mean +/- SEM), which was reflected by marked decreases in Pa-O2. Si ldenafil elicited some significant increases in cardiac index (CI) thigh do se, 142 +/- 10 to 196 +/- 13 mi kg(-1), mean +/- SEM). Mean arterial pressu re was significantly depressed after the high dose of sildenafil. Pulmonary artery pressure was decreased after high-dose sildenafil (maximum amplitud e, 16 +/- 1.6 to 14 +/- 1.8, mean +/- SEM). No significant differences betw een the three treatment groups were found. Sildenafil represents and orally active substance with phosphodiesterase V inhibitory and cardiac output-in creasing actions. Pa-O2 decrease after 50 and 100 mg of sildenafil was obse rved in the presence of significant rises in pulmonary shunt flow and Cl.