Nitrates
Medical > Therapy > General measures
Nitrates
Organic nitrate and sodium-nitroprusside are intravenous non-pulmonary selective vasodilators and have been used to assess pulmonary vasoreactivity in patients with pulmonary hypertension (Pearl et al., 1983, Packer et al., 1984). In end-stage cardiomyopathies, nitroglycerin and isosorbide dinitrate produce similar acute decreases in mean pulmonary artery pressure (Muikku et al., 1996). Compared to inhaled nitric oxide, intravenous nitric oxide donors cause systemic vasodilation and therefore may compromise right ventricular perfusion. Moreover, intravenous nitrates dilate both ventilated and poorly ventilated areas, which causes hypoxemia by worsening the ventilation-perfusion relationship (Packer et al., 1984, Schmid et al., 1999). Compared to prostaglandin E1, the vasodilation effect of nitroglycerin and sodium nitroprusside on the pulmonary circulation seams to be less potent. Conversely, due to their ability to dilate venous capacitance vessels, nitroglycerin and sodium nitroprusside decrease right and left atrial pressure more than prostaglandin E1 (Murali et al., 1992, Schmid et al., 1999). In conclusion, intravenous nitrates can be used to test pulmonary vasoreactivity, however, they do not offer advantages compared to more pulmonary selective vasodilators such as inhaled nitric oxide and intravenous prostaglandin E1. The treatment with intravenous nitrates may provoke systemic hypotension and/or hypoxemia jeopardizing right ventricular function.
References
Back to > Medical > Therapy > General measures
Nitrates
Organic nitrate and sodium-nitroprusside are intravenous non-pulmonary selective vasodilators and have been used to assess pulmonary vasoreactivity in patients with pulmonary hypertension (Pearl et al., 1983, Packer et al., 1984). In end-stage cardiomyopathies, nitroglycerin and isosorbide dinitrate produce similar acute decreases in mean pulmonary artery pressure (Muikku et al., 1996). Compared to inhaled nitric oxide, intravenous nitric oxide donors cause systemic vasodilation and therefore may compromise right ventricular perfusion. Moreover, intravenous nitrates dilate both ventilated and poorly ventilated areas, which causes hypoxemia by worsening the ventilation-perfusion relationship (Packer et al., 1984, Schmid et al., 1999). Compared to prostaglandin E1, the vasodilation effect of nitroglycerin and sodium nitroprusside on the pulmonary circulation seams to be less potent. Conversely, due to their ability to dilate venous capacitance vessels, nitroglycerin and sodium nitroprusside decrease right and left atrial pressure more than prostaglandin E1 (Murali et al., 1992, Schmid et al., 1999). In conclusion, intravenous nitrates can be used to test pulmonary vasoreactivity, however, they do not offer advantages compared to more pulmonary selective vasodilators such as inhaled nitric oxide and intravenous prostaglandin E1. The treatment with intravenous nitrates may provoke systemic hypotension and/or hypoxemia jeopardizing right ventricular function.
References
Back to > Medical > Therapy > General measures
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SSPH Research Prize 2012
Deadline for submission: April 30, 2012
Further information
Symposium "pulmonal-arterielle Hypertension im Kindesalter"
Donnerstag, 10. Mai 2012, 16.00-18.00, Bern
Further information:
5th International Congress of the Swiss Society of Pulmonary Hypertension (SSPH)
28.-29. September 2012, Thun, Congress Hotel Seepark Thun
Informationen: www.imk.ch/sgph2012
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