Cardiopulmonary effects of enprofylline. A xanthine with weak adenosine receptor antagonism in patients with severe chronic lung disease.
The acute cardiovascular effects of a new xanthine, enprofylline, were studied in patients with chronic lung disease. The studies were done during cardiac catheterization (n = 12) and by radionuclide ventriculography (n = 6). Enprofylline was given intravenously, 2 mg/kg, and measurements were done after ten and 30 min. Enprofylline reduced the mean pulmonary artery pressure from 30 +/- 10 to 26 +/- 7 mm Hg (p less than 0.05) and the mean systemic arterial pressure from 92 +/- 17 to 83 +/- 15 mm Hg (p less than 0.01), increased the heart rate from 89 +/- 15 to 100 +/- 18 beats/min (p less than 0.01) and reduced the stroke volume from 55 +/- 12 to 48 +/- 12 ml (p less than 0.05) after 30 min. Radionuclide ventriculography revealed unchanged ejection fraction of left and right ventricles after enprofylline. None of the patients experienced serious side effects of the drug. Thus, enprofylline induced modest acute cardiovascular effects with a chronotropic response together with a small vasodilation in pulmonary and systemic circulation.[1]References
- Cardiopulmonary effects of enprofylline. A xanthine with weak adenosine receptor antagonism in patients with severe chronic lung disease. Vik-Mo, H., Gulsvik, A., Folling, M. Chest (1988) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
