Circulatory effects of the PDE-inhibitors piroximone and enoximone.
1. The isolated circulatory response to intravenous application of the phosphodiesterase (PDE) inhibitors piroximone and enoximone was studied. 2. In a randomized sequence of 30 male patients undergoing elective aortocoronary bypass grafting either piroximone (0.5 mg kg(-1); n = 10) or enoximone (0.5 mg kg(-1); n = 10) were given during steady state of cardiopulmonary bypass (CPB). A group in which NaCl was given as a placebo served as a control (n = 10). 3. MAP was reduced by piroximone (maximum -23 mm Hg) and enoximone (maximum -18 mm Hg), whereas it increased in the control (+20 mm Hg). Volume of the extracorporeal circuit indicating venous pooling decreased more pronouncedly in the enoximone patients (-440 ml) than in the piroximone group (-300 ml). 4. Laser Doppler flows (LDFs) increased in both PDE-III inhibitor groups with the higher and longer increase in the enoximone-treated patients (LDF-forehead maximum +44%, LDF-forearm maximum +33%). Piroximone-induced increase in both LDFs was less pronounced with respect to both time and degree (LDF-forehead maximum +30%, LDF-forearm +12%). 5. Oxygen consumption (VO2) was significantly higher in the PDE-III inhibitor-treated than in the control patients. 6. Piroximone and enoximone showed significant vasodilatory properties at the arterial and venous side (= 'venous pooling'), from which patients with heart failure would profit. 7. Vasodilation could be observed for a longer period and was more pronounced in the enoximone-treated than in the piroximone patients. Alterations in capillary skin blood flow measured by laser Doppler technique gave evidence for an improvement in nutritive microcirculation, which was slightly more pronounced in the enoximone patients.[1]References
- Circulatory effects of the PDE-inhibitors piroximone and enoximone. Boldt, J., Knothe, C., Zickmann, B., Schindler, E., Stertmann, W.A., Hempelmann, G. British journal of clinical pharmacology. (1993) [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