Intracellular cyclic nucleotide levels can be controlled through regulation of either synthesis via respective cyclases or degradation via the phosphodiesterases (PDEs)[3]. Dipyridamole inhibits the phosphodiesterase enzyme that degrades cyclic AMP to 5’-AMP, resulting in the intraplatelet accumulation of cyclic AMP[4]. Inhibition of the erythrocytic nucleoside transport system by dipyridamole (10 μM) evokes the antiaggregatory action of adenosine in whole blood (IC50 congruent to 2 μM)[5]. In an in situ perfused rabbit lung model in which the pulmonary vascular resistance (PVR) was elevated, 0.06 μM dipyridamole reduced elevated PVR by 8.2 +/- 2.8%, and the EC50 for dipyridamole was approximately 0.2 μM[6]. In newborn lambs with persistent pulmonary hypertension of the newborn (PPHN), dipyridamole infused at 0.02 mg/kg/min for 45 min alone significantly decreased pulmonary and systemic blood pressure, decreased pulmonary vascular resistance, and increased pulmonary blood flow[7]. Some potent dipyridamole derivatives are able to increase the primary immune response in mice immunized with sheep red blood cells (SRBC). 10 mg/kg/day of the most potent substance administered in the drinking water increased the number of plaque forming cells (PFC) in spleens of these mice by a factor of about 2 when the treatment was started after immunization[8].
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