Publications by authors named "R Kadatz"

Dipyridamole appears to act in vivo by synergistically modifying several biochemical pathways, including: a) inhibition of platelet cAMP-phosphodiesterase; b) potentiation of adenosine inhibition of platelet function by blocking reuptake by vascular and blood cells, and subsequent degradation of adenosine; and possibly, c) potentiation of PGI2 antiaggregatory activity and enhancement of PGI2 biosynthesis. These independent processes inhibit platelet function by increasing platelet cAMP through both a reduction in enzymatic cAMP-degradation, and stimulation of cAMP formation via activation of adenylcyclase by adenosine and possibly PGI2. Only the inhibition of cAMP phosphodiesterase appears to be involved in the dipyridamole inhibition of isolated platelets in vitro, since adenosine and PGI2 originate in vivo from tissues other than platelets and any blood concentrations existing in vivo will disappear before platelet-rich plasma has been prepared for in vitro platelet studies.

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1. v. administration of 5,6-dimethoxy-2-(3-[(alpha-(3,4-dimethoxy) phenylethyl) methylamino] propyl)- phthalimidine (AQ-A 39) to anaesthetized animals induced dose dependents bradycardia.

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2-[(2-Methoxy-4-methylsulfinyl)phenyl]-1H-imidazo[4,5-b]-pyridine (AR-L 115 BS) (0.1--1.0 mg/kg i.

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In anaesthetized dogs, 0.03--10 mg/kg 2-[(2-methoxy-4-methylsulfinyl)-phenyl]-1H-imidazo[4,5-b]pyridine (AR-L 115 BS) i.V.

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2-(2,4-Dimethoxyphenyl)-1H-imidazo[4,5-b]-pyridine (AR-L 57 BS), 2-(4-methoxy-2-[(2-methylsulfinyl)ethoxy]-phenyl-3H-imidazo[4,5-b]pyridine (AR-L 100 BS) and 2-[(2-methoxy-4-methylsulfinyl)phenyl]-1H-imidazo[4,5-b]pyridine (AR-L 115 BS) increased force of contraction in isolated rat atria at 3-1000 mumol/l by maximally 100%. In anaesthetized cats dp/dtmax was augmented by maximally 141-216% at 0.1-10 mg/kg i.

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