TL;DR: Olprinone is a newly developed phosphodiesterase III inhibitor characterized by several properties that improves myocardial mechanical efficiency and may prevent cerebral metabolic abnormalities in heart failure.
Abstract: Olprinone is a newly developed phosphodiesterase III inhibitor characterized by several properties. First, olprinone has positive inotropic and vasodilator actions and improves myocardial mechanical efficiency. Second, olprinone augments cerebral blood flow by a direct vasodilatory effect on cerebral arteries. The cerebrovascular reactivity to olprinone is marked in patients with impaired cerebral circulation. Third, olprinone selectively improves carotid artery distensibility, which may be attributable to differences in the arterial structural components or the reactivity of smooth muscle cells to olprinone. Fourth, olprinone improves inadequate redistribution of brain perfusion and may prevent cerebral metabolic abnormalities in heart failure.
TL;DR: These compounds have proven to be very versatile reagents for heterocyclization and many diverse products can be prepared from the addition of these compounds to Nitrogen, Oxygen, Phosphorus and Sulfur containing compounds.
Abstract: Zolpidem, Necopidem, Alpidem, Saripidem, Miroprofen, Zolimidine, Olprinone and Abafungin (Figure 1) have severed as rich sources of variety of medicinal, pharmaceutical, anti-tumor, antibiotics and antiviral drugs (Figure 2) and biological properties [1-18]. These compounds represent an important class of Nitrogen, Oxygen, Phosphorus and Sulfur heterocyclic and they constitute useful intermediates in organic synthesis [19-39]. Zolpidem, Necopidem, Alpidem, Saripidem, Miroprofen, Zolimidine, Olprinone and Abafungin have proven to be very versatile reagents for heterocyclization and many diverse products can be prepared from the addition of these compounds to Nitrogen, Oxygen, Phosphorus and Sulfur containing compounds.
TL;DR: In patients with HF, the CBF of the cerebral cortex was decreased, but was increased by OL infusion, and the percent increase in CBF was significantly greater in HF than in normal subjects.
Abstract: Cerebral blood flow (CBF) is reduced in heart failure (HF) For the treatment of acute HF, a phosphodiesterase-3 inhibitor, olprinone (OL), yields an increase in myocardial contractility and a decreas
TL;DR: The ability of amrinone to scavenge reactive oxygen species at clinically relevant concentrations while not affecting neutrophil function suggests that the PDE inhibitor can be used without detriment in severely ill patients.
Abstract: Objectives: Neutrophils play an important role in ridding the body of bacteria and cellular debris. Several neutrophil functions are thought to be regulated by inotropes that increase cellular levels of cyclic adenosine monophosphate, including phosphodiesterase (PDE) inhibitors. We have investigated the effect of amrinone, milrinone, and olprinone, type III PDE (PDE-III) inhibitors, on several human neutrophil functions. Design: Prospective in vitro study. Setting: Academic research laboratory. Subjects: Neutrophils isolated from 12 healthy adult volunteers. Interventions: We measured chemotaxis, phagocytosis, reactive oxygen species production, intracellular calcium ion concentration, and cyclic adenosine monophosphate levels in neutrophils in the absence and the presence (at clinically relevant concentrations, 10 times, and 100 times those concentrations) of amrinone, milrinone, or olprinone. We also measured reactive oxygen species production under the same condition in a xanthine-xanthine oxidase system Measurements and Main Results: None of the PDE-III inhibitors impaired neutrophil chemotaxis or phagocytosis. Amrinone at clinically relevant or higher concentrations and milrinone at high concentrations reduced superoxide, hydrogen peroxide, and hydroxyl radical levels in neutrophils and in the xanthine-xanthine oxidase system. Olprinone did not have those effects, and none of the PDE-III inhibitors had an effect on intracellular calcium ion concentration or cyclic adenosine monophosphate production in neutrophils stimulated by a chemotactic factor. Conclusions: The ability of amrinone to scavenge reactive oxygen species at clinically relevant concentrations while not affecting neutrophil function suggests that the PDE inhibitor can be used without detriment in severely ill patients.
TL;DR: OLP attenuates excessive shear stress through the up‐regulation of eNOS and improves the survival rate after EHx, and the administration of Nω‐nitro‐l‐arginine methyl ester to OLP‐treated rats eliminated the effects of OLP on PV pressure and survival after Ehx.