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1 ne, and the phosphodiesterase III inhibitor, amrinone.
3 atelets in suspension were preincubated with amrinone 2.5 to 15 microg/mL; stimulated with the agonis
5 elevant concentrations of inotropes, such as amrinone and dopamine, which increase cAMP, could inhibi
7 amined the effects of 2 commonly used PDEIs, amrinone and milrinone, on cardiac cell inflammatory res
9 xpression, all were significantly reduced by amrinone, beginning at concentrations of 10 to 50 micro
10 Results showed that at the cellular level, amrinone inhibited agonist-induced Ca2+ mobilization and
12 pinephrine (0.1 to 100 ng/mL) for 15 mins or amrinone lactate (0.25 to 10 microg/mL) for 20 mins.
14 pretreated with increasing concentrations of amrinone or dopamine, or left untreated as controls, fol
16 In contrast, increasing concentrations of amrinone produced increased peak augmentation of contrac
19 this increase was not reflected by increased amrinone-stimulated generation of cyclic AMP relative to
20 ad no effect, indicating that the effects of amrinone were not due to phosphodiesterase inhibition.
21 e have previously found that vesnarinone and amrinone, when given before LPS, prevented cytokine prod
22 nonadrenergic inotropic and vasodilator drug amrinone, which elevates platelet cAMP levels, would bot
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