ライフサイエンスコーパス: milrinone

1 , and intravenous inotropes (ie, dobutamine, milrinone).

2 ization of the medicinal agents, fasudil and milrinone.

3 4+/-18% with DOB (P=0.001) and 28+/-11% with milrinone.

4 mortality rate compared with dobutamine and milrinone.

5 tality than those treated with dobutamine or milrinone.

6 teraction between etiology and the effect of milrinone.

7 cally relevant concentrations of amrinone or milrinone.

8 red more frequently in patients who received milrinone.

9 (n = 13) before and during administration of milrinone.

10 btained with and without INO at each dose of milrinone.

11 20 reversed the effects of both iloprost and milrinone.

12 ere randomly assigned to receive intravenous milrinone (0.5 mug/kg/min) (n = 22) or conventional mana

13 gned to receive a 48-hour infusion of either milrinone, 0.5 microg/kg per minute initially (n = 477),

14 The phosphodiesterase 3 (PDE 3) inhibitor milrinone (1 microM) increased the release of [3H] acety

15 induced by either spermine-NO (200 microm), milrinone (10 microm), IBMX (100 microm) or forskolin (1

16 pitalizations: dobutamine 43%, dopamine 24%, milrinone 17%, or a combination 16%.

17 (nesiritide, 20 [minimum to maximum, 0-24]; milrinone, 18 [0-23]; placebo, 20 [0-23]; P=0.38).

18 sterase-3 inhibitors cilostazol (10 muM) and milrinone (2.5 muM) restored electrical homogeneity, thu

19 se III inhibitors cilostazol (10 mumol/L) or milrinone (5 mumol/L) diminished the ER manifestations a

20 yme (PDE3) had been selectively inhibited by milrinone (5 mumol/L).

21 trol group, n=16) as a bolus and infusion or milrinone 50 microg/kg as a bolus and then 0.5 microg/kg

22 ic response to a single intravenous bolus of milrinone (50 micrograms/kg body weight) infused over 1

23 differ significantly between patients given milrinone (6 days) compared with placebo (7 days; P =.71

24 ted cardiomyopathy, 91% of patients received milrinone, 85% of patients underwent transplantation, 8%

25 imulated by spermine/NO, a NO donor, than by milrinone, a phosphodiesterase type III inhibitor.

26 of this study was to investigate the use of milrinone, a selective phosphodiesterase III inhibitor,

27 ugs, and in vivo after 3 d of treatment with milrinone, a type III cAMP phosphodiesterase inhibitor.

28 s revealed that the specific PDE3 inhibitor, milrinone, accelerated spontaneous firing by approximate

29 available inotropes, such as dobutamine and milrinone, act (directly or indirectly) by increasing cy

30 NO and milrinone administration both led to significant improve

31 in RV diastolic properties after both NO and milrinone administration suggests that these agents may

32 collected at baseline and after both NO and milrinone administration.

33 e as well as following both nitric oxide and milrinone administration.

34 The use of high-dose milrinone after pediatric congenital heart surgery reduc

35 Since milrinone, an inhibitor of cAMP phosphodiesterase (PDE)

36 d ODQ, inhibitors of cGMP production; or (c) milrinone, an inhibitor of cGMP-dependent phosphodiester

37 rskolin, an adenylate cyclase activator, and milrinone, an inhibitor of class III phosphodiesterases,

38 ors of type 3 PDE (cGMP-inhibited: CGI-PDE), milrinone and cilostamide.

39 ne (IBMX), and the PDE3 selective inhibitors milrinone and cilostazol each suppressed thrombin-induce

40 stics of inhibition of the mutant enzymes by milrinone and cilostazol, specific inhibitors of PDE3.

41 sponding values for nesiritide compared with milrinone and dobutamine were 0.59 (95% CI 0.48 to 0.73,

42 0.37 to 0.57, p < or = 0.005) compared with milrinone and dobutamine, respectively.

43 valuated the interaction between response to milrinone and etiology of HF.

44 Milrinone and INO both decrease pulmonary hypertension i

45 The milrinone and placebo groups did not differ significantl

46 s that increased cAMP levels (eg, forskolin, milrinone) and agents that decreased protein kinase C ac

47 xperiment based on solubility of cilostazol, milrinone, and 8-Br-cAMP.

48 %, 17.5%, and 11.7% in the placebo, low-dose milrinone, and high-dose milrinone groups, respectively,

49 6, and 35 were randomized to the nesiritide, milrinone, and placebo groups, respectively, and all wer

50 o not support the routine use of intravenous milrinone as an adjunct to standard therapy in the treat

51 with hypoxanthine, 8-AHA-cAMP, guanosine, or milrinone, but was ineffective in olomoucine- or roscovi

52 An intravenous bolus of milrinone can be used to test for the reversibility of p

53 was significantly lower, 18.2% (4/22) in the milrinone compared with 57.9% (11/19) in the conventiona

54 Bolus milrinone consistently decreases PVR in patients with pu

55 ction of pro-inflammatory cytokines, whereas milrinone does not.

56 Milrinone dose dependently decreased PAP, PVR, MAP, and

57 year, whereas the dobutamine, dopamine, and milrinone doses used decreased 49%, 55%, and 29% (P<0.00

58 After milrinone, eNO rose proportionally with decreased PAP (p

59 Milrinone facilitates resuscitation from prolonged VF an

60 tcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OP

61 tcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OP

62 enic mice lacking CFTR do not respond to the milrinone/forskolin combination, indicating that the eff

63 ed K(i) for cilostazol but no difference for milrinone from the recombinant PDE3A.

64 e placebo, low-dose milrinone, and high-dose milrinone groups, respectively, developed LCOS in the fi

65 Milrinone had no effect on heart rate or systemic arteri

66 Both amrinone and milrinone have significant effects on cardiac inflammato

67 heart failure (HF) etiology and response to milrinone in decompensated HF.

68 l-known clinical effects of nitric oxide and milrinone in improving pulmonary hypertension, which wer

69 ated the efficacy and safety of prophylactic milrinone in pediatric patients at high risk for develop

70 y account in part for the ineffectiveness of milrinone in the treatment of severe CHF.

71 s compared to controls, but cells exposed to milrinone in vivo exhibited an accentuation in their con

72 In contrast, milrinone increased nuclear NFkappaB translocation, iNOS

73 s appears to be an effective vasopressor for milrinone-induced hypotension.

74 ecrease in PVR correlated inversely with the milrinone-induced increase in cardiac output.

75 acebo, empirical perioperative nesiritide or milrinone infusions are not associated with improved ear

76 n these patients, but the use of dobutamine, milrinone, inhaled nitric oxide, and intravenous prostac

77 At each dose of milrinone, INO further decreased PVR but not SVR.

78 Milrinone is an intravenously active phosphodiesterase i

79 D950A, and F1004A had reduced sensitivity to milrinone (K(i) changed from 0.66 microM for the recombi

80 ressure and transpulmonary efficiency, while milrinone led to a significant increase in right ventric

81 ic changes of patients on inotropic therapy (milrinone, levosimendan, and istaroxime) and neuropeptid

82 Milrinone may be deleterious in ischemic HF, but neutral

83 Milrinone may have a bidirectional effect based on etiol

84 Cdc2a mRNA, which activates CDC2A, overcomes milrinone-mediated inhibition of oocyte maturation, indu

85 Milrinone might be helpful in patients with cardiac dysf

86 ther studies are needed to determine whether milrinone might be useful to prevent progression of earl

87 P induced by the phosphodiesterase inhibitor milrinone mirrored the actions of iloprost, suggesting t

88 luding dobutamine (n=10), epinephrine (n=8), milrinone (n=7), and dopamine (n=4) before receiving AVP

89 Neither milrinone nor H-89 changed the HR response to carbamylch

90 ght heart failure, despite administration of milrinone, norepinephrine, and nitroglycerin infusions.

91 examine the effects of both nitric oxide and milrinone on pulmonary hemodynamics and right ventricula

92 esigned to investigate the effects of NO and milrinone on RV diastolic dysfunction in the setting of

93 fects of 2 commonly used PDEIs, amrinone and milrinone, on cardiac cell inflammatory responses.

94 ure to receive 48 to 72 hours of intravenous milrinone or placebo in addition to standard therapy.

95 We hypothesized that compared with milrinone or placebo, patients assigned to receive nesir

96 ated HF to receive 48 to 72 h of intravenous milrinone or placebo.

97 patients received nitroglycerin, nesiritide, milrinone, or dobutamine were identified and reviewed (n

98 surgery were assigned to receive nesiritide, milrinone, or placebo.

99 % of hospitals), dopamine-predominant (25%), milrinone-predominant (1%), mixed dobutamine and dopamin

100 In a small pilot study, we found that milrinone reduced early mortality compared with historic

101 The use of high-dose milrinone reduced the risk of the LCOS through the final

102 Both nitric oxide and milrinone resulted in significant improvements in pulmon

103 show that the PDE3 inhibitors cilostazol and milrinone share some of common residues but interact wit

104 Milrinone significantly reduced the 1-week mortality of

105 High-dose milrinone significantly reduced the risk the development

106 Quinidine, cilostazol, and milrinone suppress the hypothermia-induced VT/VF by reve

107 mortality in PROMISE (Prospective Randomized Milrinone Survival Evaluation).

108 Trial], and PROMISE [Prospective Randomized Milrinone Survival Evaluation]) to explore gender-relate

109 utcomes in nonischemic patients treated with milrinone tended to be improved in terms of the primary

110 ated with the PDE3 inhibitors cilostazol and milrinone, then analyzed using qRT-PCR, immunoprecipitat

111 stive heart failure receiving dobutamine and milrinone therapy is presented.

112 The ability of milrinone to lower PVR in patients with heart failure ha

113 effectiveness of quinidine, cilostazol, and milrinone to prevent hypothermia-induced arrhythmias.

114 e more definitive evidence of the ability of milrinone to reduce the 1-week mortality of stage 3B ent

115 m animals that had been treated in vivo with milrinone, to the beta-adrenergic agonist isoproterenol

116 Milrinone-treated patients with ischemic etiology tended

117 ctivity increased by 25% with cilostazol and milrinone treatment (P<0.05 and P<0.01, respectively), a

118 on of ventilator-free days was longer in the milrinone treatment group (p = 0.01).

119 ery pressure was included in the model, age, milrinone use (odds ratio, 4.45; 95% confidence interval

120 e (P<0.001), ejection fraction (P=0.02), and milrinone use (odds ratio, 4.86; 95% confidence interval

121 Milrinone use is an independent risk factor for postoper

122 Milrinone use was associated with an increased risk of p

123 ve surgery did not change the association of milrinone use with postoperative AF.

124 erms of the primary end point (13.6 days for milrinone vs. 12.4 days for placebo, p = 0.055 for inter

125 were disabled by ryanodine, neither IBMX nor milrinone was able to amplify LCRs, accelerate diastolic

126 Milrinone was administered sequentially as a 30-mg/kg bo

127 When iloprost or milrinone was introduced after the initial mobilization

128 Milrinone was used in 84.8% and dobutamine in 15.2%.

129 05] for cilostazol and 2.5-fold [P<0.01] for milrinone), while macrophage CD39 mRNA and protein were

130 to determine whether empirical nesiritide or milrinone would improve the early postoperative course a

131 H) (4 degrees C) or STH containing rolipram, milrinone, zaprinast, or theophylline.