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1 , and intravenous inotropes (ie, dobutamine, milrinone).
2 tive intensity following the introduction of milrinone.
3 20 reversed the effects of both iloprost and milrinone.
4 ization of the medicinal agents, fasudil and milrinone.
5 4+/-18% with DOB (P=0.001) and 28+/-11% with milrinone.
6 stent with vasodilation also decreased after milrinone.
7  mortality rate compared with dobutamine and milrinone.
8 tality than those treated with dobutamine or milrinone.
9 teraction between etiology and the effect of milrinone.
10 cally relevant concentrations of amrinone or milrinone.
11 red more frequently in patients who received milrinone.
12 (n = 13) before and during administration of milrinone.
13 btained with and without INO at each dose of milrinone.
14 ere randomly assigned to receive intravenous milrinone (0.5 mug/kg/min) (n = 22) or conventional mana
15 gned to receive a 48-hour infusion of either milrinone, 0.5 microg/kg per minute initially (n = 477),
16    The phosphodiesterase 3 (PDE 3) inhibitor milrinone (1 microM) increased the release of [3H] acety
17  induced by either spermine-NO (200 microm), milrinone (10 microm), IBMX (100 microm) or forskolin (1
18 pitalizations: dobutamine 43%, dopamine 24%, milrinone 17%, or a combination 16%.
19  (nesiritide, 20 [minimum to maximum, 0-24]; milrinone, 18 [0-23]; placebo, 20 [0-23]; P=0.38).
20 sterase-3 inhibitors cilostazol (10 muM) and milrinone (2.5 muM) restored electrical homogeneity, thu
21 se III inhibitors cilostazol (10 mumol/L) or milrinone (5 mumol/L) diminished the ER manifestations a
22 yme (PDE3) had been selectively inhibited by milrinone (5 mumol/L).
23 trol group, n=16) as a bolus and infusion or milrinone 50 microg/kg as a bolus and then 0.5 microg/kg
24 ic response to a single intravenous bolus of milrinone (50 micrograms/kg body weight) infused over 1
25  differ significantly between patients given milrinone (6 days) compared with placebo (7 days; P =.71
26 ted cardiomyopathy, 91% of patients received milrinone, 85% of patients underwent transplantation, 8%
27 imulated by spermine/NO, a NO donor, than by milrinone, a phosphodiesterase type III inhibitor.
28  of this study was to investigate the use of milrinone, a selective phosphodiesterase III inhibitor,
29 ugs, and in vivo after 3 d of treatment with milrinone, a type III cAMP phosphodiesterase inhibitor.
30 s revealed that the specific PDE3 inhibitor, milrinone, accelerated spontaneous firing by approximate
31  available inotropes, such as dobutamine and milrinone, act (directly or indirectly) by increasing cy
32 ing undergone cardiac surgery, we found that milrinone acted as a vasodilator but did not demonstrate
33                                       NO and milrinone administration both led to significant improve
34 in RV diastolic properties after both NO and milrinone administration suggests that these agents may
35  collected at baseline and after both NO and milrinone administration.
36 e as well as following both nitric oxide and milrinone administration.
37                         The use of high-dose milrinone after pediatric congenital heart surgery reduc
38                                        Since milrinone, an inhibitor of cAMP phosphodiesterase (PDE)
39 d ODQ, inhibitors of cGMP production; or (c) milrinone, an inhibitor of cGMP-dependent phosphodiester
40 rskolin, an adenylate cyclase activator, and milrinone, an inhibitor of class III phosphodiesterases,
41  analysis were performed prior to commencing milrinone and 4-6 hours after milrinone infusion.
42 ors of type 3 PDE (cGMP-inhibited: CGI-PDE), milrinone and cilostamide.
43 ne (IBMX), and the PDE3 selective inhibitors milrinone and cilostazol each suppressed thrombin-induce
44 stics of inhibition of the mutant enzymes by milrinone and cilostazol, specific inhibitors of PDE3.
45 nic shock, no significant difference between milrinone and dobutamine was found with respect to the p
46 sponding values for nesiritide compared with milrinone and dobutamine were 0.59 (95% CI 0.48 to 0.73,
47  0.37 to 0.57, p < or = 0.005) compared with milrinone and dobutamine, respectively.
48 valuated the interaction between response to milrinone and etiology of HF.
49 linical worsening after discontinuation (eg, milrinone and flosequinan); and 4) persistence of favora
50                                              Milrinone and INO both decrease pulmonary hypertension i
51                                          The milrinone and placebo groups did not differ significantl
52 s that increased cAMP levels (eg, forskolin, milrinone) and agents that decreased protein kinase C ac
53 xperiment based on solubility of cilostazol, milrinone, and 8-Br-cAMP.
54 %, 17.5%, and 11.7% in the placebo, low-dose milrinone, and high-dose milrinone groups, respectively,
55 6, and 35 were randomized to the nesiritide, milrinone, and placebo groups, respectively, and all wer
56 o not support the routine use of intravenous milrinone as an adjunct to standard therapy in the treat
57 with hypoxanthine, 8-AHA-cAMP, guanosine, or milrinone, but was ineffective in olomoucine- or roscovi
58                      An intravenous bolus of milrinone can be used to test for the reversibility of p
59 was significantly lower, 18.2% (4/22) in the milrinone compared with 57.9% (11/19) in the conventiona
60                                        Bolus milrinone consistently decreases PVR in patients with pu
61 ction of pro-inflammatory cytokines, whereas milrinone does not.
62                                              Milrinone dose dependently decreased PAP, PVR, MAP, and
63  year, whereas the dobutamine, dopamine, and milrinone doses used decreased 49%, 55%, and 29% (P<0.00
64                                        After milrinone, eNO rose proportionally with decreased PAP (p
65                                              Milrinone facilitates resuscitation from prolonged VF an
66 tcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OP
67 tcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OP
68 enic mice lacking CFTR do not respond to the milrinone/forskolin combination, indicating that the eff
69 ed K(i) for cilostazol but no difference for milrinone from the recombinant PDE3A.
70 ent occurred in 47 participants (49%) in the milrinone group and in 52 participants (54%) in the dobu
71 e placebo, low-dose milrinone, and high-dose milrinone groups, respectively, developed LCOS in the fi
72                                              Milrinone had no effect on heart rate or systemic arteri
73                            Both amrinone and milrinone have significant effects on cardiac inflammato
74  heart failure (HF) etiology and response to milrinone in decompensated HF.
75 l-known clinical effects of nitric oxide and milrinone in improving pulmonary hypertension, which wer
76 ated the efficacy and safety of prophylactic milrinone in pediatric patients at high risk for develop
77 y account in part for the ineffectiveness of milrinone in the treatment of severe CHF.
78 s compared to controls, but cells exposed to milrinone in vivo exhibited an accentuation in their con
79                                 In contrast, milrinone increased nuclear NFkappaB translocation, iNOS
80 s appears to be an effective vasopressor for milrinone-induced hypotension.
81 ecrease in PVR correlated inversely with the milrinone-induced increase in cardiac output.
82 atory failure (OR=0.28 [CI, 0.11-0.70]), and milrinone infusion (OR=0.32 [CI, 0.15-0.67]).
83  to commencing milrinone and 4-6 hours after milrinone infusion.
84 acebo, empirical perioperative nesiritide or milrinone infusions are not associated with improved ear
85 n these patients, but the use of dobutamine, milrinone, inhaled nitric oxide, and intravenous prostac
86                              At each dose of milrinone, INO further decreased PVR but not SVR.
87                                              Milrinone is an inodilator widely used in the postoperat
88                                              Milrinone is an intravenously active phosphodiesterase i
89 D950A, and F1004A had reduced sensitivity to milrinone (K(i) changed from 0.66 microM for the recombi
90 ressure and transpulmonary efficiency, while milrinone led to a significant increase in right ventric
91 ic changes of patients on inotropic therapy (milrinone, levosimendan, and istaroxime) and neuropeptid
92                                              Milrinone may be deleterious in ischemic HF, but neutral
93                                              Milrinone may have a bidirectional effect based on etiol
94 Cdc2a mRNA, which activates CDC2A, overcomes milrinone-mediated inhibition of oocyte maturation, indu
95                                              Milrinone might be helpful in patients with cardiac dysf
96 ther studies are needed to determine whether milrinone might be useful to prevent progression of earl
97 P induced by the phosphodiesterase inhibitor milrinone mirrored the actions of iloprost, suggesting t
98 luding dobutamine (n=10), epinephrine (n=8), milrinone (n=7), and dopamine (n=4) before receiving AVP
99                                      Neither milrinone nor H-89 changed the HR response to carbamylch
100 ght heart failure, despite administration of milrinone, norepinephrine, and nitroglycerin infusions.
101 examine the effects of both nitric oxide and milrinone on pulmonary hemodynamics and right ventricula
102 esigned to investigate the effects of NO and milrinone on RV diastolic dysfunction in the setting of
103             We sought to study the effect of milrinone on the vasculature and its effects on the vent
104 fects of 2 commonly used PDEIs, amrinone and milrinone, on cardiac cell inflammatory responses.
105 d patients with cardiogenic shock to receive milrinone or dobutamine in a double-blind fashion.
106 ure to receive 48 to 72 hours of intravenous milrinone or placebo in addition to standard therapy.
107           We hypothesized that compared with milrinone or placebo, patients assigned to receive nesir
108 ated HF to receive 48 to 72 h of intravenous milrinone or placebo.
109 patients received nitroglycerin, nesiritide, milrinone, or dobutamine were identified and reviewed (n
110 surgery were assigned to receive nesiritide, milrinone, or placebo.
111 % of hospitals), dopamine-predominant (25%), milrinone-predominant (1%), mixed dobutamine and dopamin
112        In a small pilot study, we found that milrinone reduced early mortality compared with historic
113                                              Milrinone reduced myocardial oxygen consumption (0.15+/-
114                         The use of high-dose milrinone reduced the risk of the LCOS through the final
115                        Both nitric oxide and milrinone resulted in significant improvements in pulmon
116 show that the PDE3 inhibitors cilostazol and milrinone share some of common residues but interact wit
117                      Measured noninvasively, milrinone significantly increased LV ejection fraction (
118                                              Milrinone significantly reduced the 1-week mortality of
119                                    High-dose milrinone significantly reduced the risk the development
120                   Quinidine, cilostazol, and milrinone suppress the hypothermia-induced VT/VF by reve
121 mortality in PROMISE (Prospective Randomized Milrinone Survival Evaluation).
122  Trial], and PROMISE [Prospective Randomized Milrinone Survival Evaluation]) to explore gender-relate
123 utcomes in nonischemic patients treated with milrinone tended to be improved in terms of the primary
124 ated with the PDE3 inhibitors cilostazol and milrinone, then analyzed using qRT-PCR, immunoprecipitat
125 stive heart failure receiving dobutamine and milrinone therapy is presented.
126 d adjustment and following bolus intravenous milrinone to assess changes in loading conditions and co
127                               The ability of milrinone to lower PVR in patients with heart failure ha
128  effectiveness of quinidine, cilostazol, and milrinone to prevent hypothermia-induced arrhythmias.
129 e more definitive evidence of the ability of milrinone to reduce the 1-week mortality of stage 3B ent
130 m animals that had been treated in vivo with milrinone, to the beta-adrenergic agonist isoproterenol
131                                              Milrinone-treated patients with ischemic etiology tended
132 ctivity increased by 25% with cilostazol and milrinone treatment (P<0.05 and P<0.01, respectively), a
133 on of ventilator-free days was longer in the milrinone treatment group (p = 0.01).
134 ery pressure was included in the model, age, milrinone use (odds ratio, 4.45; 95% confidence interval
135 e (P<0.001), ejection fraction (P=0.02), and milrinone use (odds ratio, 4.86; 95% confidence interval
136                                              Milrinone use is an independent risk factor for postoper
137                                              Milrinone use was associated with an increased risk of p
138 ve surgery did not change the association of milrinone use with postoperative AF.
139 erms of the primary end point (13.6 days for milrinone vs. 12.4 days for placebo, p = 0.055 for inter
140 were disabled by ryanodine, neither IBMX nor milrinone was able to amplify LCRs, accelerate diastolic
141                                              Milrinone was administered sequentially as a 30-mg/kg bo
142                             When iloprost or milrinone was introduced after the initial mobilization
143                                              Milrinone was used in 84.8% and dobutamine in 15.2%.
144 05] for cilostazol and 2.5-fold [P<0.01] for milrinone), while macrophage CD39 mRNA and protein were
145 to determine whether empirical nesiritide or milrinone would improve the early postoperative course a
146 H) (4 degrees C) or STH containing rolipram, milrinone, zaprinast, or theophylline.

 
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