ライフサイエンスコーパス: pulmonary congestion

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1 uated TAC induced myocardial hypertrophy and pulmonary congestion.

2 ng and cardiomyocyte apoptosis and minimized pulmonary congestion.

3 when combined with near-threshold levels of pulmonary congestion.

4 en delivered during near-threshold levels of pulmonary congestion.

5 ted RAR responses to substance P and to mild pulmonary congestion.

6 intrathoracic impedance, which is related to pulmonary congestion.

7 hypoperfusion = 14 (3%), Group B = isolated pulmonary congestion = 32 (6%), Group C = isolated hypop

8 hmias, heart block, asystole, development of pulmonary congestion, acute mitral regurgitation and car

9 We sought to evaluate the frequency of pulmonary congestion and associated clinical and hemodyn

10 ic constriction, S2814A mice did not exhibit pulmonary congestion and had reduced levels of atrial na

11 implantation, possibly because of decreased pulmonary congestion and improved renal perfusion.

12 s with development of biventricular failure, pulmonary congestion, and death.

13 al signs, symptoms, radiographic evidence of pulmonary congestion, and echocardiographic evidence of

14 he increase in RAR activity produced by mild pulmonary congestion, and evokes an augmented response f

15 Such fluid retention can ultimately lead to pulmonary congestion, ascites or peripheral edema.

16 Absence of pulmonary congestion at initial clinical evaluation does

17 had 141 adjudicated HF hospitalizations with pulmonary congestion at least 60 days after implantation

18 KO mice showed reduced cardiac hypertrophy, pulmonary congestion, concentric LV wall thickness, LV d

19 zed that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from pre-clin

20 Virus infection is followed by intense pulmonary congestion due to an extensive influx of macro

21 ant proportion of patients with shock had no pulmonary congestion (Group C = 28%, 95% CI, 24% to 31%)

22 ary, lung ultrasound can detect asymptomatic pulmonary congestion in hemodialysis patients, and the r

23 Including the degree of pulmonary congestion in the model significantly improved

24 The prevalence of pulmonary congestion in the setting of CS is uncertain.

25 Pulmonary congestion is highly prevalent and often asymp

26 were divided into four groups: Group A = no pulmonary congestion/no hypoperfusion = 14 (3%), Group B

27 ce P augments the stimulatory effect of mild pulmonary congestion on RAR activity, most probably by e

28 (2) clinical pulmonary edema, (3) radiologic pulmonary congestion or edema, or (4) left ventricular s

29 m of atrial natriuretic peptide, may improve pulmonary congestion via vasodilation and enhanced diure

30 Mild pulmonary congestion was produced by inflating a balloon

31 Near-threshold levels of pulmonary congestion were produced by increasing left at

32 ed serious adverse events: not transplanted- pulmonary congestion with epilepticus (likely not relate

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