ライフサイエンスコーパス: right ventricular hypertrophy

1 e of rats with established PAH and decreased right ventricular hypertrophy.

2 hickening of the pulmonary artery media, and right ventricular hypertrophy.

3 ization of peripheral pulmonary arteries and right ventricular hypertrophy.

4 ncrease in pulmonary vascular remodeling and right ventricular hypertrophy.

5 ed with raised pulmonary artery pressure and right ventricular hypertrophy.

6 ressures, pulmonary vascular remodeling, and right ventricular hypertrophy.

7 ery pressure, diminished cardiac output, and right ventricular hypertrophy.

8 is echocardiogram revealed profound left and right ventricular hypertrophy.

9 artery pressure (pulmonary hypertension) and right ventricular hypertrophy.

10 cardiocytes from control cats and cats with right ventricular hypertrophy.

11 actile dysfunction seen in pressure-overload right ventricular hypertrophy.

12 icular systolic pressure >30 mm Hg exhibited right ventricular hypertrophy and an increase in the num

13 We therefore examined a canine model of right ventricular hypertrophy and failure (RVHF) in whic

14 AH, Egln1(Tie2) mice exhibited unprecedented right ventricular hypertrophy and failure and progressiv

15 l injury, angioproliferative remodeling, and right ventricular hypertrophy and failure.

16 onary arterial hypertension and pathological right ventricular hypertrophy and failure.

17 s pulmonary arterial hypertension leading to right ventricular hypertrophy and heart failure.

18 However, only A-17 reduced hypoxia-induced right ventricular hypertrophy and improved pulmonary art

19 resistance, pulmonary artery remodeling, and right ventricular hypertrophy and improving functional c

20 entricular systolic pressure associated with right ventricular hypertrophy and increased peripheral p

21 g, P<0.05) coupled with a small reduction in right ventricular hypertrophy and inhibition of pulmonar

22 There was also right ventricular hypertrophy and pathological evidence

23 In the athymic rat, imatinib decreased right ventricular hypertrophy and pulmonary arteriolar m

24 n of right ventricular systolic pressure and right ventricular hypertrophy and pulmonary vascular rem

25 Hypoxia-induced increases in right ventricular hypertrophy and pulmonary vascular rem

26 Simvastatin treatment reduced right ventricular hypertrophy and reduced proliferation

27 c chamber, developed pulmonary hypertension, right ventricular hypertrophy and wall-thickening in pul

28 sensitivity, and complete regression of PAH, right ventricular hypertrophy, and abnormal pulmonary ar

29 iated with reductions in pulmonary pressure, right ventricular hypertrophy, and abnormally musculariz

30 s significant pulmonary vascular remodeling, right ventricular hypertrophy, and decreased lung alveol

31 ent for 3 weeks dose-dependently reduced PH, right ventricular hypertrophy, and distal pulmonary arte

32 monary artery pressure, vascular remodeling, right ventricular hypertrophy, and fibrosis in compariso

33 levated right ventricular systolic pressure, right ventricular hypertrophy, and loss of small arterie

34 stem cell abnormalities in vascular injury, right ventricular hypertrophy, and morbidity associated

35 ment of systolic right ventricular pressure, right ventricular hypertrophy, and percentage of remodel

36 ight ventricular systolic pressure increase, right ventricular hypertrophy, and pulmonary vessel wall

37 t ventricular systolic pressure, significant right ventricular hypertrophy, and striking vascular rem

38 halted and attenuated the development of PH, right ventricular hypertrophy, and vascular remodeling i

39 hloroquine prevented the development of PAH, right ventricular hypertrophy, and vascular remodelling

40 lability controlled pulmonary vascular tone, right ventricular hypertrophy, and vascular structural r

41 nduces polycythemia, pulmonary hypertension, right ventricular hypertrophy, and weight loss.

42 creased right ventricular systolic pressure, right ventricular hypertrophy, as well as collagen depos

43 ater right ventricular systolic pressure and right ventricular hypertrophy at baseline, which increas

44 ulmonary vascular remodeling, and reduce the right ventricular hypertrophy characteristic of PH.

45 lmonary vascular remodeling, and reduces the right ventricular hypertrophy characteristic of PH.

46 ular muscularization but a similar degree of right ventricular hypertrophy compared with wild-type mi

47 These changes resulted in right ventricular hypertrophy, confirming hemodynamicall

48 Although PH and right ventricular hypertrophy developed by 2 weeks after

49 ses pulmonary arterial pressure and inhibits right ventricular hypertrophy in a rat model of PAH.

50 eathing 10% oxygen for 3 weeks produced less right ventricular hypertrophy in cPLA(2alpha)(-/-) than

51 After 5 weeks, MRI showed right ventricular hypertrophy in MCT(+)/ACEI(-) rats.

52 GP treatment caused alveolar enlargement and right ventricular hypertrophy in mice.

53 mation, pulmonary arterial hypertension, and right ventricular hypertrophy in rats.

54 ry resistance, functional residual capacity, right ventricular hypertrophy index, and total cell coun

55 so reduced pulmonary vascular remodeling and right ventricular hypertrophy indicating a role for Grem

56 class I HDAC inhibitor only modestly reduced right ventricular hypertrophy, it had multiple beneficia

57 essures, and this occurs before the onset of right ventricular hypertrophy or pulmonary arterial remo

58 pressure but without a significant effect on right ventricular hypertrophy or vascular remodeling.

59 Mutant mice display right ventricular hypertrophy, overriding aorta, ventric

60 icantly delayed development of polycythemia, right ventricular hypertrophy, pulmonary hypertension, a

61 heless, monocrotaline exposure did not cause right ventricular hypertrophy, pulmonary hypertension, o

62 PAH was assessed in mice via measurement of right ventricular hypertrophy, pulmonary vascular remode

63 exposure to CO reverses established PAH and right ventricular hypertrophy, restoring right ventricul

64 nary arterial pressures (53 +/- 2 mm Hg) and right ventricular hypertrophy (right ventricle/[left ven

65 gle-skinned myocytes isolated from rats with right ventricular hypertrophy (RVH) and control rats.

66 ide-treated rats also had significantly less right ventricular hypertrophy (RVH) and pulmonary arteri

67 ), hypertensive lung structural changes, and right ventricular hypertrophy (RVH) caused by prolonged

68 s of electrocardiographic (ECG) criteria for right ventricular hypertrophy (RVH) measured by cardiac

69 timal pattern of remodeling developed severe right ventricular hypertrophy (RVH) whereas animals with

70 us deletion of the Cav-1 gene develop PH and right ventricular hypertrophy (RVH).

71 These animals also have marked right ventricular hypertrophy, suggesting a chronic incr

72 ated cats during and after the completion of right ventricular hypertrophy; the left ventricle from e

73 zation and decreased pulmonary hypertension, right ventricular hypertrophy, vascular remodeling, vasc

74 In contrast, adaptive right ventricular hypertrophy was less than anticipated.

75 However, right ventricular hypertrophy was unchanged despite atte

76 tribute to pulmonary vascular remodeling and right ventricular hypertrophy, we tested the hypothesis

77 ted right ventricular systolic pressures and right ventricular hypertrophy with corresponding pulmona