ライフサイエンスコーパス: RVH

1 RVH also increased myocardial expression of inflammatory

2 RVH and RVH+S had similarly increased arterial pressure

3 RVH was defined using sex-specific normative equations b

4 RVH was induced by pulmonary artery constriction for 36

5 gs were studied after 12 wk: normal (n = 7), RVH (n = 7), or RVH+simvastatin (RVH+S; 80 mg/d; n = 6).

6 s maladaptive RVH is imprecise, but adaptive RVH is associated with better functional capacity and su

7 load and mass some patients develop adaptive RVH (concentric with retained RV function), while others

8 rgic signaling, and metabolism than adaptive RVH, and these derangements often involve the left ventr

9 hese findings indicate that the EF hands and RVH domain act as a functional unit during Ca(2+)-induce

10 this agent did not protect the EF hands and RVH domain from trypsin cleavage.

11 he development of pulmonary hypertension and RVH, and promotes regression of pulmonary arterial neoin

12 oped pulmonary artery medial hypertrophy and RVH, which was normalized by administration of AP-Cav.

13 Neointimal lesions and RVH were similar whether injury preceded pneumonectomy o

14 ssion could affect the development of PH and RVH remains unknown.

15 pulmonary artery medial hypertrophy, PH, and RVH.

16 RVH and RVH+S had similarly increased arterial pressure and seru

17 r blockade decreased PAP in utero, decreased RVH and distal muscularization of small pulmonary arteri

18 cose oxidation is beneficial in experimental RVH and can be achieved by inhibition of pyruvate dehydr

19 r remodeling and hypertrophy in experimental RVH independent of lipid lowering.

20 (62.9 MBq +/- 40.7) baseline acquisition for RVH and a high activity (303.4 MBq +/- 48.1) acquisition

21 The recommended ECG screening criteria for RVH are not sufficiently sensitive or specific for scree

22 The ECG screening criteria for RVH from the 2009 American Heart Association Recommendat

23 Current ECG criteria for RVH were based on cadaveric dissection in small studies.

24 ific (many >95%) but had low sensitivity for RVH by cMRI.

25 of NMDAR-DeltaCa(2+) signalling in MNCs from RVH rats, partly due to blunted endoplasmic reticulum Ca

26 arger and prolonged DeltaCa(2+) in MNCs from RVH rats.

27 4) had higher mPAP (40 +/- 9 mm Hg), greater RVH, and more severe pulmonary arterial neointimal forma

28 A total of 6% had RVH, which was generally mild.

29 on of images in patients suspected of having RVH or obstruction compared with administration of lower

30 o contains an N-terminal recoverin homology (RVH) domain that is related to the N termini of the reco

31 spected of having renovascular hypertension (RVH) were randomly selected from archived databases and

32 tructure in swine renovascular hypertension (RVH) would be improved by simvastatin treatment.

33 not in MNCs from renovascular hypertensive (RVH) rats.

34 MNCs of sham and renovascular hypertensive (RVH) rats.

35 MNCs in sham and renovascular hypertensive (RVH) rats.

36 y cells (MNCs) in renovascular hypertensive (RVH) rats.

37 ng in right ventricular failure/hypertrophy (RVH) are poorly understood.

38 he ET axis is upregulated in RV hypertrophy (RVH) and that ERAs have direct effects on the RV myocard

39 RV hypertrophy (RVH) triggered by pressure overload is initially compens

40 rom rats with right ventricular hypertrophy (RVH) and control rats.

41 ficantly less right ventricular hypertrophy (RVH) and pulmonary arterial neointimal formation.

42 changes, and right ventricular hypertrophy (RVH) caused by prolonged closure of the ductus arteriosu

43 criteria for right ventricular hypertrophy (RVH) measured by cardiac magnetic resonance imaging (cMR

44 eloped severe right ventricular hypertrophy (RVH) whereas animals with a medial hypertrophy pattern o

45 evelop PH and right ventricular hypertrophy (RVH).

46 ed also to higher ongoing firing activity in RVH rats.

47 ibuting in turn to higher firing activity in RVH rats.

48 R1-NR2A-D subunit expression were altered in RVH rats.

49 expression of NMDAR subunits were altered in RVH rats.

50 an upregulation of the myocardial ET axis in RVH.

51 GRK2 interactions has therapeutic benefit in RVH.

52 rats, but this effect was largely blunted in RVH rats.

53 els/cm(2); P < 0.05), which was decreased in RVH+S (72.5 +/- 14.9 vessels/cm(2)), whereas capillary d

54 ition of IA and enhanced MNC excitability in RVH rats.

55 e-1-receptor signaling, which is impaired in RVH.

56 -positive, PVN-RVLM (OT-PVN-RVLM) neurons in RVH rats.

57 ltaCa(2+) responses in sham rats, but not in RVH rats.

58 f sham rats, but this effect was occluded in RVH rats, thus equalizing the magnitude and time course

59 Acute inotropic support in RVH is best accomplished by dobutamine, reflecting its b

60 The enhanced endogenous glutamate tone in RVH rats was not due to blunted glutamate transporter ac

61 ine) versus pulmonary artery banding-induced RVH (PAB-RVH).

62 Maladaptive RVH shares metabolic abnormalities with cancer including

63 Clinically, maladaptive RVH is characterized by increased N-terminal pro-brain n

64 function), while others develop maladaptive RVH, characterized by dilatation, fibrosis, and RV failu

65 In maladaptive RVH there is reduced inotrope responsiveness because of

66 At the molecular level, maladaptive RVH displays greater impairment of angiogenesis, adrener

67 fferentiation of adaptive versus maladaptive RVH is imprecise, but adaptive RVH is associated with be

68 sensitive or specific for screening for mild RVH in adults without clinical cardiovascular disease.

69 of remodeling (MCT only) developed moderate RVH compared with control animals.

70 Compared with normal, RVH showed increased spatial density of microvessels (16

71 and positively correlated with the degree of RVH (RV thickness/body surface area; r(2)=0.838 and r(2)

72 Q 123 treatment prevented the development of RVH as determined by the ratio of the right ventricle/le

73 bated NMDAR-DeltaCa(2+) responses in MNCs of RVH rats affected both somatic and dendritic compartment

74 e in somatodendritic compartments of MNCs of RVH rats, and (2) that a blunted ER Ca(2+) buffering cap

75 s sharply increased in compensating phase of RVH tissues but was lost in decompensation phase of RVH.

76 ng the transition from compensating phase of RVH toward decompensation phase of RVH.

77 sues but was lost in decompensation phase of RVH.

78 phase of RVH toward decompensation phase of RVH.

79 after 12 wk: normal (n = 7), RVH (n = 7), or RVH+simvastatin (RVH+S; 80 mg/d; n = 6).

80 suspected of having obstruction (P = .80) or RVH (P = .24).

81 us pulmonary artery banding-induced RVH (PAB-RVH).

82 In PAH-RVH versus PAB-RVH there was greater downregulation of beta1-, alpha1-

83 m; P<0.001) were lower in PAH-RVH versus PAB-RVH.

84 or downregulation also occurred in human PAH-RVH.

85 ed with pulmonary arterial hypertension (PAH-RVH; SU5416+chronic-hypoxia or Monocrotaline) versus pul

86 In PAH-RVH versus PAB-RVH there was greater downregulation of b

87 s 244.1+/-12.4 m; P<0.001) were lower in PAH-RVH versus PAB-RVH.

88 c receptors impairs inotropic reserve in PAH-RVH.

89 function in renovascular hypertensive rats (RVH).

90 drenergic remodeling were compared in rodent RVH associated with pulmonary arterial hypertension (PAH

91 Neointimal lesions and severe RVH developed in these animals but were not seen in anim

92 Despite similar RVH, cardiac output (58.3+/-4.9 versus 82.9+/-4.8 mL/min

93 al (n = 7), RVH (n = 7), or RVH+simvastatin (RVH+S; 80 mg/d; n = 6).

94 Confocal immunohistochemistry showed that RVH myocardial ET type A (but not type B) receptor and E

95 the EF hands protected sites within both the RVH domain and EF hands from trypsin cleavage and increa

96 nt DGK alpha fragment that included both the RVH domain and EF hands.

97 ship (Hill coefficient) was decreased in the RVH group at SL = 2.0 microns (4.3 +/- 0.4 versus 3.1 +/

98 Maximal force was increased in the RVH group: 1.20 +/- 0.10 versus 1.62 +/- 0.13 mg at SL =

99 half-maximal activation was increased in the RVH group: 2.64 +/- 0.13 versus 3.47 +/- 0.22 mumol/L at

100 Maximal tension, however, was reduced in the RVH group: 24.3 +/- 1.91 versus 37.5 +/- 2.92 mN/mm2 at

101 Deletion of the RVH domain resulted in loss of Ca(2+)-dependent activati

102 As with Ca(2+), this activation required the RVH domain.

103 samples, and from rats with normal RV versus RVH attributable to PAH.

104 e effects of ERAs on the RV in patients with RVH and PAH.

105 RV myocardial samples from 34 patients with RVH were compared with 16 nonhypertrophied RV samples, a