ライフサイエンスコーパス: hemodynamic load

1 itochondrial biogenesis genes in response to hemodynamic load.

2 hagy in heart disease elicited by changes in hemodynamic load.

3 ntial of functioning heart in the absence of hemodynamic load.

4 Both of them are induced by hemodynamic load.

5 th and function in response to an increasing hemodynamic load.

6 nduction system is sensitive to variation in hemodynamic load.

7 ong others, abnormal tissue architecture and hemodynamic load.

8 rtrophy and atrophy secondary to a transient hemodynamic load.

9 atrophy are temporally related to changes in hemodynamic load.

10 suggesting potential alterations in cardiac hemodynamic load.

11 because of an arterial hypertension-induced hemodynamic load.

12 maladaptive response of the heart to chronic hemodynamic loads.

13 mice, or even when hearts were subjected to hemodynamic loading.

14 ex mechanical signals generated by pulsatile hemodynamic loading.

15 of vascular remodeling to restore normative hemodynamic loading.

16 These findings suggest that increased hemodynamic load adversely affects endocardial function

17 art is critical for functional adaptation to hemodynamic load and nutrient environment.

18 In our previous work, we examined hemodynamic loading and aortic arch growth in the chick

19 of cardiac cells to mechanical stress during hemodynamic loading and unloading.

20 dissection, or rupture are influenced by the hemodynamic loads and mechanical properties of the wall.

21 R was related to severity of AS, increase in hemodynamic load, and reduction in diastolic perfusion t

22 te the relationships between aging, elevated hemodynamic load, cardiac mechanics, and LV remodeling i

23 The relationship between exercise hemodynamics, loading conditions, and medical treatment

24 The left ventricular hemodynamic load differs between aortic regurgitation (A

25 t pressure-volume measurement, was used as a hemodynamic (loading) feature.

26 However, the pulsatile component of hemodynamic load has not been evaluated in this model.

27 impairment was related to aortic valve area, hemodynamic load imposed, and diastolic perfusion rather

28 rdium is critically dependent on the type of hemodynamic load imposed, mandates that cardiac hypertro

29 Hemodynamic loading imposed by 7 days of transverse aort

30 imary rate-limiting event in the response to hemodynamic loading in vivo and that p300 availability d

31 s are appropriate to compensate their higher hemodynamic load, in OB increase in LV mass exceeds this

32 mpound, arjunolic acid (AA), in ameliorating hemodynamic load-induced cardiac fibrosis and identified

33 Reduction of hemodynamic load is a primary factor underlying several

34 tial cardiac response to a fixed increase in hemodynamic load is an increase in cardiac mass.

35 Although reducing the hemodynamic load is known to improve myocardial fibrosis

36 an easily measurable correlate of pulsatile hemodynamic load, is an independent predictor of risk of

37 ication of a morphological sign of increased hemodynamic load may be important in asymptomatic aortic

38 er, suggests that the pulsatile component of hemodynamic load may play a fundamental role in both the

39 injury, cardiac remodeling is influenced by hemodynamic load, neurohormonal activation and other fac

40 CTB) or reduced (left atrial ligation, LAL) hemodynamic loading of the embryonic heart.

41 osed that the response of aortic SMCs to the hemodynamic load on a structurally defective aorta is th

42 ophy (LVH) in obesity results from increased hemodynamic load or altered neurohormonal signaling rema

43 n response to pathological stressors such as hemodynamic load or ischemia, cardiac myocytes downregul

44 uent increase in distal arterial caliber and hemodynamic load precipitates the flow-dependent develop

45 elative contribution of myocyte hypertrophy, hemodynamic load, severity of AS, and coronary perfusion

46 le can all be precisely manipulated to apply hemodynamic loading to culture cells.