ライフサイエンスコーパス: hemodynamic load

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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 maladaptive response of the heart to chronic hemodynamic loads.

11 ex mechanical signals generated by pulsatile hemodynamic loading.

12 of vascular remodeling to restore normative hemodynamic loading.

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

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

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

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

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

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

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

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

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

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

23 Hemodynamic loading imposed by 7 days of transverse aort

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

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

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

27 Reduction of hemodynamic load is a primary factor underlying several

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

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

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

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

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

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

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

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

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

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

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

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

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