ライフサイエンスコーパス: venous congestion

1 nsplantation, two from graft loss because of venous congestion.

2 and muscle via local mechanisms secondary to venous congestion.

3 The flaps failed in the DIEP group due to venous congestion.

4 against this background of chronic pulmonary venous congestion.

5 onstriction that characterizes this model of venous congestion.

6 lus epithelium, decreased villus height, and venous congestion.

7 icular preload, dilates, and causes systemic venous congestion.

8 oad or during exercise, leading to pulmonary venous congestion.

9 quired retransplantation and none because of venous congestion.

10 sis, lowering venous pressures and relieving venous congestion(3-8).

11 is preserved, safeguarding both grafts from venous congestion; all reconstructions can be performed

12 Patients present with systemic and pulmonary venous congestion and atrial fibrillation and have a poo

13 t premature mortality associated with marked venous congestion and dilated cardiomyopathy.

14 Venous congestion and edema within the optic nerve relat

15 ed standing with resultant gravity-dependent venous congestion and inflammatory vasculitis.

16 suggest an association between intracranial venous congestion and SANS.

17 monstrated by the absence of graft loss from venous congestion and superior graft survival.

18 consequences of diastolic dysfunction (e.g., venous congestion), and the second is to eliminate or re

19 stimulation of forearm mechanoreceptors with venous congestion, and during ischemia produced by forea

20 ubmucosal edema, infiltration of leukocytes, venous congestion, and hemorrhage.

21 vere hepatic necrosis, likely from prolonged venous congestion, and the patient required repeat trans

22 ory of some vortex vein varices, implicating venous congestion as an instigator and venous collateral

23 tive hyperemia) and during venous occlusion (venous congestion), as assessed with skin capillaroscopy

24 Venous congestion due to TR may lead to end-organ dysfun

25 ged as a novel imaging biomarker of systemic venous congestion, identifying right heart failure and a

26 We further identify that venous congestion is common and identifies patients with

27 Venous congestion is the most important hemodynamic fact

28 Venous congestion of the epiescleral and retinal vessels

29 The effects of acute pulmonary venous congestion on the activity of rapidly adapting re

30 ccur secondary to persistent chronic passive venous congestion or decreased cardiac output resulting

31 patients with concomitant signs of cerebral venous congestion (p = 0.06), while no significant assoc

32 r limb arterial blood flow is sustained when venous congestion pressure is raised using small cumulat

33 sis that the application of small cumulative venous congestion pressure steps is associated with a re

34 e to transient (10 s duration) elevations of venous congestion pressure to 90 mmHg, after which the c

35 tibial arterial peak blood flux at 58.3 mmHg venous congestion pressure was 102.2 +/- 2.3% of the con

36 Cumulative small steps in venous congestion pressure were used to study the effect

37 M. control arterial blood flow at the lowest venous congestion pressure, 4.8 +/- 0.1 mmHg, was 2.77 +

38 At the highest venous congestion pressure, 59.2 +/- 0.2 mmHg, arterial

39 b arterial blood flow and blood flux at each venous congestion pressure, assuming that both mean arte

40 It is concluded that chronic pulmonary venous congestion resulting from destruction of the mitr

41 body weight) are mostly related to systemic venous congestion secondary to various mechanisms includ

42 During ischemia but not during venous congestion, SSNA increased more compared with con

43 ain at some point in their lives, and pelvic venous congestion syndrome (PVCS) is the cause of this p

44 est tertiles of capillary recruitment during venous congestion yielded an odds ratio of 2.89 (95% con