ライフサイエンスコーパス: venous congestion

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

2 and muscle via local mechanisms secondary to venous congestion.

3 against this background of chronic pulmonary venous congestion.

4 onstriction that characterizes this model of venous congestion.

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

6 quired retransplantation and none because of venous congestion.

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

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

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

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

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

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

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

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

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

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

17 Venous congestion is the most important hemodynamic fact

18 Venous congestion of the epiescleral and retinal vessels

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

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

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

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

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

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

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

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

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

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

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

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

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

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