ライフサイエンスコーパス: myocardial stunning

1 ion that follows brief periods of ischemia ("myocardial stunning").

2 cardiopulmonary resuscitation, indicative of myocardial stunning.

3 own of MyBP-C during reperfusion may prolong myocardial stunning.

4 generation or swelling and failed to prevent myocardial stunning.

5 ase of ischemic preconditioning (PC) against myocardial stunning.

6 15 patients showed improved or no effect on myocardial stunning.

7 cardioprotective effects of late PC against myocardial stunning.

8 chondrial (SOD2) isoforms to protect against myocardial stunning.

9 Reactive oxygen species (ROS) contribute to myocardial stunning.

10 sed echocardiography to assess intradialytic myocardial stunning.

11 and function in a canine model of repetitive myocardial stunning.

12 not have any delayed deleterious actions on myocardial stunning.

13 d whether this gene therapy protects against myocardial stunning.

14 change further, suggesting the induction of myocardial stunning.

15 P<0.05), indicating a late PC effect against myocardial stunning.

16 ours after the sixth reperfusion, indicating myocardial stunning.

17 ing postdobutamine recovery, consistent with myocardial stunning.

18 -dependent myofilament proteolysis underlies myocardial stunning.

19 time course of late preconditioning against myocardial stunning.

20 I, in some species, has been associated with myocardial stunning.

21 eperfusion of the first sequence, indicating myocardial stunning.

22 ors considered in the etiology of HD-induced myocardial stunning.

23 ar systolic dysfunction caused by repetitive myocardial stunning.

24 ic episodes confer marked protection against myocardial stunning 1-3 d later (late preconditioning [P

25 nce of O/R (group V, n = 5), the severity of myocardial stunning 24 h later was not modified.

26 n of L-NA did not exacerbate the severity of myocardial stunning 24 hours later; therefore, the absen

27 ns renders the heart relatively resistant to myocardial "stunning" 24 hours later (late preconditioni

28 us free radical concentration and ameliorate myocardial stunning after ischemia-reperfusion.

29 d flow by 40% for 90 minutes, and subsequent myocardial stunning after reperfusion in chronically ins

30 ting (CABG) similarly may be associated with myocardial stunning and cell necrosis associated with is

31 acute myocardial infarction (MI) because of myocardial stunning and compensatory hyperkinesia in non

32 survival that relates to the time course of myocardial stunning and differs transmurally in relation

33 This process is known as myocardial stunning and has important clinical ramificat

34 tter understanding of the pathophysiology of myocardial stunning and hibernation is important for a m

35 he end point reflecting irreversible injury, myocardial stunning and hibernation result from reversib

36 A3 adenosine receptor agonist, in models of myocardial stunning and infarction in chronically instru

37 ioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicatin

38 ioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicatin

39 and aberrant cellular processes, leading to myocardial stunning, arrhythmias, and ultimately cell da

40 ROS and MPT have been implicated in myocardial stunning associated with reperfusion in ische

41 inding that ROS contribute to the genesis of myocardial stunning but, at the same time, trigger the d

42 -7% before the 6th CS, reflecting persistent myocardial stunning, but baseline CBF was not changed.

43 se (SOD) without catalase fails to alleviate myocardial stunning, but extracellular SOD (Ec-SOD) may

44 have been implicated in the pathogenesis of myocardial stunning, but the precise mechanism by which

45 of brief coronary occlusions induces severe myocardial stunning, but when the same sequence is repea

46 To test the hypothesis that persistent myocardial stunning can lead to hibernating myocardium,

47 In summary, repetitive myocardial stunning commonly seen in chronic multivessel

48 In phase I (studies of myocardial stunning), conscious rabbits underwent a sequ

49 r (LV) myocardial wall motion abnormalities (myocardial stunning) due to segmental hypoperfusion.

50 Although doxycycline did not improve myocardial stunning following coronary artery bypass gra

51 The magnitude and time course of myocardial stunning from cardiac arrest is unknown.

52 s of reperfusion, and the differentiation of myocardial stunning from myocardial necrosis.

53 DETA/NO-induced late PC effect against both myocardial stunning (groups VII through X) and myocardia

54 The mechanism of myocardial stunning has been studied extensively in rode

55 ally relevant time after ischemia eliminates myocardial stunning in conscious pigs during augmented c

56 strate that the mechanism of late PC against myocardial stunning in conscious rabbits involves a PKC-

57 ly blocks the development of late PC against myocardial stunning in conscious rabbits, indicating tha

58 Understanding the genes up-regulated during myocardial stunning, including those not previously desc

59 provement of ventricular function in chronic myocardial stunning is associated with restoration of mi

60 Myocardial stunning is characterized by decreased myofil

61 of cardiac troponin I (cTnI) proteolysis in myocardial stunning is not fully understood.

62 Myocardial stunning is observed clinically and must be r

63 Full recovery of this postresuscitation myocardial stunning is seen by 48 h in this experimental

64 Myocardial stunning may cause prolonged left ventricular

65 Possible poststress myocardial stunning may have caused gated Tl LVEFs to ov

66 ose produced by XO + P, mimic the effects of myocardial stunning on cardiac excitation-contraction co

67 (b) antioxidant therapy markedly attenuates myocardial stunning on day 1, indicating that ROS play a

68 ective as antioxidant therapy in attenuating myocardial stunning on day 1, it has no effect on late p

69 This study compared the effects of porcine myocardial stunning on the uptake of [18F]-fluorodeoxygl

70 r 4 h after the 10th reperfusion, indicating myocardial "stunning." On days 2 and 3, however, the rec

71 sfunction after acute MI may be secondary to myocardial stunning or necrosis.

72 6), designed to produce different degrees of myocardial stunning; or (c) a single episode of 2 minute

73 In phase I (studies of myocardial stunning), rabbits were subjected to six 4-mi

74 Thus, late preconditioning against myocardial stunning requires > 6 hours to develop, lasts

75 iopulmonary resuscitation and is mediated by myocardial stunning resulting from mitochondrial electro

76 owever, hibernation may represent persistent myocardial stunning resulting from repeated episodes of

77 metabolic changes associated with repetitive myocardial stunning seen in chronic multivessel coronary

78 ults in recurrent segmental ischemic injury (myocardial stunning) that drives cumulative cardiac dama

79 In contrast, in DCA pigs, myocardial stunning was ameliorated (P<0.05).

80 al perfusion and metabolism, suggesting that myocardial stunning was common.

81 Myocardial stunning was induced in conscious pigs by cor

82 pigs with regional cardiac denervation (CD), myocardial stunning was intensified, ie, at 12 hours rep

83 The severity of myocardial stunning was measured as the total deficit of

84 s observed during dobutamine stress, and (3) myocardial stunning was observed during postdobutamine r

85 In the absence of DCA, myocardial stunning was observed; ie, wall thickening wa

86 kening (a measure of the overall severity of myocardial stunning) was reduced by 68% (control, 129 +/

87 In a canine model of repetitive myocardial stunning, we showed that carvedilol, a non-se

88 Significant myocardial stunning with subsequent improvement of ventr

89 he heart with substantial protection against myocardial stunning without the need for concomitant adm