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 ase of ischemic preconditioning (PC) against myocardial stunning.

3 cardioprotective effects of late PC against myocardial stunning.

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

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

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

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

8 not have any delayed deleterious actions on myocardial stunning.

9 d whether this gene therapy protects against myocardial stunning.

10 change further, suggesting the induction of myocardial stunning.

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

12 ours after the sixth reperfusion, indicating myocardial stunning.

13 ing postdobutamine recovery, consistent with myocardial stunning.

14 -dependent myofilament proteolysis underlies myocardial stunning.

15 time course of late preconditioning against myocardial stunning.

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

17 eperfusion of the first sequence, indicating myocardial stunning.

18 generation or swelling and failed to prevent myocardial stunning.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 -7% before the 6th CS, reflecting persistent myocardial stunning, but baseline CBF was not changed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Myocardial stunning is characterized by decreased myofil

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

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

53 Myocardial stunning may cause prolonged left ventricular

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 Myocardial stunning was induced in conscious pigs by cor

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

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

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

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

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

75 Significant myocardial stunning with subsequent improvement of ventr

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