ライフサイエンスコーパス: myocardial ischaemia

1 stress echocardiography to detect or exclude myocardial ischaemia.

2 n of Hand1 is protective in a mouse model of myocardial ischaemia.

3 ception to the central nervous system during myocardial ischaemia.

4 ors released from activated platelets during myocardial ischaemia.

5 ardiac spinal afferents are activated during myocardial ischaemia.

6 n progress in some disease states, including myocardial ischaemia.

7 n and T wave changes characteristic of acute myocardial ischaemia.

8 cardiogenic sympathoexcitatory reflex during myocardial ischaemia.

9 e therapy using angiogenic growth factors in myocardial ischaemia.

10 g gross distension, possibly associated with myocardial ischaemia.

11 c acid production is associated closely with myocardial ischaemia.

12 cardiac sympathetic C-fibre afferents during myocardial ischaemia.

13 fied according to their response to 5 min of myocardial ischaemia.

14 ts (i.e. prostaglandins (PGs)) occurs during myocardial ischaemia.

15 tamine stress in the presence and absence of myocardial ischaemia.

16 We conclude that during early myocardial ischaemia, a major component of [K+]o accumul

17 Myocardial ischaemia activates blood platelets and cardi

18 Myocardial ischaemia activates blood platelets, which in

19 Myocardial ischaemia activates cardiac sympathetic affer

20 n of p38-MAPK by dual phosphorylation during myocardial ischaemia aggravates lethal injury.

21 ated tool for the non-invasive evaluation of myocardial ischaemia and enables the recording of heart

22 e patients aged 18-85 years with evidence of myocardial ischaemia and one or two de-novo native lesio

23 e patients aged 18-85 years with evidence of myocardial ischaemia and one or two de-novo native lesio

24 During myocardial ischaemia and reperfusion, tirofiban, a speci

25 These findings show acute myocardial ischaemia and subacute myocardial microinfarc

26 detected in cardiomyopathies, heart failure, myocardial ischaemia, and hypertrophy.

27 de in obtunding cardiovascular responses and myocardial ischaemia, and the provision of effective per

28 We have focused on acute myocardial ischaemia as it is the most strikingly proarr

29 depletion of cellular energy reserves (e.g. myocardial ischaemia), ATP generated from glycolysis may

30 most widely used test for the assessment of myocardial ischaemia, but its diagnostic accuracy is rep

31 tion of cardiac sympathetic afferents during myocardial ischaemia causes angina and induces important

32 Myocardial ischaemia causes the release of metabolites s

33 In the absence of myocardial ischaemia, dobutamine stress is associated wi

34 The dose-limiting toxic effect was myocardial ischaemia due to excessive prolongation of sy

35 Using a non-human primate model of myocardial ischaemia followed by reperfusion, we show th

36 sed the activity of cardiac afferents during myocardial ischaemia from 1.5 +/- 0.4 to 0.8 +/- 0.4 imp

37 etermined whether individuals with transient myocardial ischaemia had different autonomic responses t

38 h usually causes cell volume changes, during myocardial ischaemia, hypertrophy and heart failure.

39 Incremental atrial pacing was used to induce myocardial ischaemia in 18 patients with coronary artery

40 ) activity and LV remodelling in response to myocardial ischaemia in vivo.

41 us studies have shown that a brief period of myocardial ischaemia increases endothelin in cardiac ven

42 study was to test the hypothesis that acute myocardial ischaemia increases QT dispersion measured fr

43 These results demonstrate that myocardial ischaemia induced by incremental atrial pacin

44 sensitive cardiac visceral afferents during myocardial ischaemia induces both angina and cardiovascu

45 utamine stress is augmented as the burden of myocardial ischaemia is increased.

46 Chest pain caused by myocardial ischaemia is mediated by cardiac sympathetic

47 g the precise mechanism of activation during myocardial ischaemia is of considerable importance, sinc

48 Responses of cardiac afferents to myocardial ischaemia, lactic acid, sodium lactate, acidi

49 inistration of ET-1 (n = 7) and to recurrent myocardial ischaemia (n = 7).

50 istration of U46619 (n = 6) and to recurrent myocardial ischaemia (n = 7).

51 onymized electronic medical records from the Myocardial Ischaemia National Audit Project and the Gene

52 in England and Wales were obtained from the Myocardial Ischaemia National Audit Project between Janu

53 propensity score analyses, of data from the Myocardial Ischaemia National Audit Project for patients

54 nal English and Welsh registry data from the Myocardial Ischaemia National Audit Project.

55 NT] 63) and decrease (OR 0.36, 0.26-0.50) in myocardial ischaemia (NNT 16) at the expense of an incre

56 depletion and Ca(2+) overload occur, such as myocardial ischaemia or anoxia.

57 anisms and the relevance of these results to myocardial ischaemia or hypoxia is considered.

58 The PROVE IT and the Myocardial Ischaemia Reduction with Aggressive Cholester

59 cture that can be selectively removed during myocardial ischaemia reperfusion by mu-calpain proteolys

60 ctive effects of short-term exercise against myocardial ischaemia-reperfusion injury in male and fema

61 g processes in atherosclerosis, vascular and myocardial ischaemia-reperfusion injury, and heart failu

62 patient that experiences an episode of acute myocardial ischaemia-reperfusion injury.

63 ement activation is a recognised mediator of myocardial ischaemia-reperfusion-injury (IRI) and cardio

64 p38-MAPK pathway plays an important role in myocardial ischaemia/reperfusion injury and has been imp

65 rction, non-fatal stroke, heart failure, and myocardial ischaemia, safety outcomes of perioperative b

66 Five minutes of myocardial ischaemia stimulated all 38 cardiac afferents

67 Five minutes of myocardial ischaemia stimulated all 39 cardiac afferents

68 These data indicate that during myocardial ischaemia the activated platelets stimulate c

69 However, under conditions of myocardial ischaemia, there was a directionally opposite

70 es to activation of cardiac afferents during myocardial ischaemia through direct stimulation of ET(A)

71 o the activation of cardiac afferents during myocardial ischaemia through direct stimulation of TP re