ライフサイエンスコーパス: myocardial contractility

1 CSAR activation in the normal state enhances myocardial contractility.

2 tion is inherently independent of underlying myocardial contractility.

3 now understood to be a critical repressor of myocardial contractility.

4 expression in the human RV and its impact on myocardial contractility.

5 he RV and the impact of this upregulation on myocardial contractility.

6 artner phospholamban (PLN) are essential for myocardial contractility.

7 ulating intracellular Ca(2+) homeostasis and myocardial contractility.

8 concentration, plasma oncotic pressure, and myocardial contractility.

9 s by which activated p38alpha MAPK depresses myocardial contractility.

10 whether Arg inhibition would increase basal myocardial contractility.

11 n analysis allows quantitative assessment of myocardial contractility.

12 d is therefore of interest as a regulator of myocardial contractility.

13 n interactions that could lead to diminished myocardial contractility.

14 uppression of dobutamine-induced increase in myocardial contractility.

15 neovascularization and improve perfusion and myocardial contractility.

16 Ca2+ release, leading to variable effects on myocardial contractility.

17 eart development and is important for normal myocardial contractility.

18 nificant role in the autocrine regulation of myocardial contractility.

19 O in oxidative phosphorylation and, in turn, myocardial contractility.

20 ding effects on the systemic circulation and myocardial contractility.

21 ements of endocardial voltage potentials and myocardial contractility.

22 and volume, which defines a single state of myocardial contractility.

23 coplasmic reticulum Ca2+-ATPase activity and myocardial contractility.

24 estation, with no significant alterations in myocardial contractility.

25 al inducible nitric oxide synthase decreases myocardial contractility.

26 t-mediated glutathione efflux and maintained myocardial contractility.

27 lase activity and an increased inhibition of myocardial contractility.

28 significant changes in oxygen extraction or myocardial contractility.

29 pigs showed significantly better recovery of myocardial contractility 3 months after infarction injur

30 inine (L-NNA) on free radical generation and myocardial contractility after ischemia-reperfusion.

31 Myocardial contractility and blood flow provide essentia

32 ction due to the effect of V1a activation on myocardial contractility and cell growth.

33 We found that myocardial contractility and CRC activity were decreased

34 at TLR2 signaling contributes to the loss of myocardial contractility and cytokine production in the

35 ibitors are cardiotonic agents that increase myocardial contractility and decrease vascular smooth mu

36 metabolic abnormalities, including decreased myocardial contractility and decreased plasma ionized ca

37 -Cytokine-induced NO production depresses myocardial contractility and has been shown to be cytoto

38 t ventricular cardiac myocytes as a model of myocardial contractility and in whole blood from childre

39 osis, ventricular arrhythmias, and decreased myocardial contractility and left ventricular pressure.

40 HF is characterized by a marked decrease in myocardial contractility and loss of pump function.

41 importance of acidic N' region in regulating myocardial contractility and mediating the response of t

42 troponin I (cTnI) phosphorylation modulates myocardial contractility and relaxation during beta-adre

43 Myocardial contractility and relaxation were continuousl

44 To study the effects of tachycardia on myocardial contractility and relaxation, we evaluated th

45 ic receptors is pivotal in the regulation of myocardial contractility and remodeling.

46 n of Sca-1 causes primary cardiac defects in myocardial contractility and repair consistent with impa

47 espite their importance in the regulation of myocardial contractility and rhythm.

48 ures of dilated cardiomyopathy (DCM) are low myocardial contractility and risk of thromboembolism.

49 Decreases in myocardial contractility and shortening of ventricular s

50 ic oxide (NO) modulates autonomic effects on myocardial contractility and sinus and atrioventricular

51 study the rate related effects of sotalol on myocardial contractility and to test the hypothesis that

52 Regional myocardial contractility and wall thickness were used in

53 ure associated with lower ejection fraction, myocardial contractility, and greater force developed by

54 I alters biventricular systolic function, RV myocardial contractility, and LV diastolic performance.

55 and results in enhanced calcium transients, myocardial contractility, and relaxation that may have f

56 and diminished myocardial contractility are important factors leading t

57 LV strain/strain rate, surrogate measures of myocardial contractility, are reduced in pediatric PH an

58 lic stresses and heart rate increased, while myocardial contractility, as reflected by LV dP/dt and m

59 red hPSC-CMs as powerful models for studying myocardial contractility at the cellular level.

60 gh beta-adrenergic stimuli are essential for myocardial contractility, beta-blockers have a proven be

61 les (blood pressure, stroke volume [SV], and myocardial contractility), but the relative strength and

62 mprovements in functional parameters such as myocardial contractility by echocardiography, perfusion

63 acterized by chamber enlargement and reduced myocardial contractility, decreases in beta-adrenergic r

64 Epinephrine increases myocardial contractility, decreases the duration of syst

65 Myocardial contractility depends on Ca2+ release from an

66 tions were used to track changes in regional myocardial contractility, geometry, and perfusion.

67 he effects of veno-venous ultrafiltration on myocardial contractility in children undergoing cardiopu

68 It had no effect on myocardial contractility in isolated mouse cardiac myocy

69 Microtubule depolymerization normalized myocardial contractility in papillary muscles of PAB cat

70 Nitric oxide inhibits beta-adrenergic myocardial contractility in patients with heart failure.

71 ed acidic N' region results in a decrease in myocardial contractility in the cTnI(Delta2-11) mice dem

72 We conclude that SMT is beneficial to myocardial contractility in this model of endotoxemia, w

73 Myocardial contractility in transgenic mice, as assessed

74 amban is necessary for optimal regulation of myocardial contractility in vivo.

75 mediating its optimal regulatory effects on myocardial contractility in vivo.

76 Insulin can alter myocardial contractility, in part through an effect on t

77 wditch 139 years ago as the observation that myocardial contractility increases proportionally with i

78 Poor myocardial contractility is a very important issue in vi

79 Myocardial contractility is constantly changing from bea

80 Myocardial contractility is generally believed to be inc

81 t a volatile anaesthetic-induced decrease in myocardial contractility is mediated by a reduction in i

82 annel (CRC) activity is a mechanism by which myocardial contractility is reduced in endotoxemia; b) t

83 We assessed myocardial contractility, myocardial nitric oxide conten

84 PPA had little effect on myocardial contractility of normal hearts until the high

85 e systolic dysfunction results from impaired myocardial contractility or altered loading conditions i

86 Hypothermia does not decrease myocardial contractility or induce hypotension if hypovo

87 not develop hypoxia, acidosis, alteration in myocardial contractility, or arrhythmias.

88 formation imaging might more closely reflect myocardial contractility than traditional measures of sy

89 serve), diastolic function (compliance), and myocardial contractility (the slope of the relationship

90 and regulate cardiac performance, from acute myocardial contractility to chronic gene expression and

91 The aim of this work was to evaluate myocardial contractility using the end-systolic wall str

92 mited, diastolic function was preserved, and myocardial contractility was altered (Emax=2.6+/-0.3 mm

93 Myocardial contractility was followed up by cardiac magn

94 Myocardial contractility was inversely determined from p

95 mited, ventricular compliance decreased, and myocardial contractility was preserved.

96 mice, echocardiographic analysis showed that myocardial contractility was reduced to 14 +/- 1% of con

97 Because NOS1 positively modulates myocardial contractility, we determined whether Arg inhi

98 y increased glutathione efflux and decreased myocardial contractility when compared with control anim

99 sses unique inotropic properties, increasing myocardial contractility while simultaneously reducing c

100 n femoral resistance arteries, and increased myocardial contractility with sympathetic dominance.

101 mendan is a calcium sensitizer that enhances myocardial contractility without increasing myocardial o

102 al application of inotropic compounds drives myocardial contractility without systemic side effects.