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

1 in proportion to the reduced O2 delivery and myocardial oxygen consumption .

2 , MAP is mean arterial pressure, and MVO2 is myocardial oxygen consumption).

3 ase and, as a consequence, fails to decrease myocardial oxygen consumption.

4 rformance without necessarily increasing the myocardial oxygen consumption.

5 riod improved LV function without increasing myocardial oxygen consumption.

6 s modestly reduced by L-NNA at all levels of myocardial oxygen consumption.

7 s the groundwork for calculation of regional myocardial oxygen consumption.

8 surements, these data were used to calculate myocardial oxygen consumption.

9 sed from ATP hydrolysis, but not in terms of myocardial oxygen consumption.

10 onary vascular dilation, and NO can modulate myocardial oxygen consumption.

11 oronary flow without commensurate changes in myocardial oxygen consumption.

12 Milrinone reduced myocardial oxygen consumption (0.15+/-0.06 versus 0.16+/

13 There was increased myocardial oxygen consumption (0.16+/-0.07 versus 0.14+/

14 increased mechanical efficiency (stroke work/myocardial oxygen consumption; +122+/-42%; P=0.04).

15 ogs, but not controls, allopurinol decreased myocardial oxygen consumption (-49+/-4.6%; P=0.002) and

16 lure has been associated with a reduction in myocardial oxygen consumption and an improvement in myoc

17 performed to determine the effects of CHF on myocardial oxygen consumption and coronary blood flow du

18 wever, the slope of the relationship between myocardial oxygen consumption and coronary venous oxygen

19 tabolic signalling factor is proportional to myocardial oxygen consumption and delivery is proportion

20 tabolic signalling factor is proportional to myocardial oxygen consumption and delivery is proportion

21 ardiac failure was associated with decreased myocardial oxygen consumption and failure of oxygen cons

22 Myocardial oxygen consumption and FAO were increased 3-

23 baseline cardiac metabolism, but attenuates myocardial oxygen consumption and glucose oxidation in r

24 mponent of CIMR, with increased gradients of myocardial oxygen consumption and impaired diastolic fil

25 Whereas higher doses may increase myocardial oxygen consumption and induce arrhythmias, di

26 de of NO synthesis resulted in elevations in myocardial oxygen consumption and reductions in myocardi

27 ncy was assessed by the relationship between myocardial oxygen consumption and total pressure-volume

28 xtensively for the noninvasive assessment of myocardial oxygen consumption and viability with PET.

29 gh workload groups had a similar increase in myocardial oxygen consumption ( and cardiac power.

30 elated with lower valvuloarterial impedance, myocardial oxygen consumption, and improved myocardial e

31 Myocardial work correlates with myocardial oxygen consumption, and work efficiency can a

32 Myocardial oxygen consumption before ischemia was 4.58 +

33 r, in HF, des-acyl and acyl ghrelin enhanced myocardial oxygen consumption by 10.2+/-3.5% and 9.9+/-3

34 initial increase and subsequent reduction in myocardial oxygen consumption during disease progression

35 Myocardial oxygen consumption during exercise was signif

36 thood, and are sufficient to maintain normal myocardial oxygen consumption during stressed conditions

37 t that beta-adrenergic stimulation increases myocardial oxygen consumption during ventricular fibrill

38 that xanthine oxidase inhibitors can reduce myocardial oxygen consumption for a particular stroke vo

39 d flow and coronary vascular resistance, and myocardial oxygen consumption (four pigs).

40 notropes; however, these agents can increase myocardial oxygen consumption, impair tissue perfusion,

41 DMA increase heart rate, blood pressure, and myocardial oxygen consumption in a magnitude similar to

42 there was a 31% and 23% increase in unloaded myocardial oxygen consumption in healthy and postischemi

43 3-butanedione monoxide abolished all surplus myocardial oxygen consumption in the OM-treated hearts.

44 adykinin (10(-4) mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40

45 radykinin- or carbachol-induced reduction of myocardial oxygen consumption in vitro, and this effect

46 nges in CBV with handgrip were linked to the myocardial oxygen consumption in women but not in men.

47 Myocardial oxygen consumption increased (P = 0.04) from

48 Before inhibition of NO synthesis, myocardial oxygen consumption increased approximately 3.

49 Myocardial oxygen consumption increased versus baseline

50 Myocardial oxygen consumption is determined by regulatio

51 e mortality due to increased tachycardia and myocardial oxygen consumption leading to arrhythmia and

52 beta- and alpha1-adrenergic effects increase myocardial oxygen consumption, magnify global myocardial

53 d for noninvasive quantification of regional myocardial oxygen consumption (MMRO2, mL.min-1 x 100 g-1

54 In nondiabetic dogs, exercise increased myocardial oxygen consumption (MVO(2)) 3.4-fold, myocard

55 betes, myocardial fatty acid utilization and myocardial oxygen consumption (MVo(2)) are increased, an

56 sine receptor blockade fails to alter CBF or myocardial oxygen consumption (MVO(2)) in the normal hea

57 acid (FFA) and insulin levels, we quantified myocardial oxygen consumption (MVo(2)), glucose, and fat

58 Myocardial blood flow (MBF), myocardial oxygen consumption (MVO(2)), myocardial fatty

59 measurements of myocardial blood flow (MBF), myocardial oxygen consumption (MVO(2)), myocardial gluco

60 action, 29+/-3%) were instrumented to assess myocardial oxygen consumption (MVO(2)), peak rate of ris

61 unction do so while concomitantly increasing myocardial oxygen consumption (MVO(2)).

62 Myocardial oxygen consumption (MVO2) and fatty acid upta

63 C]acetate for the noninvasive measurement of myocardial oxygen consumption (MVO2) and myocardial bloo

64 se humans and animals demonstrated increased myocardial oxygen consumption (MVO2) and reduced cardiac

65 ricular (LV) function without an increase in myocardial oxygen consumption (MVO2) and thus improves L

66 S) plays an important role in the control of myocardial oxygen consumption (MVO2) by nitric oxide (NO

67 etate has been validated as a PET tracer for myocardial oxygen consumption (MVO2) in animals and huma

68 To investigate the theory of decreased myocardial oxygen consumption (MVo2) in dynamic cardiomy

69 Myocardial oxygen consumption (MVO2) of LV tissue was me

70 It has been shown that myocardial oxygen consumption (MVO2) of the hypertrophie

71 d parabiotic rabbit heart Langendorff model, myocardial oxygen consumption (MVO2) was compared in hea

72 l myocardial pressure (P(tm)) and indices of myocardial oxygen consumption (MVO2) were determined in

73 In normal conscious dogs, L-NMMA increased myocardial oxygen consumption (MVO2) while lowering left

74 n of NO synthase (NOS) caused an increase of myocardial oxygen consumption (MVO2).

75 ondrial electron transport chain to regulate myocardial oxygen consumption (MVO2).

76 etermination of myocardial blood flow (MBF); myocardial oxygen consumption (MVO2); myocardial glucose

77 Empagliflozin did not change myocardial oxygen consumption or MEE.

78 re were no associated significant changes in myocardial oxygen consumption, or its major correlates w

79 unloaded mode, the low-Hb group showed lower myocardial oxygen consumption ( P < 0.001), a higher art

80 myocardial efficiency defined as stroke work/myocardial oxygen consumption (r=0.63-0.65; all P<0.01).

81 ts enhanced cardiac efficiency by decreasing myocardial oxygen consumption rates.

82 Although myocardial oxygen consumption responses were similar bet

83 Regression analysis of measurements of myocardial oxygen consumption showed that there was a st

84 ts the relationship between cardiac work and myocardial oxygen consumption, suggesting that endogenou

85 Cardiac efficiency was assessed by relating myocardial oxygen consumption to the cardiac work indice

86 hemodynamics and tissue perfusion and reduce myocardial oxygen consumption, until adequate anti-arrhy

87 The increased unloaded myocardial oxygen consumption was confirmed in OM-treate

88 Under all perfusion conditions, myocardial oxygen consumption was higher in ob/ob hearts

89 Myocardial oxygen consumption was invasively determined

90 Likewise, myocardial oxygen consumption was lower at rest in contr

91 ffer in HOCM compared with controls, whereas myocardial oxygen consumption was lower in HOCM.

92 Myocardial oxygen consumption was measured polarographic

93 Resting myocardial oxygen consumption was reduced (63+/-3 versus

94 rterial impedance (ie, global afterload) and myocardial oxygen consumption were reduced by -11% and -

95 umic developed pressure, coronary flows, and myocardial oxygen consumption were significantly improve

96 left ventricular end-diastolic pressure and myocardial oxygen consumption while increasing ejection

97 Myocardial oxygen consumption with dobutamine increased