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 rformance without necessarily increasing the myocardial oxygen consumption.

4 riod improved LV function without increasing myocardial oxygen consumption.

5 ase and, as a consequence, fails to decrease 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 increased mechanical efficiency (stroke work/myocardial oxygen consumption; +122+/-42%; P=0.04).

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

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

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

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

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

18 Myocardial oxygen consumption and FAO were increased 3-

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

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

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

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

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

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

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

26 Myocardial oxygen consumption before ischemia was 4.58 +

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

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

29 Myocardial oxygen consumption during exercise was signif

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

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

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

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

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

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

36 3-butanedione monoxide abolished all surplus myocardial oxygen consumption in the OM-treated hearts.

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

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

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

40 Myocardial oxygen consumption increased (P = 0.04) from

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

42 Myocardial oxygen consumption increased versus baseline

43 Myocardial oxygen consumption is determined by regulatio

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

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

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

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

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

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

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

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

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

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

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

55 Myocardial oxygen consumption (MVO2) and fatty acid upta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Although myocardial oxygen consumption responses were similar bet

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

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

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

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

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

78 Myocardial oxygen consumption was invasively determined

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

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

81 Myocardial oxygen consumption was measured polarographic

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

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

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

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

86 Myocardial oxygen consumption with dobutamine increased