ライフサイエンスコーパス: developed pressure

1 displayed significantly enhanced recovery of developed pressure.

2 hosphates using 31P-NMR and left-ventricular developed pressure.

3 creased heart rate and peak left ventricular developed pressure.

4 left and right ventricles for measurement of developed pressure.

5 4+/-1 versus 23+/-1.6 mm Hg; Langendorff LV developed pressure, 105+/-4 versus 62+/-9 mm Hg, P<.001

6 beats/min, p < 0.05) and a decrease in peak developed pressure (153 +/- 21 vs. 180 +/- 16 mm Hg, p <

7 ed indexes of functional recovery, including developed pressure (38 +/- 3 versus 69 +/- 7 mm Hg) and

8 Isolated heart function (LV developed pressure 58+/-2 versus 72+/-3 mm Hg, P:=0.004)

9 ed significantly greater recovery of maximum developed pressure (70 +/- 4% in control versus 77 +/- 2

10 sure (450% vs. 33%, p < 0.01) and reduced LV developed pressure (9% vs. 33%, p < 0.01), LV positive (

11 ondrial reactive oxygen species, improved LV developed pressure (92+/-5 vs. 28+/-10 mmHg, P<0.001), a

12 had a 28% decrease in peak left ventricular developed pressure, a 30% decrease in +dP/ dt, and a 23%

13 The developed pressure after administration of isoproterenol

14 Peak left ventricular developed pressure and +/-dp/dt were significantly lower

15 In isolated perfused hearts, developed pressure and -dP/dt were significantly improve

16 resulted in an increase in left ventricular developed pressure and an increase in [Ca2+]SR.

17 icular recovery was demonstrated by improved developed pressure and aortic flow and reduced myocardia

18 IPC significantly increased left ventricular developed pressure and decreased infarct size in wild-ty

19 p 2 was found to have significantly impaired developed pressure and diastolic relaxation and an incre

20 tion fraction and increased left ventricular developed pressure and end diastolic pressure.

21 nt, enhanced fetal LV developed pressure, RV developed pressure and HR responses to carbachol (P < 0.

22 , suppressed fetal LV developed pressure, RV developed pressure and HR responses to isoprenaline (P <

23 Recovery of left ventricular developed pressure and infarct size were measured as ind

24 Left ventricular developed pressure and ischemic contracture were assesse

25 i.e., a marked reduction in left ventricular developed pressure and maximal rate of development of le

26 Developed pressure and oxygen consumption were better pr

27 tion, consisting of a better preservation of developed pressure and positive and negative dP/dt after

28 ntricular function was assessed by measuring developed pressure and rate pressure product in Langendo

29 Left ventricular developed pressure and rate pressure product were signif

30 ed postischemic recovery of left ventricular developed pressure and reduced infarct size.

31 llowing measurement of left ventricular (LV) developed pressure and right ventricular (RV) developed

32 Preischemic left ventricular developed pressures and +dP/dtmax, as well as -dP/dtmin,

33 contraction and relaxation, left ventricular developed pressure, and cardiac output compared with non

34 ment in postischemic end-diastolic pressure, developed pressure, and rate-pressure product, which was

35 e at 1 and 4 months after MI, as was peak LV developed pressure at 1 month after MI.

36 ed at the end of ischemia, and the return of developed pressure at reperfusion was greater (P<0.05).

37 Rapid VR increased developed pressure by 15% (92.2 +/- 23.7 [mean +/- SD] v

38 cardiac function, IGF-1 increased isovolumic developed pressure by 24% above baseline.

39 ioning recovered 70+/-7% of left ventricular developed pressure compared with 43+/-8% recovery in non

40 Isovolumic developed pressure, coronary flow, and oxygen consumptio

41 Recovery of postischemic isovolumic developed pressure, coronary flows, and MVO2 were compar

42 Isovolumic developed pressure, coronary flows, and myocardial oxyge

43 ylephrine-induced increase in heart rate and developed pressure could be blocked with an alpha-1 anta

44 On warming to 37 degrees C, arteries developed pressure-dependent myogenic tone, and this was

45 intracardiac balloon volume at which maximal developed pressure (DevP) occurred.

46 ardial protection, as evidenced by increased developed pressure (DP) (53.3 +/- 4.3 versus 35.4 +/- 1.

47 30 and 90 minutes of reperfusion, LV maximum developed pressure (DP), dP/dt, CBF, and oxygen consumpt

48 and the first derivative of left ventricular developed pressure (dP/dt), slope of the end-systolic pr

49 TAT-AKAD also had a pronounced effect on developed pressure (-dP/dt), consistent with a delayed r

50 Peak left ventricular developed pressure, +/-dp/dt, oxygen consumption (MVO(2)

51 n the absence of eniporide, left ventricular developed pressure, end-diastolic pressure, and coronary

52 eveloped pressure and right ventricular (RV) developed pressure, heart rate (HR), coronary perfusion

53 y of left ventricular diastolic pressure and developed pressure, however, were improved significantly

54 eperfusion, the heart rate multiplied by the developed pressure (HRxDP) in the wild-type and SOD1(+/-

55 ecrosis, better recovery of left-ventricular developed pressure, improved phosphocreatine recovery, a

56 +/- 3% to 67 +/- 5%) and slightly increased developed pressure in hypoxic hearts (67 +/- 5% to 72 +/

57 s but did not alter postischemic recovery of developed pressure in isolated chronically hypoxic (FIO(

58 Left-ventricular-developed pressure in isolated isovolumic hearts, normal

59 ed postischemic recovery of left ventricular developed pressure in isolated normoxic (FIO(2)=0.21) he

60 blocker, L-calchin reduced peak systolic and developed pressure in isolated rat heart Langendorff pre

61 In contrast, at 4 months after MI, peak LV developed pressure in KO mice was higher than in WT mice

62 ) increased the recovery of left ventricular developed pressure in normoxic hearts to values not diff

63 cium transient amplitude, concomitant with a developed pressure increase; however, there was no incre

64 urs of reperfusion, maximum left ventricular developed pressure increased from 87.0+/-6.8 mm Hg (mean

65 The peak LV developed pressure/ISO dose response was shifted rightwa

66 eristics and on recovery of left ventricular developed pressure (LVDP) after 20 minutes of global isc

67 ) led to a 61% reduction in left ventricular developed pressure (LVDP) and a 57% reduction in the pre

68 d by measuring the index of left-ventricular developed pressure (LVDP) and contractility (dP/dt) befo

69 howed increased recovery of left ventricular developed pressure (LVDP) and decreased infarct size aft

70 coronary flow and preserved left ventricular developed pressure (LVDP) and dP/dtmax, indexes of cardi

71 Recovery of left ventricular developed pressure (LVDP) and infarct size were measured

72 ed postischemic recovery of left ventricular developed pressure (LVDP) and reduced infarct size compa

73 Left ventricular developed pressure (LVDP) and the cytochrome a,a3 redox

74 s have improved recovery of left ventricular developed pressure (LVDP) compared with wild-type (WT) h

75 Recovery of left ventricular developed pressure (LVDP) of ischemic hearts treated wit

76 he postischemic recovery of left ventricular developed pressure (LVDP) was 15+/-2% in controls and wa

77 mbinant EPO treatment while left-ventricular-developed pressure (LVDP) was measured continuously to a

78 Optical APs were mapped when measuring LV developed pressure (LVDP), coronary flow rate and oxygen

79 easured during reperfusion; left ventricular developed pressure (LVDP), end diastolic pressure (EDP),

80 reduction in coronary flow, left ventricular developed pressure (LVDP), or the first derivative of LV

81 ed recovery of postischemic left ventricular developed pressure (LVDP).

82 Recovery of left ventricular developed pressure (LVDP; percentage of initial preische

83 The percentage of recovery of developed pressure (mean+/-SEM) for control, glibenclami

84 LV developed pressure measured over a range of LV volumes w

85 mals in groups 3 and 4 demonstrated improved developed pressure, normal relaxation and diastolic stif

86 ter 16 minutes; P<0.05) and in LV dP/dt at a developed pressure of 40 mm Hg (LV dP/dt(40)) (-179+/-54

87 as were phosphocreatine and left ventricular-developed pressure on reperfusion.

88 opy in isolated hearts (14% decrease in peak developed pressure), papillary muscles (53% decrease in

89 In vivo left ventricular systolic developed pressure per gram as well as endocardial fract

90 oped an impaired heart-rate-left-ventricular-developed pressure product in response to high workload

91 hanges in LV volume (r=.79) and function (LV developed pressure, r=-.81).

92 At 20 minutes of reflow, isovolumic developed pressure recovered completely in the antioxida

93 st injury resulting from zero-flow ischemia (developed pressure recovered to 67+/-6% versus 31+/-12%

94 in HSP than in CON hearts: left ventricular developed pressure recovery was 72.4+/-6.4% versus 59.7+

95 greater in HSP versus CON: Left ventricular developed pressure recovery was 76.7+/-3.9% versus 60.5+

96 pressures and decreased percent recovery of developed pressure relative to WT hearts.

97 (84% versus 29% of initial left ventricular developed pressure, respectively).

98 The peak ISO LV developed pressure response was similar between WKY and

99 ut not cortisol treatment, enhanced fetal LV developed pressure, RV developed pressure and HR respons

100 not cortisol treatment, suppressed fetal LV developed pressure, RV developed pressure and HR respons

101 increased postischemic left ventricular (LV) developed pressure to 79.5 + or - 9.47 mmHg compared to

102 n), the hazard ratio for new pressure ulcers developed (pressure ulcer prevention care bundle relativ

103 with a sharper slope of the left ventricular developed pressure-volume curve and a reduced slope of t

104 esulting from low-flow ischemia (recovery of developed pressure was 40+/-8% versus 37+/-7% in C and D

105 LV developed pressure was better preserved in hearts from T

106 l and energetic compromise: left ventricular developed pressure was depressed by 20%, and cardiac pho

107 (2) Left ventricular developed pressure was depressed in transplanted hearts

108 control hearts, recovery of left ventricular developed pressure was increased in rhEPO-perfused heart

109 Peak LV developed pressure was reduced to a similar degree after

110 complete recovery of diastolic pressure and developed pressure was seen irrespective of when Ucn was

111 Systolic function (percentage recovery of developed pressure) was measured over a range of volumes

112 ic (30 minutes of reperfusion) diastolic and developed pressure were compared among the groups.

113 and positive pressure derivatives as well as developed pressures were significantly higher in both hs

114 AC recovered 53% of initial left ventricular developed pressure, whereas hearts treated with NAC alon

115 Percentage recovery of developed pressure with pinacidil (60.3%+/-3.1%) was not

116 s were made of rate-pressure product (RPP=LV developed pressure x heart rate), phosphorus-containing