ライフサイエンスコーパス: developed pressure

1 creased heart rate and peak left ventricular developed pressure.

2 displayed significantly enhanced recovery of developed pressure.

3 hosphates using 31P-NMR and 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 Dobutamine increased both developed pressure and heart rate accompanied by decreas

22 Dobutamine increased both developed pressure and heart rate accompanied by decreas

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

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

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

26 Left ventricular developed pressure and ischemic contracture were assesse

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

28 Developed pressure and oxygen consumption were better pr

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

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

31 Left ventricular developed pressure and rate pressure product were signif

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

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

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

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

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

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

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

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

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

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

42 Isovolumic developed pressure, coronary flow, and oxygen consumptio

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

44 Isovolumic developed pressure, coronary flows, and myocardial oxyge

45 (calculated as the product of heart rate and developed pressure), correlated with functional recovery

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

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

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

49 ft (LV) and right (RV) ventricles to measure developed pressure (DP = systolic minus diastolic).

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

51 30 and 90 minutes of reperfusion, LV maximum developed pressure (DP), dP/dt, CBF, and oxygen consumpt

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

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

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

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

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

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

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

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

60 +/- 3% to 67 +/- 5%) and slightly increased developed pressure in hypoxic hearts (67 +/- 5% to 72 +/

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 decreased the amplitude of left-ventricular developed pressure (LVDP) at baseline and accelerated th

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

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

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

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

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

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

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

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

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

88 a under the curve, AUC, for left ventricular developed pressure, LVDP: 1767.3 +/- 929.5 vs. 492.7 +/-

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

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

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

92 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

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

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

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

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

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

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

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

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

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

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

103 (84% versus 29% of initial left ventricular developed pressure, respectively).

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

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

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

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

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

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

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

111 LV developed pressure was better preserved in hearts from T

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

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

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

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

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

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

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

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

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

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

122 In contrast, the TA1 increased developed pressure without any effect on heart rate, lef

123 In contrast, the TA1 increased developed pressure without any effect on heart rate, lef

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