ライフサイエンスコーパス: LVDP

1 LVDP recovery was 34+/-4% in controls and was improved t

2 LVDP recovery was expressed as percent of baseline readi

3 LVDP recovery was significantly reduced in ARTg mice com

4 before ischemia did not significantly alter LVDP recovery.

5 At 50% perfusate oxygenation, APD and LVDP were significantly higher in LWHs perfused with TOL

6 ffect of PC and HOE was readily apparent and LVDP recovery with PC+HOE (66+/-2%) was almost double th

7 ntrol hearts was 26 +/- 5% of their baseline LVDP, whereas hearts pretreated with EPO exhibited signi

8 In contrast, LVDP recovery and infarct size were unchanged in Tie2-CY

9 WT hearts with 250 nM 9,10-DiHOME decreased LVDP recovery compared to vehicle (16 vs. 31%, respectiv

10 ure to the multipollutant mixtures decreased LVDP, baseline rate of left ventricular contraction (dP/

11 days before ischemia significantly decreased LVDP recovery; however, perfusion of WT hearts with indo

12 n of acute multipollutant mixtures decreases LVDP and cardiac contractility in isolated non-ischemic

13 rol 3.9+/-0.6 nmol ATP/min/mg) and depressed LVDP (49+/-3% of baseline; P<.05).

14 stischemic succinate administration enhanced LVDP recovery after IR (89+/-8% of baseline; P<.05).

15 Final LVDP was 95+/-5 mm Hg in I/R hearts perfused with PMNs a

16 Recovery of function (LVDP) after global ischemia in hearts from COX-1(-/-) an

17 sfunction, as evidence by a 93% reduction in LVDP at 45 minutes of reperfusion and a 91% reduction in

18 M-LVDP, and E/E' >15 identified increased M-LVDP.

19 E/E' <8 accurately predicted normal M-LVDP, and E/E' >15 identified increased M-LVDP.

20 eters, and the mean LV diastolic pressure (M-LVDP) was used as a surrogate for mean left atrial press

21 meters of transmitral flow correlated with M-LVDP only when ejection fraction <50%.

22 us (E/E') showed a better correlation with M-LVDP than did other Doppler variables for all levels of

23 s an excellent predictor of an elevated mean LVDP.

24 ltant ratio (E/e') correlates well with mean LVDP.

25 pressure (LVDP), or the first derivative of LVDP (dP/dtmax) was observed at the end of the observati

26 treatment improved post-ischemic recovery of LVDP (58.5+/-4.8% vs. 22.0+/-6.3% in control) and reduce

27 ion of COX-1 and COX-2 decreases recovery of LVDP after ischemia; however, acute perfusion with indom

28 = 9), resulted in 80.2 +/- 6.7% recovery of LVDP and 77.0 +/- 8.6% recovery of PRP.

29 perfusion significantly improved recovery of LVDP and reduced infarct size.

30 Postischemic recovery of LVDP in COX-1(-/-) and COX-2(-/-) was unchanged by perfu

31 The post-ischemic recovery of LVDP in the untreated control hearts was 26 +/- 5% of th

32 Improved recovery of LVDP was matched by reduced creatine kinase leakage in a

33 tracture, increases postischemic recovery of LVDP, and reduces infarct size.

34 DOG addition improved postischemic LVDP (67+/-6%; P<0.001 compared with control), but in co

35 itioning significantly improved postischemic LVDP recovery in COX-1(-/-), COX-2(-/-), and WT mice.

36 arts and abolishes the improved postischemic LVDP recovery in CYP2J2 Tr hearts.

37 and ISO-induced improvement in postischemic LVDP and infarct size.

38 the ISO-induced improvement in postischemic LVDP and infarct size.

39 ion after ischemia, recovery of postischemic LVDP and size of infarct were examined.

40 re group had better recovery of postischemic LVDP and smaller infarct size.

41 GSNO increased recovery of postischemic LVDP in GA-treated normoxic and hypoxic hearts to baseli

42 found that PC had no effect on postischemic LVDP or infarct size in beta2-AR-/-.

43 ore ischemia results in reduced postischemic LVDP recovery in WT hearts and abolishes the improved po

44 ure (LVDP; percentage of initial preischemic LVDP), measured after 30 minutes of reflow, was improved

45 very of left ventricular developed pressure (LVDP) after 20 minutes of global ischemia and 40 minutes

46 tion in left ventricular developed pressure (LVDP) and a 57% reduction in the pressure-rate product (

47 ndex of left-ventricular developed pressure (LVDP) and contractility (dP/dt) before ischemia.

48 very of left ventricular developed pressure (LVDP) and decreased infarct size after I/R.

49 eserved left ventricular developed pressure (LVDP) and dP/dtmax, indexes of cardiac contractile funct

50 very of left ventricular developed pressure (LVDP) and infarct size were measured.

51 very of left ventricular developed pressure (LVDP) and reduced infarct size compared with control hea

52 Left ventricular developed pressure (LVDP) and the cytochrome a,a3 redox state (near infrared

53 very of left ventricular developed pressure (LVDP) compared with wild-type (WT) hearts after 20 minut

54 very of left ventricular developed pressure (LVDP) of ischemic hearts treated with CSIL at 1 min of i

55 very of left ventricular developed pressure (LVDP) was 15+/-2% in controls and was improved to 45+/-7

56 t while left-ventricular-developed pressure (LVDP) was measured continuously to assess contractile fu

57 mapped when measuring LV developed pressure (LVDP), coronary flow rate and oxygen consumption in LANG

58 fusion; left ventricular developed pressure (LVDP), end diastolic pressure (EDP), and ATP were measur

59 y flow, left ventricular developed pressure (LVDP), or the first derivative of LVDP (dP/dtmax) was ob

60 schemic left ventricular developed pressure (LVDP).

61 very of left ventricular developed pressure (LVDP; percentage of initial preischemic LVDP), measured

62 sure of left ventricular diastolic pressure (LVDP) early after acute myocardial infarction (MI).

63 2-CYP2C8 Tr hearts had significantly reduced LVDP recovery (from 21 to 14%) and increased infarct siz

64 The LVDP of hearts treated with CSIL at 5, 10, and 20 min wa