ライフサイエンスコーパス: left ventricular developed pressure

1 and reversibly decreased heart rate and peak left ventricular developed pressure.

2 red high-energy phosphates using 31P-NMR and left-ventricular developed pressure.

3 Septic rats had a 28% decrease in peak left ventricular developed pressure, a 30% decrease in +

4 Peak left ventricular developed pressure and +/-dp/dt were si

5 or isoproterenol resulted in an increase in left ventricular developed pressure and an increase in [

6 IPC significantly increased left ventricular developed pressure and decreased infarc

7 d +dP/dt and ejection fraction and increased left ventricular developed pressure and end diastolic pr

8 Recovery of left ventricular developed pressure and infarct size wer

9 Left ventricular developed pressure and ischemic contrac

10 diac depression (i.e., a marked reduction in left ventricular developed pressure and maximal rate of

11 Left ventricular developed pressure and rate pressure pr

12 nificantly improved postischemic recovery of left ventricular developed pressure and reduced infarct

13 Preischemic left ventricular developed pressures and +dP/dtmax, as w

14 greater rates of contraction and relaxation, left ventricular developed pressure, and cardiac output

15 ycle of preconditioning recovered 70+/-7% of left ventricular developed pressure compared with 43+/-8

16 s were measured, and the first derivative of left ventricular developed pressure (dP/dt), slope of th

17 Peak left ventricular developed pressure, +/-dp/dt, oxygen co

18 In the absence of eniporide, left ventricular developed pressure, end-diastolic press

19 s had much less necrosis, better recovery of left-ventricular developed pressure, improved phosphocre

20 cromol/L) increased postischemic recovery of left ventricular developed pressure in isolated normoxic

21 akalim (1 mumol/L) increased the recovery of left ventricular developed pressure in normoxic hearts t

22 Left-ventricular-developed pressure in isolated isovolum

23 After 24 hours of reperfusion, maximum left ventricular developed pressure increased from 87.0+

24 unctional characteristics and on recovery of left ventricular developed pressure (LVDP) after 20 minu

25 MNs alone (n = 10) led to a 61% reduction in left ventricular developed pressure (LVDP) and a 57% red

26 YP2J2 Tr hearts showed increased recovery of left ventricular developed pressure (LVDP) and decreased

27 ams/rat improved coronary flow and preserved left ventricular developed pressure (LVDP) and dP/dtmax,

28 Recovery of left ventricular developed pressure (LVDP) and infarct s

29 nificantly improved postischemic recovery of left ventricular developed pressure (LVDP) and reduced i

30 Left ventricular developed pressure (LVDP) and the cytoc

31 CYP2J2 Tr hearts have improved recovery of left ventricular developed pressure (LVDP) compared with

32 Recovery of left ventricular developed pressure (LVDP) of ischemic h

33 onged ischemia, the postischemic recovery of left ventricular developed pressure (LVDP) was 15+/-2% i

34 mic injury) was measured during reperfusion; left ventricular developed pressure (LVDP), end diastoli

35 No significant reduction in coronary flow, left ventricular developed pressure (LVDP), or the first

36 c hypoxia increased recovery of postischemic left ventricular developed pressure (LVDP).

37 Recovery of left ventricular developed pressure (LVDP; percentage of

38 ction was assessed by measuring the index of left-ventricular developed pressure (LVDP) and contracti

39 nce of brief recombinant EPO treatment while left-ventricular-developed pressure (LVDP) was measured

40 during ischemia, as were phosphocreatine and left ventricular-developed pressure on reperfusion.

41 usion, they developed an impaired heart-rate-left-ventricular-developed pressure product in response

42 ction was greater in HSP than in CON hearts: left ventricular developed pressure recovery was 72.4+/-

43 chemic+/-SEM) was greater in HSP versus CON: Left ventricular developed pressure recovery was 76.7+/-

44 untreated hearts (84% versus 29% of initial left ventricular developed pressure, respectively).

45 s was associated with a sharper slope of the left ventricular developed pressure-volume curve and a r

46 vivable functional and energetic compromise: left ventricular developed pressure was depressed by 20%

47 (2) Left ventricular developed pressure was depressed in tra

48 saline-perfused control hearts, recovery of left ventricular developed pressure was increased in rhE

49 nce of 4 mmol/L NAC recovered 53% of initial left ventricular developed pressure, whereas hearts trea