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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        Inhibiting NCX with SEA0400 abolished LVDP depression caused by increasing [Na(+)](o) at basel
5  before ischemia did not significantly alter LVDP recovery.
6        At 50% perfusate oxygenation, APD and LVDP were significantly higher in LWHs perfused with TOL
7 ffect of PC and HOE was readily apparent and LVDP recovery with PC+HOE (66+/-2%) was almost double th
8 ntrol hearts was 26 +/- 5% of their baseline LVDP, whereas hearts pretreated with EPO exhibited signi
9                          Concordance between LVDP and lactate was assessed during 4 h using cutoffs f
10                                 In contrast, LVDP recovery and infarct size were unchanged in Tie2-CY
11  WT hearts with 250 nM 9,10-DiHOME decreased LVDP recovery compared to vehicle (16 vs. 31%, respectiv
12 ure to the multipollutant mixtures decreased LVDP, baseline rate of left ventricular contraction (dP/
13               Ischemia-reperfusion decreased LVDP in all hearts with return of intrinsic activity, an
14 days before ischemia significantly decreased LVDP recovery; however, perfusion of WT hearts with indo
15 n of acute multipollutant mixtures decreases LVDP and cardiac contractility in isolated non-ischemic
16 rol 3.9+/-0.6 nmol ATP/min/mg) and depressed LVDP (49+/-3% of baseline; P<.05).
17 stischemic succinate administration enhanced LVDP recovery after IR (89+/-8% of baseline; P<.05).
18                                        Final LVDP was 95+/-5 mm Hg in I/R hearts perfused with PMNs a
19 te was assessed during 4 h using cutoffs for LVDP of 70 mm Hg and for lactate of 10 mmol/L.
20        Measurements of contractile function (LVDP) and metabolism (lactate levels) were deemed concor
21                        Recovery of function (LVDP) after global ischemia in hearts from COX-1(-/-) an
22 ed concordant in 7 hearts with either a high LVDP (mean 100 mm Hg) with low lactate (mean 6.7 mmol/L)
23 ts were deemed discordant: 4 hearts had high LVDP (mean 124 mm Hg), despite high lactate levels 17.3
24 sfunction, as evidence by a 93% reduction in LVDP at 45 minutes of reperfusion and a 91% reduction in
25 with low lactate (mean 6.7 mmol/L)) or a low LVDP (15 mm Hg) with high lactate (mean 17.3 mmol/).
26 gh lactate levels 17.3 mmol/L) and 1 had low LVDP (54 mm Hg) but low lactate (6.9 mmol/L).
27  M-LVDP, and E/E' >15 identified increased M-LVDP.
28        E/E' <8 accurately predicted normal M-LVDP, and E/E' >15 identified increased M-LVDP.
29 eters, and the mean LV diastolic pressure (M-LVDP) was used as a surrogate for mean left atrial press
30 meters of transmitral flow correlated with M-LVDP only when ejection fraction <50%.
31 us (E/E') showed a better correlation with M-LVDP than did other Doppler variables for all levels of
32 s an excellent predictor of an elevated mean LVDP.
33 ltant ratio (E/e') correlates well with mean LVDP.
34  pressure (LVDP), or the first derivative of LVDP (dP/dtmax) was observed at the end of the observati
35 treatment improved post-ischemic recovery of LVDP (58.5+/-4.8% vs. 22.0+/-6.3% in control) and reduce
36 ion of COX-1 and COX-2 decreases recovery of LVDP after ischemia; however, acute perfusion with indom
37  = 9), resulted in 80.2 +/- 6.7% recovery of LVDP and 77.0 +/- 8.6% recovery of PRP.
38 perfusion significantly improved recovery of LVDP and reduced infarct size.
39                     Postischemic recovery of LVDP in COX-1(-/-) and COX-2(-/-) was unchanged by perfu
40                The post-ischemic recovery of LVDP in the untreated control hearts was 26 +/- 5% of th
41                         Improved recovery of LVDP was matched by reduced creatine kinase leakage in a
42 tracture, increases postischemic recovery of LVDP, and reduces infarct size.
43           DOG addition improved postischemic LVDP (67+/-6%; P<0.001 compared with control), but in co
44 itioning significantly improved postischemic LVDP recovery in COX-1(-/-), COX-2(-/-), and WT mice.
45 arts and abolishes the improved postischemic LVDP recovery in CYP2J2 Tr hearts.
46  and ISO-induced improvement in postischemic LVDP and infarct size.
47  the ISO-induced improvement in postischemic LVDP and infarct size.
48 ion after ischemia, recovery of postischemic LVDP and size of infarct were examined.
49 re group had better recovery of postischemic LVDP and smaller infarct size.
50      GSNO increased recovery of postischemic LVDP in GA-treated normoxic and hypoxic hearts to baseli
51  found that PC had no effect on postischemic LVDP or infarct size in beta2-AR-/-.
52 ore ischemia results in reduced postischemic LVDP recovery in WT hearts and abolishes the improved po
53 ure (LVDP; percentage of initial preischemic LVDP), measured after 30 minutes of reflow, was improved
54 very of left ventricular developed pressure (LVDP) after 20 minutes of global ischemia and 40 minutes
55 tion in left ventricular developed pressure (LVDP) and a 57% reduction in the pressure-rate product (
56 ndex of left-ventricular developed pressure (LVDP) and contractility (dP/dt) before ischemia.
57 very of left ventricular developed pressure (LVDP) and decreased infarct size after I/R.
58 eserved left ventricular developed pressure (LVDP) and dP/dtmax, indexes of cardiac contractile funct
59 very of left ventricular developed pressure (LVDP) and infarct size were measured.
60 very of left ventricular developed pressure (LVDP) and reduced infarct size compared with control hea
61         Left ventricular developed pressure (LVDP) and the cytochrome a,a3 redox state (near infrared
62 tude of left-ventricular developed pressure (LVDP) at baseline and accelerated the onset of ischemic
63 very of left ventricular developed pressure (LVDP) compared with wild-type (WT) hearts after 20 minut
64 very of left ventricular developed pressure (LVDP) of ischemic hearts treated with CSIL at 1 min of i
65 very of left ventricular developed pressure (LVDP) was 15+/-2% in controls and was improved to 45+/-7
66 t while left-ventricular-developed pressure (LVDP) was measured continuously to assess contractile fu
67 mapped when measuring LV developed pressure (LVDP), coronary flow rate and oxygen consumption in LANG
68 fusion; left ventricular developed pressure (LVDP), end diastolic pressure (EDP), and ATP were measur
69 y flow, left ventricular developed pressure (LVDP), or the first derivative of LVDP (dP/dtmax) was ob
70 schemic left ventricular developed pressure (LVDP).
71 very of left ventricular developed pressure (LVDP; percentage of initial preischemic LVDP), measured
72 sure of left ventricular diastolic pressure (LVDP) early after acute myocardial infarction (MI).
73 UC, for left ventricular developed pressure, LVDP: 1767.3 +/- 929.5 vs. 492.7 +/- 308.1; myocardial c
74 2-CYP2C8 Tr hearts had significantly reduced LVDP recovery (from 21 to 14%) and increased infarct siz
75                                          The LVDP of hearts treated with CSIL at 5, 10, and 20 min wa