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. 2016 Sep 12;11(9):e0162632. doi: 10.1371/journal.pone.0162632

Table 1. Effect of L2 on cardiac contractility in normoxic hearts.

Normoxic study n HR LVDP LVEDP dPmax/dt dPmin/dt
(bpm) (mmHg) (mmHg) (mmHg/s) (mmHg/s)
Control study 8
Stabilisation 290 ± 9 116 ± 3.6 15.44 ± 2 3876 ± 42 -2356 ± 87
Vehicle 276 ± 12 109 ± 2.3 14.23 ± 3 3571 ± 76 -2120 ± 32
BNP study 14
Stabilisation 288 ± 18 109 ± 5.6 16.28 ± 1 4053 ± 63 -2293 ± 106
Vehicle 271 ± 10 110 ± 3.7 15.84 ± 1 3673 ± 211 -2095 ± 97
BNP (10 nM) 277 ± 11 102 ± 3.3 15.03 ± 1 3425 ± 187 -2332 ± 105
L2 study 10
Stabilisation 272 ± 13 112 ± 4 15.26 ± 2 4132 ± 21 -242 1 ± 87
Vehicle 266 ± 11 116 ± 2 15.47 ± 2 4087 ± 98 -2582 ± 78
L2 (100 nM) 287 ± 17 106 ± 5 14.74 ± 2 3958 ± 110 -2427 ± 107
L2 (200 nM) 291 ± 21 104 ± 7 15.55 ± 1 3993 ± 121 -2421 ± 92

Data are mean ± S.E.M. Heart rate (HR), left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximum (dPmax/dt) and minimum (dPmin/dt) rate of rise of ventricular pressure were recorded before and after L2 or BNP perfusion, at stabilisation period and 50 min after drug perfusion. bpm, beat per minute.