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. Author manuscript; available in PMC: 2016 Feb 26.
Published in final edited form as: Sci Transl Med. 2015 Mar 4;7(277):277ra31. doi: 10.1126/scitranslmed.aaa0154

Fig. 2. Paroxetine treatment after MI enhances in vivo LV hemodynamic function and restores βAR inotropic reserve.

Fig. 2

.<br>Hemodynamics were recorded from wild-type (WT) mice treated with vehicle, fluoxetine (fluox), or paroxetine (parox) at 6 weeks after MI (after 4 weeks of treatment) compared to sham. (A) Representative LV dP/dt hemodynamic recordings. Arrows mark administration of ISO. (B) Quantification of mean systemic pressure. (C to E) Quantification of (C) HR, (D) LV +dP/dt average maximum (*P = 0.0234 and 0.0130, **P = 0.0008, ***P ≤ 0.0001), and (E) LV −dP/dt average minimum at baseline and with increasing doses of ISO (0.1 to 10 ng) (*P = 0.0105 and 0.0134 for sham, and 0.0280 for MI; **P = 0.0058, 0.0040, and 0.0087, respectively). bpm, beats per minute. (F) Quantification of LVEDP at baseline (no ISO) 6 weeks after sham and MI (**P = 0.005). Statistics are relative to corresponding sham or MI vehicle by two-or one-way ANOVA as appropriate. n = 12 to 15 per group.