Table 2. Haemodynamic parameters in N106-infused Serca2a knockout mice.
| Baseline (n=3) | Vehicle (n=3) | Baseline (n=8) | N106 (n=8) | |
|---|---|---|---|---|
| ESPVR slope (mm Hg μl−1) | 3.6±0.8 | 3.5±0.5 | 3.8±0.6 | 3.9±0.7 |
| +dP/dtmax (mm Hg s−1) | 2360.7±597.0 | 2023.6±674.9 | 3064.2±489.5 | 2917.8±412.9 |
| Pmax (mm Hg) | 62.9±6.3 | 67.4±11.8 | 74.0±4.5 | 75.0±4.4 |
| τ (ms) | 10.1±2.0 | 10.2±1.1 | 10.7±1.1 | 11.2±1.0 |
| HR (bpm) | 315.2±34.6 | 291.5±36.3 | 348.8±44.1 | 311.2±16.1 |
+dP/dtmax LV maximal contraction rate (inotropic response); ESPVR, end systolic pressure–volume relationship; HR, heart rate; N106, N-(4-methoxybenzo[d]thiazol-2-yl)-5-(4-methoxyphenyl)-1,3,4-oxadiazol-2-amine; Pmax, maximal pressure; TAC, transverse aortic constriction; τ, time constant of isovolumetric relaxation
Eight-week-old male cardiac-specific Serca2a-deficient mice received tamoxifen intraperitoneally (1 mg per day for 4 days). Four weeks after, ESPVR slope, maximal pressure, +dP/dtmax, τ and HR were recorded both at baseline and in response to 1 mg kg−1 of N106 administered via cannulation of the right internal jugular vein. Either vehicle or N106 had no effects on haemodynamic parameters in these mice. Data are represented as mean±s.e.m. Statistics were performed using a Student's t-test.