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. 2010 Jul;160(6):1408–1416. doi: 10.1111/j.1476-5381.2010.00793.x

Table 1.

Haemodynamics, β-adrenoceptor density and noradrenaline concentration, morphology and MAP kinase activation during the progression of HF

Sham HF1 HF2 HF3
Heart rate (bpm) 224 ± 5 263 ± 10A 277 ± 10A 258 ± 15
LVEDD (mm) 17.0 ± 0.3 18.7 ± 0.4A 19.3 ± 0.3A 19.6 ± 0.5AB
Fractional shortening (%) 30.0 ± 1.7 19.1 ± 0.7A 15.9 ± 0.7A 10.3 ± 1.3AB
Noradrenaline (ng·mL−1) 1.33 ± 0.17 2.87 ± 0.69A 4.03 ± 0.81A 3.83 ± 0.64A
ß-Adrenoceptor density (fmol·mg−1) 67 ± 5 45 ± 2A 47 ± 2A 41 ± 3A
Cardiomyocyte cross-sectional area (µm2) 242 ± 11 266 ± 4 299 ± 8AB 334 ± 7ABC
Number of TUNEL-positive cardiomyocytes [/(1000*mm2)] 4 ± 2 23 ± 5A 16 ± 4 50 ± 8ABC
Phospho p38-MAPK/total p38-MAPK (relative to sham) 1.00 ± 0.24 0.54 ± 0.09 0.65 ± 0.24 2.34 ± 0.54ABC
Phospho HSP27/total HSP27 (relative to sham) 1.00 ± 0.42 1.75 ± 0.24 1.01 ± 0.14 2.58 ± 0.60AC

Mean ± SEM.

A

p < 0.05 versus Sham.

B

p < 0.05 versus HF1.

C

p < 0.05 versus HF2.

HF1, heart failure rabbits, 1 week (n = 7); HF2, heart failure rabbits, 2 weeks (n = 7); HF3, heart failure rabbits, 3 weeks (n = 8); LVEDD, left ventricular end-diastolic diameter; Sham, sham-operated rabbits (n = 7); TUNEL, TdT-mediated dUTP nick end labelling.