Table 2.

cTnI-ND, but not cTnT-ND, increased contractility of isolated cardiomyocytes in the absence of external load

	No Iso		30 nM Iso
	Wild Type	cTnI-ND	Wild Type	cTnI-ND
Shortening amplitude, %	3.45 ± 0.55	6.90 ± 0.64**	13.52 ± 1.24‡	15.49 ± 0.81‡
Shortening velocity, μm/s	121.56 ± 21.47	235.00 ± 32.68*	433.21 ± 56.10‡	509.14 ± 43.36‡
Relengthening velocity, μm/s	87.24 ± 15.32	205.99 ± 31.83*	402.69 ± 58.23‡	486.56 ± 35.04‡

	No Iso		30 nM Iso
	Wild Type	cTnT-ND	Wild Type	cTnT-ND
Shortening amplitude, %	9.06 ± 1.11	6.88 ± 1.11	18.49 ± 2.28‡	23.45 ± 6.46‡
Shortening velocity, μm/s	329.13 ± 38.29	266.92 ± 45.70	582.85 ± 93.79‡	566.29 ± 85.32‡
Relengthening velocity, μm/s	294.36 ± 36.02	224.67 ± 41.36	587.57 ± 103.34‡	497.78 ± 74.66‡

cTnI-ND cardiomyocytes paced at 2 Hz had significantly increased contractile amplitude and maximal shortening and relengthening velocities in the absence of isoproterenol (Iso) compared with wild-type controls (

^*P < 0.05;

^**P < 0.01), whereas cTnT-ND cardiomyocytes paced at 2 Hz showed no significant change in the baseline contractile amplitude and maximal shortening and relengthening velocities compared with wild-type controls. Iso treatment increased the contractility of all 3 groups (

^‡P < 0.01) and diminished the difference between cTnI-ND and wild-type cells. Data are means ± SE (for cTnI-ND data, n = 4 hearts in each group; for cTnT-ND data, n = 6 hearts in wild-type group and n = 7 hearts in cTnT-ND group). At least 3–5 cells were studied for each heart and pooled for statistical analysis.