Table 4.

Percent change of functional parameters of cTnI-ND and cTnT-ND hearts relative to wild-type control

	No Iso		30 nM Iso
	cTnI-ND	cTnT-ND	cTnI-ND	cTnT-ND
Resting cell length	−12.0 ± 4.5*	+5.8 ± 2.7#	N/A	N/A
Resting cell width	−4.2 ± 2.0	−2.4 ± 0.1	N/A	N/A
Resting sarcomere length	−1.0 ± 0.4	−1.4 ± 0.4	N/A	N/A
Amplitude of cell shortening	+100.1 ± 18.4**	−24.1 ± 12.2##	+14.6 ± 6.0	+26.8 ± 35.0
Shortening velocity	+93.3 ± 26.9*	−18.9 ± 13.9##	+17.5 ± 10.0	−2.8 ± 15.0##
Relengthening velocity	+136.1 ± 36.5*	−23.7 ± 14.1##	+20.8 ± 8.7	−15.3 ± 12.7##
Baseline cytosolic Ca2+	+1.4 ± 4.5	+3.3 ± 3.5	+2.4 ± 4.2	+6.7 ± 3.6
Peak cytosolic Ca2+	+7.7 ± 9.1	+4.4 ± 4.8	+6.0 ± 9.1	+4.7 ± 4.5
TR25	−20.3 ± 4.3*	−11.0 ± 7.6	−17.9 ± 4.4*	+3.8 ± 8.4#
TR75	−15.8 ± 3.2*	−21.0 ± 5.7*	−17.0 ± 3.5*	−22.6 ± 4.4**

From the primary data shown in Tables 1–3, the effects of cTnI-ND and cTnT-ND on cardiomyocyte function were calculated as %change relative to wild-type controls (+, increase; −, decrease). Data are means ± SE. cTnI-ND but not cTnT-ND cardiomyocytes had shorter slack length with no change in sarcomere length and increased baseline contractile amplitude and shortening and relengthening velocities. cTnI-ND and cTnT-ND cardiomyocytes both had significantly shorter times to TR₇₅ at baseline or in the presence of 30 nM Iso. cTnI-ND but not cTnT-ND cardiomyocytes also had shorter times to TR₂₅ at baseline or in the presence of 30 nM Iso.

^*P < 0.05;

^**P < 0.01 compared with wild-type control.

^#P < 0.05;

^##P < 0.01, cTnI-ND compared with cTnT-ND.