Table 1.

TLR3 deficiency attenuated cardiac dysfunction in CLP-induced sepsis

Group	Heart rate	%EF	%FS	LVESD(mm)	LVEDD(mm)	SV(mmHg*μl)	CO(μl)
WT pre- CLP	440.9 ± 21.72	61.2 ± 5.49	32.4 ± 3.99	2.2 ± 0.34	5.5 ± 0.33	33816.9 ± 3279.01	15170.2 ± 1609.34
WT CLP	368.1 ± 40.52*	45.5 ± 7.32*	22.8 ± 8.15*	0.6 ± 0.13*	1.3 ± 0.51*	6696.6 ± 3787.75*	2483.9 ± 1241.00*
TLR3−/− pre-CLP	454.2 ± 19.34	61.8 ± 6.93	33.0 ± 5.25	2.1 ± 0.39	5.6 ± 0.61	34270.8 ± 5730.02	17249.0 ± 3648.22
TLR3−/− CLP	392.8 ± 6.55 #	62.6 ± 6.08#	33.2 ± 4.58#	1.5 ± 0.58#	4.4 ± 0.65#	28924.5 ± 6411.69#	12682.1 ± 3525.39#

TLR3 deficiency attenuated cardiac dysfunction in CLP-induced sepsis. TLR3^−/− mice (n=12) and WT mice (n=12) were subjected to CLP. Cardiac function was examined by echocardiography before and 6 hrs after CLP. EF: Ejection fraction; FS: Fractional Shortening; LVESD: left ventricle end systolic diameter; LVEDD: left ventricle end diastolic diameter; SV: Stroke volume; CO: cardiac output.

^*p<0.01, compared with the WT pre-CLP

^#p<0.01, compared with the WT CLP