Th2 Regulation of Viral Myocarditis in Mice: Different Roles for TLR3 versus TRIF in Progression to Chronic Disease

Table 2

In vivo hemodynamics of recombinant (r)IL-33-treated TLR3-deficient mice during acute CVB3 myocarditis (day 10 pi) based on pressure-volume analysis.

Parameter	PBS	rIL-33	P value
Heart rate	560 ± 12.0	555 ± 7.6	0.75
Developed pressure	66 ± 5.6	82 ± 3.9	0.04
EDP	11 ± 1.6	6 ± 0.8	0.04
dP/dT Max	4891 ± 537	7177 ± 523	0.01
dP/dT Min	−3597 ± 446	−6168 ± 850	0.02
EF	54 ± 4.0	60 ± 2.8	0.24
ESV	8 ± 1.6	5 ± 1.7	0.27
EDV	17 ± 1.9	14 ± 3.2	0.34
CO	5.0 ± 0.43	4.5 ± 0.96	0.58
PMX	4 ± 0.7	6 ± 0.7	0.03
PRSW	35 ± 6.0	62 ± 11.2	0.04
Ees	5 ± 0.4	14 ± 1.0	0.00001
E Max	13 ± 2.7	32 ± 3.9	0.002
Ea/Ees	1.7 ± 0.18	0.89 ± 0.19	0.01

CO, cardiac output (μL/min); dP/dT max, peak rate of pressure rise (mmHg/s); dP/dT min, peak rate of pressure decline (mmHg/s); EDV, end diastolic volume (μL); Ees, LV end systolic elastance; EF, ejection fraction (%); developed pressure, (ESP-EDP) (mmHg); ESV, end systolic volume (μL); PRSW, preload recruitable stroke work; PMX, maximum ventricular power (mW); Ea/Ees, arterial elastance normalized to Ees; E Max, slope of line from end systole to end diastole. P values compare PBS-treated TLR3−/− to rIL-33-treated TLR3−/− by Student’s t-test at day 10 pi. Data are shown as mean ± SEM for 11 to 12 mice/group. All mice were infected with CVB3 10 days prior to assessment.