OBJECTIVE: To determine biventricular cardiac function in pneumovirus-induced acute lung injury in spontaneously breathing mice. DESIGN: Experimental animal study. SETTING: Animal laboratory. SUBJECTS: C57Bl/6 mice. INTERVENTION: Mice were inoculated with the rodent pneumovirus, pneumonia virus of mice. MEASUREMENTS AND MAIN RESULTS: Pneumonia virus of mice-infected mice were studied for right and left ventricular function variables by high-field strength (7 Tesla) cardiac MRI at specific time points during the course of disease compared with baseline. One day before and at peak disease severity, pneumonia virus of mice-infected mice showed significant right and left ventricular systolic and diastolic volume changes, with a progressive decrease in stroke volume and ejection fraction. No evidence for viral myocarditis or viral presence in heart tissue was found. CONCLUSIONS: These findings show adverse pulmonary-cardiac interaction in pneumovirus-induced acute lung injury, unrelated to direct virus-mediated effects on the heart.
OBJECTIVE: To determine biventricular cardiac function in pneumovirus-induced acute lung injury in spontaneously breathing mice. DESIGN: Experimental animal study. SETTING: Animal laboratory. SUBJECTS: C57Bl/6 mice. INTERVENTION: Mice were inoculated with the rodent pneumovirus, pneumonia virus of mice. MEASUREMENTS AND MAIN RESULTS:Pneumonia virus of mice-infected mice were studied for right and left ventricular function variables by high-field strength (7 Tesla) cardiac MRI at specific time points during the course of disease compared with baseline. One day before and at peak disease severity, pneumonia virus of mice-infected mice showed significant right and left ventricular systolic and diastolic volume changes, with a progressive decrease in stroke volume and ejection fraction. No evidence for viral myocarditis or viral presence in heart tissue was found. CONCLUSIONS: These findings show adverse pulmonary-cardiac interaction in pneumovirus-induced acute lung injury, unrelated to direct virus-mediated effects on the heart.