INHALATION OF ENVIRONMENTALLY PESISTENT FREE RADICALS ALTER LEFT VENTRICULAR FUNCTION IN VIVO.
Document Type
Presentation
Start Date
22-10-2010 3:00 PM
End Date
22-10-2010 4:30 PM
Description
Epidemiological data consistently link exposure to increased fine airborne particulate matter with increased cardiovascular morbidity and mortality. We have shown that during combustion, halogenated hydrocarbons chemisorb to the surface of transition metal-oxide-containing particles and form an environmentally persistent free radical (EPFR) capable of continuous redox cycling. The purpose of this study was to determine whether inhalation of EPFRs adversely affects baseline cardiac function in na·ive rats. To test the physiological effects of EPFRs we developed a surrogate particle system, dichlorobenzene-230 (DCB230). Rats were exposed to either vehicle or DCB230 via nose only inhalation for 20 min/day for 7 days. 24 hrs after the final exposure, the rats were anesthetized, intubated and left ventricular function was measured using a Millar pressure-volume catheter. Exposure to DCB230 (~600μg/m3) increased systolic function as evidenced by augmented dP/dt, stroke work (SW), ejection fraction and cardiac output (CO). This dose also increased diastolic function as evidenced by decreases in the end diastolic pressure and an increase in the relaxation constant Tau W. After exposure to DCB230 (~1000μg/m3) diastolic function was further enhanced. However, end diastolic volume, stroke volume and CO were significantly decreased, while measures of contractility (dP/dt, end systolic pressure and SW) were at control level. These data indicate that the higher cone. of DCB230 reduced ventricular filling which may reflect an increase in pulmonary vascular resistance due to lung inflammation. The mechanism underlying the increased function produced by the lower DCB230 cone. is less clear but may reflect sympathetic stimulation due to a milder pulmonary inflammation. These data show that inhalational exposure to EPFR can significantly affect cardiac function in vivo and that pulmonary inflammation may play a contributory role. Support P20ES013648, P20RR 18766.
Recommended Citation
Mahne, Sarah; Dellinger, B.; and Varner, K. J., "INHALATION OF ENVIRONMENTALLY PESISTENT FREE RADICALS ALTER LEFT VENTRICULAR FUNCTION IN VIVO." (2010). Dr. Joseph M. Moerschbaecher, III Graduate Research Day. 12.
https://digitalscholar.lsuhsc.edu/grad_rs/2010/poster2/12
INHALATION OF ENVIRONMENTALLY PESISTENT FREE RADICALS ALTER LEFT VENTRICULAR FUNCTION IN VIVO.
Epidemiological data consistently link exposure to increased fine airborne particulate matter with increased cardiovascular morbidity and mortality. We have shown that during combustion, halogenated hydrocarbons chemisorb to the surface of transition metal-oxide-containing particles and form an environmentally persistent free radical (EPFR) capable of continuous redox cycling. The purpose of this study was to determine whether inhalation of EPFRs adversely affects baseline cardiac function in na·ive rats. To test the physiological effects of EPFRs we developed a surrogate particle system, dichlorobenzene-230 (DCB230). Rats were exposed to either vehicle or DCB230 via nose only inhalation for 20 min/day for 7 days. 24 hrs after the final exposure, the rats were anesthetized, intubated and left ventricular function was measured using a Millar pressure-volume catheter. Exposure to DCB230 (~600μg/m3) increased systolic function as evidenced by augmented dP/dt, stroke work (SW), ejection fraction and cardiac output (CO). This dose also increased diastolic function as evidenced by decreases in the end diastolic pressure and an increase in the relaxation constant Tau W. After exposure to DCB230 (~1000μg/m3) diastolic function was further enhanced. However, end diastolic volume, stroke volume and CO were significantly decreased, while measures of contractility (dP/dt, end systolic pressure and SW) were at control level. These data indicate that the higher cone. of DCB230 reduced ventricular filling which may reflect an increase in pulmonary vascular resistance due to lung inflammation. The mechanism underlying the increased function produced by the lower DCB230 cone. is less clear but may reflect sympathetic stimulation due to a milder pulmonary inflammation. These data show that inhalational exposure to EPFR can significantly affect cardiac function in vivo and that pulmonary inflammation may play a contributory role. Support P20ES013648, P20RR 18766.
Comments
See abstract book page 56