Related Experiment Video
Updated: Jun 19, 2026
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
Published on: March 21, 2021
Enhanced death signaling in ozone-exposed ischemic-reperfused hearts
Rama Surya Prakash Perepu1, Carlos Garcia, David Dostal
1Department of Biological & Health Sciences, Texas A&M University Kingsville, Kingsville, TX, USA.
Insights
Chronic ozone exposure increases heart damage from ischemia-reperfusion (I/R) injury. This air pollutant may worsen cardiovascular disease (CVD) by increasing oxidative stress and inflammation.
Area of Science:
- Environmental Health
- Cardiovascular Physiology
- Toxicology
Background:
- Cardiovascular diseases (CVD) remain a leading cause of death, with some cases lacking clear risk factors.
- Air pollution, specifically ozone, is increasingly implicated in cardiovascular pathology.
- Environmental pollutants may contribute to the pathophysiology of CVD.
Purpose of the Study:
- To investigate the hypothesis that chronic ozone exposure sensitizes the heart to ischemia-reperfusion (I/R) injury.
- To determine the effects of ozone exposure on cardiac function following I/R in an isolated heart model.
Main Methods:
- Sprague-Dawley rats were exposed to filtered air or 0.8 ppm ozone for 8 hours/day over 28 and 56 days.
- Isolated hearts underwent 30 minutes of global ischemia followed by 60 minutes of reperfusion.
- Cardiac function parameters (LVDP, dP/dt, LVEDP) and myocardial markers (TNF-alpha, lipid peroxidation, SOD, IL-10) were assessed.
Main Results:
- Ozone-exposed hearts showed significantly reduced cardiac function (LVDP, +dP/dt, -dP/dt) and increased LVEDP after I/R compared to controls.
- Enhanced I/R injury in ozone-exposed hearts correlated with increased myocardial TNF-alpha and lipid peroxidation.
- Decreased myocardial superoxide dismutase (SOD) and IL-10 activities were observed in ozone-exposed hearts.
Conclusions:
- Chronic ozone exposure exacerbates myocardial sensitivity to I/R injury.
- Ozone-induced cardiac dysfunction appears to be mediated by increased oxidative stress and inflammatory responses.
- Environmental pollutants like ozone represent a significant, underappreciated risk factor for cardiovascular events.
Abstract:
Although numerous advancements made in the field of human health have resulted in reduced deaths due to cardiovascular diseases (CVD), many patients with cardiac disease show no established risk. Therefore, other unknown factors may be responsible for the pathophysiology of CVD. Out of 350,000 sudden cardiac deaths each year in the United States, 60,000 deaths have been related to air pollution, suggesting a detrimental role of environmental pollutants in the development of CVD. The present study tested our hypothesis that chronic ozone exposure enhances the sensitivity to ischemia-reperfusion (I/R) injury in isolated perfused hearts. Sprague-Dawley rats were continuously exposed for 8 h/day for 28 and 56 days to filtered air or 0.8 ppm ozone. Isolated hearts were subjected to 30 min of global ischemia followed by 60 min of reperfusion. Cardiac function after I/R measured as left ventricular developed pressure (LVDP), +dP/dt, -dP/dt, and left ventricular end diastolic pressure (LVEDP) was significantly decreased and increased respectively in ozone-exposed I/R hearts compared to I/R hearts exposed to filtered air. The enhanced sensitivity to I/R injury upon ozone exposure was associated with increased myocardial TNF-alpha levels and lipid peroxidation and decreased myocardial activities of superoxidase dismutase (SOD) and IL-10. These data suggest that ozone-induced sensitivity to myocardial I/R injury may be due to promoting levels of oxidative stress as well as inflammatory mediators.
