Acute cardiac dysfunction after short-term diesel exhaust particles exposure

Area of Science:

• Environmental Health
• Cardiovascular Physiology
• Toxicology

Background:

• Epidemiological studies link particulate matter exposure to acute heart failure.
• Mechanisms underlying this association require further investigation.

Purpose of the Study:

• To investigate the acute cardiac hemodynamic effects of diesel exhaust particles (DEPs).
• To explore the mechanisms involved in DEP-induced cardiac dysfunction.

Main Methods:

• Male Sprague-Dawley rats were exposed intra-tracheally to low (250 microg) or high (500 microg) doses of DEPs or saline placebo.
• Cardiac systolic and diastolic functions were assessed using dP/dt(40) and maximal negative dP/dt.
• Heart rate variability (HRV), cardiac IL-1beta, troponin I, and plasma IL-1beta and IL-6 were measured.

Main Results:

• Both low and high DEP doses significantly worsened cardiac systolic and diastolic function compared to controls.
• DEP exposure reduced SDNN and increased low frequency HRV.
• Elevated cardiac IL-1beta, troponin I, and plasma IL-1beta and IL-6 were observed in DEP-exposed groups.

Conclusions:

• Acute exposure to diesel exhaust particles induces cardiac systolic and diastolic dysfunction in rats.
• These effects are associated with altered heart rate variability, increased cardiac inflammation, and myocardial damage.