Cardiovascular and lung inflammatory effects induced by systemically administered diesel exhaust particles in rats.

@article{Nemmar2007CardiovascularAL,
  title={Cardiovascular and lung inflammatory effects induced by systemically administered diesel exhaust particles in rats.},
  author={Abderrahim Nemmar and Sultan Al-Maskari and Badreldin H. Ali and Issa S. Al-Amri},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2007},
  volume={292 3},
  pages={
          L664-70
        }
}
Pollution by particulates has consistently been associated with increased cardiorespiratory morbidity and mortality. It has been suggested that ultrafine particles, of which diesel exhaust particles (DEP) are significant contributors, are able to translocate from the airways into the bloodstream in vivo. In the present study, we assessed the effect of systemic administration of DEP on cardiovascular and respiratory parameters. DEP were administered into the tail vein of rats, and heart rate… 
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Repeated exposure to DEP induced lung and systemic inflammation characterized by TNFα release, increased SBP, and accelerated coagulation, and curcumin is a potent anti-inflammatory agent that prevents the release of TNF α and protects against the pulmonary and cardiovascular effects of DEP.
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It is concluded that the presence of DEP in the lung aggravated the renal, pulmonary, and systemic effects of CP-induced ARF, and Histopathological changes in lungs ofDEP-treated rats were aggravated by the combination of CP + DEP.
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TLDR
Experimental evidence is provided that exposure to particulate air pollution can exacerbate the vascular damage seen in patients with CKD, and Phenylephrine‐induced decreases in RBF and increases in systolic and diastolic blood pressure were severely potentiated in rats exposed to DP, and these actions were significantly augmented in AD‐treated rats.
Acute cardiovascular and inflammatory toxicity induced by inhalation of diesel and biodiesel exhaust particles.
TLDR
Biodiesel was more toxic than diesel because it promoted cardiovascular alterations as well as pulmonary and systemic inflammation.
The Salutary Effects of Catalpol on Diesel Exhaust Particles-Induced Thrombogenic Changes and Cardiac Oxidative Stress, Inflammation and Apoptosis
TLDR
Catalpol significantly ameliorated DEPs–induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.
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