title: Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats.
abstract: BACKGROUND
  Air pollution exposure affects autonomic function, heart rate, blood pressure and left ventricular function. While the mechanism for these effects is uncertain, several studies have reported that air pollution exposure modifies activity of the carotid body, the major organ that senses changes in arterial oxygen and carbon dioxide levels, and elicits downstream changes in autonomic control and cardiac function.
  
  
  OBJECTIVE
  We hypothesized that exposure to acrolein, an unsaturated aldehyde and mucosal irritant found in cigarette smoke and diesel exhaust, would activate the carotid body chemoreceptor response and lead to secondary cardiovascular responses in rats.
  
  
  METHODS
  Spontaneously hypertensive (SH) rats were exposed once for 3 h to 3 ppm acrolein gas or filtered air in whole body plethysmograph chambers. To determine if the carotid body mediated acrolein-induced cardiovascular responses, rats were pretreated with an inhibitor of cystathionine γ-lyase (CSE), an enzyme essential for carotid body signal transduction.
  
  
  RESULTS
  Acrolein exposure induced several cardiovascular effects. Systolic, diastolic and mean arterial blood pressure increased during exposure, while cardiac contractility decreased 1 day after exposure. The cardiovascular effects were associated with decreases in pO2, breathing frequency and expiratory time, and increases in sympathetic tone during exposure followed by parasympathetic dominance after exposure. The CSE inhibitor prevented the cardiovascular effects of acrolein exposure.
  
  
  CONCLUSIONS
  Pretreatment with the CSE inhibitor prevented the cardiovascular effects of acrolein, suggesting that the cardiovascular responses with acrolein may be mediated by carotid body-triggered changes in autonomic tone. (This abstract does not reflect EPA policy.).
authors.affiliation: Curriculum in Toxicology, University of North Carolina , Chapel Hill, NC , USA .
authors.forename: Christina M
authors.initials: CM
authors.lastname: Perez
authors.forename: Mehdi S
authors.initials: MS
authors.lastname: Hazari
authors.forename: Allen D
authors.initials: AD
authors.lastname: Ledbetter
authors.forename: Najwa
authors.initials: N
authors.lastname: Haykal-Coates
authors.forename: Alex P
authors.initials: AP
authors.lastname: Carll
authors.forename: Wayne E
authors.initials: WE
authors.lastname: Cascio
authors.forename: Darrell W
authors.initials: DW
authors.lastname: Winsett
authors.forename: Daniel L
authors.initials: DL
authors.lastname: Costa
authors.forename: Aimen K
authors.initials: AK
authors.lastname: Farraj
mesh_terms: D000171:Acrolein / Q000633:toxicity*; D000480:Alkynes / Q000494:pharmacology*; D000818:Animals; D001784:Blood Gas Analysis; D002344:Carotid Body / Q000502:physiology*; D003542:Cystathionine gamma-Lyase / Q000037:antagonists & inhibitors*; D005998:Glycine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D000480:Alkynes; C009055:propargylglycine; D000171:Acrolein; D003542:Cystathionine gamma-Lyase; D005998:Glycine
keywords: Acrolein; blood pressure; carotid body; pO2; spontaneously hypertensive rat