Carbon monoxide exposure in rat heart: evidence for two modes of toxicity.
Rat hearts were perfused for 30 min with buffer equilibrated with CO. Mean data for hearts exposed to 0.01% CO show a 15% decrease in heart rate (HR) during exposure followed by recovery, with a further 17% decrease post exposure. Examination of time courses from individual perfusions shows that in 10 hearts exposed to 0.01% CO HR responded in different ways: no response (5 hearts); decrease during exposure followed by recovery (3 hearts); and decrease post exposure (2 hearts). There was a strong association between CO-induced HR decrease and release of creatine kinase into the perfusate, both of which were not prevented by the antioxidants, ascorbate, and Trolox C. Perfusate flow rate declined post exposure (4.9% and 8.9% with 0.01% and 0.05% CO, respectively) and this was prevented by antioxidants. CO may have two, independent, cardiotoxic effects; these may be mediated by CO-induced elevation of oxidant production, H2O2 in one case and peroxynitrite in the other.
Patel
Ashvin P
AP
School of Biological Sciences, University of Plymouth, Plymouth PL4 8AA, Devon, UK.
Moody
A John
AJ
Sneyd
J Robert
JR
Handy
Richard D
RD
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002245:Carbon Dioxide / Q000494:pharmacology; D002249:Carbon Monoxide Poisoning; D003402:Creatine Kinase / Q000032:analysis; D006321:Heart / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D000975:Antioxidants; D002245:Carbon Dioxide; D003402:Creatine Kinase