Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

The aim of this study was to define the status of the myocardium in selecte d human cases of acute, fatal carbon monoxide intoxication and the myocardi al changes in rats exposed to carbon monoxide in relation to the type of ca rdiac arrest and the effects of reoxygenation following pre-fatal CO intoxi cation. The human study consisted of 26 cases (17 accidental and 9 suicide) of acute, fatal CO intoxication, without evidence of obstructive coronary atherosclerosis or history of ischemic heart disease which were compared wi th 45 cases of fatal head trauma in subjects who died instantaneously (26 c ases) or within 1-12 h (19 cases). Inhalation of a lethal dose of CO in rat s was compared with sub-lethal doses plus reoxygenation with and without pr e-treatment by a betablocker. In all human and experimental histological se ctions, changes were normalised per mm(2) area. Tn the human cases the myoc ardium did not show any ischemic types of changes or other lesions. Only in "three accidental" cases a few, small foci of coagulative myocytolysis wer e detected. In the case of spontaneous death in 31 rats following CO intoxi cation, no pathological myocardial changes were seen. Of the 15 "reoxygenat ed" rats, 2 of the 7 spontaneous deaths presented coagulative myocytolysis with 15 +/- 6 foci and 381 +/- 255 necrotic myocells. All the eight rats sa crificed at 3 h had coagulative myocytolysis with 5 +/- 4 foci and 60 +/- 4 7 myocells. Of the 24 reoxygenated rats pre-treated with a betablocker, 5 d ied spontaneously after a short survival and 2 of these showed 11 +/- 9 foc i and 21 +/- 20 myocells. The 19 rats sacrificed after 3 h all presented co agulative myocytolysis with figures of 75 +/- 43 and 356 +/- 301 with 0.5 m g/kg of propranolol hydrochloride and 55 +/- 45 and 253 +/- 216 with 2 mg/k g, respectively.