Bradycardia cyanide exposure

Time to incapacitation for the 100, 102, 123, 147, and 156 ppm concentrations were 19, 16, 15, 8, and 8 min, respectively the relationship between exposure and time to incapacitation was linear. During exposures, effects consisted of hyperventilation (within 30 s), loss of consciousness, and bradycardia with arrhythmias and T-wave abnormalities recoveries were rapid after exposure. The animal inhaling 147 ppm stopped breathing after 27 min and required resuscitation. Two additional exposures were terminated prior to the end of the 30 min due to severe signs. Animals rapidly recovered and were active during the first 10 min after exposure even though blood cyanide remained at levels that initially caused incapacitation. Purser (1984) states that the hyperventilatory response followed by incapacitation occurs at >80 ppm, but neither paper (Purser 1984 Purser et al. 1984) provides the experimental data for the 80 ppm concentration. At 180 ppm, hyperventilation occured almost immediately, and at 90 ppm the response was delayed for 20 min. 

Bradycardia, arrhythmias, and T-wave abnormalities were observed in monkeys exposed to 100 ppm hydrogen cyanide (96 ppm cyanide) for 30 minutes (Purser et al. 1984). Increased cardiac-specific creatinine phosphokinase activity was measured in blood samples from rats 2 hours after 12.5 minutes of exposure to 200 ppm hydrogen cyanide (192 ppm cyanide) for 20 days at 4-day intervals (O Flaherty and Thomas 1982). However, no treatment-related changes were found in the hearts at histopathology. In addition, no cardiovascular effects were reported at necropsy in rats and monkeys exposed to 25 ppm cyanogen (50 ppm cyanide) for 6 months (Lewis et al. 1984). 

Results of in vitro studies suggest an interaction between calcium ions and cyanide in cardiovascular effects (Allen and Smith 1985 Robinson et al. 1985a). It has been demonstrated that exposure to cyanide in metabolically depleted ferret papillary muscle eventually results in elevated intracellular calcium levels, but only after a substantial contracture develops (Allen and Smith 1985). The authors proposed that intracellular calcium may precipitate cell damage and arrhythmias. The mechanism by which calcium levels are raised was not determined. Franchini and Krieger (1993) produced selective denervation of the aortic and carotid bifurcation areas, and confirmed the carotid body chemoreceptor origin of cardiovascular, respiratory and certain behavioral responses to cyanide in rats. Bradycardia and hyperventilation induced by cyanide are typical responses evoked by carotid body chemoreceptor stimulation (Franchini and Krieger 1993). 

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