Abstract
Small doses of NaCN (250 micrograms.kg-1) intravenously injected into normal anesthetized Wistar rats, provoked immediate hyperventilation, bradycardia and systemic hypotension. These effects resulted mostly from peripheral chemoreceptor (PCR) stimulation. In totally baro- and chemodenervated rats (CDN), the drug induced hypoventilation, reduction in O2 consumption, prolonged bradycardia and systemic hypotension, characteristics of direct intoxication. In hyperoxic rats, hyperventilation was reduced. Bradycardia was suppressed with reduction in the systemic hypotension. These modifications arose partly from a reduction in PCR excitability and partly from a direct O2 activity counteracting cyanide poisoning. After chemical sympathetic denervation, rats presented prolonged and enlarged hyperventilation, bradycardia and systemic hypotension due to loss of adaptive baroreflex responses. Cyanide effects are predominantly reflexes in intact rats but these reactions mask the direct toxic effect of the drug which cannot be totally neglected.
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