Bilateral carotid occlusion (BCO) was performed in pentobarbital anesthetized adult rats neonatally treated with capsaicin (50 mg/kg, sc, CNT rats). Pressor and ventilatory responses to BCO in CNT rats were compared with those of littermate controls injected with a same volume of solvent (olive oil, 0.1 ml). Capsaicin was used in order to produce partial degeneration of unmyelinated C fibres related to baroreflexes and peripheral chemoreflexes. In control rats, BCO provoked in less than 5 s, hyperventilation, hypocapnia and hyperoxia. Systemic arterial hypertension and tachycardia developed more slowly. They were maximum at 65 s. At this time, ventilation was returned to control values. Hyperventilation results from the stimulation of the carotid chemoreceptors by stagnant asphyxia generated by the blood flow stop. Hypertension and tachycardia are provoked by an increase in the orthosympathetic outflow when carotid baroreceptors are unloaded. In a first time, chemoreceptors stimulation tends to oppose to the increase of heart rate in normal rats. In a second one, development of hypertension is autolimited by the stimulation of the aortic baroreceptors particularly effective in rats. Simultaneously the hyperoxic inhibition from aortic chemoreceptors, the central hypocapnia and the reperfusion of the carotid bodies lead to the suppression of hyperventilation. As hyperventilation decreases when hypertension develops, even in rats with vago-sympathetic section at low cervical level, the part of aortic baroreceptors effects is probably reduced except for the fibres travelling through superior laryngeal nerves. Carotid bodies reperfusion seems to predominate. Before any manipulations, CNT rats had lower heart rate and systemic blood pressure than controls. During BCO, initial hyperventilation was moderately prolonged as hypertension slowly developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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Reflex and direct effects of sodium cyanide in anesthetized rats.

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.

Anesthesia↗

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