Hypoxia as a cause of bradycardia during amygdala stimulation in monkey

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Abstract
Electrical stimulation of the amygdala in squirrel monkeys anesthetized with chloralose (6 cycles/sec, 30-60 sec) results in hypertension, hypoventilation, and a bradycardia abolished by va-gotomy. Such stimulation results in a significant fall of mean pH (7.345 to 7.264), Po2 (87.8 to 52.3 mm Hg) and rise of Pco2 (40.8 to 44.5 mm Hg). The bradycardia and hypertension from stimulation are blocked by simultaneous artificial ventilation or tracheal perfusion with 100% O2. Tracheal occlusion produces qualitatively similar changes in blood pressure, heart rate, and blood gases. However, respiratory distress and struggling occur which are inhibited by amygdala stimulation. Hypertension and bradycardia also occur with spontaneous apnea, or with inhalation of N2 but not 9% CO2 or intravenous HC1. The bradycardia elicited by amygdala stimulation in the monkey is a chemoreceptor reflex response to hypoxia induced by the hypoventilation. The amygdala may selectively block respiratory and behavioral but not cardiovascular chemoreceptor reflex responses. This mechanism may serve to adjust blood gases to match appropriate behavior.